Cardiology Basics

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Medicine and Surgery - Channel A - 3rd year

Unwinder : Dario Benivegna Matter : Cardiology Date : 03/05/19 code reviewer : Andrea Bolelli Prof : Bugiardini Sbobina : No. 1
Introduction to the course

Recommended books:
• Harrison - Principles of internal medicine
• Braunwald heart disease
• European Cardiology Society - https://www.escardio.org/Guidelines%20 (collection of extremely detailed articles and guidelines both from a clinical and
physiopathological point of view).
• Arrhythmology online course - http://corsoecg.zeronovetre.it/
The professor advises to consult above all the guidelines of the European Cardiology Society if you want to deepen the topics.
Every year in Italy about 270000 people die from heart diseases, followed by oncological diseases (about 160000). In third place are COPDs with around 8000
deaths per year. The "epidemic" of our century is therefore fundamentally connected to two subjects: cardiology and oncology. A third subject is emerging, cardio-
oncology: certain therapies used in the oncology field (for example therapies against lymphomas that lead to survival of the affected patient even at 15 years) are
toxic to the heart leading to heart failure.
ISCHEMIC CARDIOPATHY
The term ischemic heart disease includes a series of clinical pictures that have in common the development of myocardial ischemia, that is, of a suffering or
damage of the myocardial cells consequent to an insufficient supply of oxygen with respect to their metabolic demands.
Myocardial ischemia occurs when coronary flow is inadequate to meet myocardial oxygen consumption (MVO2). [Slide]
The chronic ischemic heart disease is a stable condition in which the patient has coronary stenosis that restrict the flow and consequently lead to hypoxia
cardiac tissue that causes a pain during physical exertion ( stable angina ) that leads the subject to stop from its activities . [Sbobine 2017/2018] Most of the
chronic ischemic heart diseases are subsequent to the acute event: following a heart attack, in which the patient survives, more easily the subject will have stable
exercise angina.
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The acute coronary syndromes lead to death or the possibility of death (90% of acute coronary syndromes is by a broken atherosclerotic plaque).
. They are divided into:
• Unstable angina
• Sudden death
• Myocardial infarction , in turn divided into:
or STEMI or NSTEMI
The sudden death is a condition in which the patient "dies without even realizing it" (the teacher gives the example of a senior who died in bed at night). To know
the cause of the death, an autoptic finding will be necessary, however the chances that the patient died of a heart attack are higher than the other possibilities due
to the incidence of the disease. Another probable cause is pulmonary embolism. The anatomical findings have shown that sudden death is often due to ulceration
of atheromatous plaques that lead to atherothrombosis because after ulceration the platelets cause thrombosis due to occlusion of the vessel.
Sudden deaths are mainly due to silent ischemias, that is, small, asymptomatic, repeated ischemic phenomena that cause chronic ischemic heart disease.
[Sbobine 2017/2018]
Myocardial infarction can be:
• Subendocardial ( NSTEMI - myocardial infarction without over-leveling of the ST tract, therefore with under-leveling of the ST tract or without anything);
• Transmural ( STEMI - with over-leveling of the ST section); it is a heart attack ranging from subendocardium to subepicardium ("ventricle hole").
The infarction of the subepicardium is not present because the conductance vessels, i.e. the anterior descending , the circumflex and the right coronary artery
run on the subepicardium, and send oxygen to the subendocardium through small vessels that penetrate the wall. To make the blood flow move, Bernoulli's law is
necessary, given by the ratio between the pressure difference and the resistances ( ΔP / R) . If the inlet pressure is equal to the outlet pressure, the flow does not
move. Crossing the entire wall of the subepicardium and bringing the blood to the subendocardium means crossing an area of high resistance, therefore it is
necessary to create a ΔP between the subepicardium and the subendocardium. The inlet pressure of the subepicardial vessels is about 100 mmHg, that in the end
will be about 60 mmHg and that of the subendocardial vessels will be around 30 mmHg. This means that the latter region is more vulnerable because "if you close
the switch" [if there should be a stenosis upstream ed.] It is the one that has the least chance of being sprayed so for this reason ischemia always arises from
subendocardium and goes towards the subepicardium. The only necrosis that can start from the subepicardium and involve the subendocardium is the external
one, that is, a pericarditis .
If there is a complete occlusion (STEMI) an angioplasty must be done immediately, if there is an incomplete occlusion, the intervention is not always necessary.
The probability of mortality increases by 1.5% every 15 minutes that pass.
STEMI AND NSTEMI are united by necrosis of myocardial cells. There are increasingly sensitive markers that allow you to identify a necrosis. Troponin high
sensitivity is used today .
Unstable angina , which is characterized by a sub-leveling of the ST tract and pain, differs from the NSTEMI because the former does not cause the release of the
troponin since the coronary artery closes and reopens quickly enough not to cause necrosis, the second yes. The more the sensitivity of the marker increases, the
more the diagnosis of unstable angina decreases and that of NSTEMI increases.
Stable angina affects subjects during physical activity and disappears with rest, chronic ischemic heart disease is more general and also includes silent ischemias.
In the event that the troponins are absent and the STs under-leveled will be a sign of an unstable angina, which affects resting subjects unlike the stable one that
arises under stress, it will be treated as a NSTEMI infarction for therapeutic convenience because the difference is only a little troponin, that is, we have not yet had
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necrosis. [Sbobine 2017/2018]
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[the professor tells of a patient suffering from "hibernated myocardium" who pumped 20% of ejection fraction. The subject had 3 almost totally occluded vessels so
that the heart pumped less to consume less. Following an operation in which the occlusions were removed, the heart began to function normally. This is an
example of chronic ischemic heart disease.]
Silent ischemia is very common. 40% of people do not feel anything before the "black day", that is, the day they feel pain because there is a heart attack. 40% of
people say they had small pains before the heart attack, the problem is that they are hardly pains that are correctly recognized by the patient. 20% have a
completely silent condition, randomly discovering that they have had a heart attack through a visit to the doctor. This occurrence is more frequent in the diabetic for
diabetic neuropathy which softens the sense of pain. Epidemiology
Ischemic heart disease is by far the most common heart disease (number of new cases occurring in a certain period of time in a population) and prevalence
(number of cases affected by the disease in a population at any given time) in developed countries.
In the United States, approximately 550,000 people die from ischemic heart disease every year and the prevalence of the disease is about 13 million individuals. In
Italy, cardiovascular diseases cause about 45% of global mortality, and ischemic heart disease is in turn responsible for 35% of deaths due to cardiovascular
diseases, with an annual number of deaths equal to about 130,000. The incidence of myocardial infarction is around 120,000 new cases per year. The prevalence
of ischemic heart disease in the Italian population is less known, but it is probably around 4%, with a similar prevalence of previous myocardial infarction and
history of angina pectoris. In Italy, therefore, more than 2 million people with ischemic heart disease live in its various forms. [Slide]
The worldwide mortality rate of ischemia heart disease is approximately 8 million people per year, in second place we find the stroke with about 6 million deaths per
year. Below are lower respiratory tract infections and COPD with around 3 million deaths. Deaths from trachea, bronchial and lung cancers are about 1.7 million
(which becomes many more if all types of cancer are considered but without overcoming cardiovascular diseases), those from road accidents are 1.34 million.
The prevalence of acute coronary syndromes increases with age, especially above 50 years of age but this obviously does not mean that heart attacks cannot
occur under 50 years of age. Furthermore, there is a prevalence in men before the age of 50 but, following menopause, in which the protective power of estrogens
in women begins to decline, the prevalence between men and women tends to become equal.
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Risk factors
There are 4 traditional (or Framingham) risk factors :
1) Cigarette smoking 2) Diabetes mellitus 3) Hypertension 4) Hypercholesterolemia
Other "classic" risk factors are:

• Not editable:
o Age (male> 45 years; woman> 55 years) o Familiarity : 32,000 genes are involved in myocardial infarction. It is essential to ask the patient if parents
and / or siblings had cardiac infarction and if so, one must ask if it occurred before the age of 65. If the heart attack happened after 65 then there is no
familiarity. If this risk factor is present, much more important screening tests will be performed. o Gender o Race or ethnicity : Indians develop coronary
heart disease and diabetes a great deal. The Japanese develop stroke a lot, much less heart attacks. It is not yet known what the reasons are. The black
breed is more prone to suffer from vasospastic infarction [Sbobine 2017/2018]
• Modifiable:
o Obesity : particularly widespread in the United States and mainly affects the lower social strata. In addition, obesity also includes traditional risk factors
such as hypercholesterolemia, hypertension, diabetes (or a pre-diabetic state) and possibly also smoking. The indices that can be used to establish obesity
are the circumference of the abdomen (different between men and women) and the BMI which determines whether a subject is obese when he is ≥ 30kg / m
2
or Sedentary lifestyle (goes hand in hand with obesity) : it is recommended, especially in the elderly, to do moderate physical activity, which consists of
20 minutes a day for at least 5 days a week of a brisk walk. o Hormone replacement therapy (for women only): until 1995-1996 hormones were given to
many women who entered menopause because the protective role of estrogen towards atherosclerosis was highlighted. Then there was a higher mortality,
a higher incidence of breast cancer and a higher incidence of deep vein thrombosis. o Polycystic ovary syndrome (for women only) o Gestational
hypertension (for women only) o Gestational diabetes mellitus (for women only)
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o Pre-eclwide / Eclampsia (for women only) : they found correlations without explanation in some studies between these gestational problems and the
onset of ischemia in women. o Socio-economic state : a low socio-economic state very often leads to obesity and to
depression is therefore an indirect risk factor. o Depression : it is prevalent in women. We know that if a person has had a heart attack he goes into
depression has a higher mortality. It is an aggravating circumstance of those who survived the heart attack which leads to an increase in the probability of
death in the post-infarct course. There are many hypotheses. According to the professor, it is linked to the hypothalamic-pituitary axis and to serotonin.
Serotonin is similar to dopamine, it cushions movements. If we pass from the activation of the parasympathetic to that of the sympathetic, dopamine
modulates this step avoiding that there is too sudden a variation. The lack of dopamine leads to a sympathetic rebound which can cause various damages
such as ruptures of stenosis. This is however an unconfirmed hypothesis. o Psycho - social stress o Alcohol [the professor claims that according to him
it is a risk factor handed down and that it is not certain that it can actually predispose to coronary heart disease in small quantities] o Some drugs: they
are the major tricyclic antidepressant drugs that can trigger fatal arrhythmias and can also occur at the coronary level. Some medications used against
breast cancer can induce myocardial infarction. o Hypertrophy of the left ventricle: it leads to an enlargement of the ventricle but not of the coronary
arteries, thus leading to ischemia because not enough oxygen will arrive to "feed" the whole heart. o Nutrition : the incidence of myocardial infarction is:
▪ 150 out of 100,000 inhabitants for France and Italy;
▪ 350 out of 100,000 inhabitants for the United States;
▪ 250 out of 100,000 inhabitants for the United Kingdom. Modern cardiology gives disproportionate importance to nutrition and it is believed that the
Mediterranean diet is the healthiest, nutrition has both a qualitative and quantitative role (it affects both the quality and quantity of food eaten). [Sbobine
2017/2018]
For myocardial infarction the incidence is higher for men (5: 1) but, for the same number of men and women with infarction, mortality is higher for
women by 30%.
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The professor does not mention the risk factors contained in the slides, only mentioning that the ApoB / ApoA1 ratio would seem to be a risk factor within the
aspect of hypercholesterolemia.
As for inflammation, there is no evidence that it is a direct factor in the pathogenesis of atherosclerosis.
• Emerging risk factors:
o Periodontal diseases (dental field). o Reactive protein C (PCR): it is a marker of inflammation, a risk factor for the onset of atherosclerosis, it is assessed as
an index for the presence of atherosclerosis → PCR is indirectly related to heart attack because having high levels exposes it at an increased risk of
atherosclerosis which in turn is a risk factor for heart attack, when trying to correlate PCR directly to heart attack, no results were obtained → Chlamydia was
accused of being responsible for heart attacks and it was done a clinical trial (sub-branch of the TEST-IT), by administering antibiotics the PCR remained
unchanged and therefore the hypothesis was refuted → it was concluded that myocardial infarction is the culmination of many other pathological processes
(atherosclerosis, inflammation and others) . Ridker Trial Jupiter : only subjects with normal cholesterol and elevated PCR were recruited, one part was
randomized and treated with statins and one with placebo, the arm treated with statins had less mortality because the cholesterol responsible for 'atherosclerosis.
[Sbobine 2017/2018]
Heart attack symptoms

The typical pain of the heart attack is retrosternal which radiates to the jaw, sometimes it can also radiate to the limbs, more commonly to the right one.
The first clinical trials conducted on ischemic heart disease up to '98, including those on the use of aspirin, which comprise 1/3 of all the subjects studied so far,
were only men since the incidence in women is lower and this would have lengthened the search time. This, however, led to the death of many women as their
reaction to the drug was not identical to that of men (in women it can lead to cerebral hemorrhage). This is to make it clear that there are biological differences
between men and women.
About 70% of women do not have the typical pain of the heart attack, have a more precordial or sometimes epigastric pain. This is called atypical pain .
Furthermore, it has been seen that women's coronaries tend to open and close more easily than in men, leading to intermittent pain. All this leads to a delay in
hospitalization and these could be a reason for the higher mortality of women. Coronary arteries
The big branches are 3: on the left the common trunk from which the circumflex and the anterior descendant come off, on the right instead the right coronary
arises .
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The weakest layer of the heart is the subendocardium, since the conductance vessels flow into the subepicardium. The anterior descending coronary has many
more branches of the circumflex artery → the occlusion of the anterior descending coronary in its proximal tract (called widow stenosis, as it has a higher
incidence in men than women) causes greater damage than a stenosis in the more distal tract. The intensity of the damage depends on the occlusion point: the
further upstream the stenosis of the vessel occurs, the more serious the consequences will be as the quantity of non-perfused tissue will be greater.
Coronary dominance:
• right dominance, the right coronary arises from a posterior descendant which irrigates most of the posterior part of the heart;
• left dominance, the posterior part of the heart is sprayed for most of the circumflex artery.
It is always preferable that the circumflex artery is closed because it has a smaller spraying area and it is easier to intervene with an angioplasty. [Sbobine
2017/2018] Physiology of the coronary arteries
Conductance vessels: they are conduction vessels, they do not prevent flow except in the case of stenosis. Resistance vessels: it is the sub-epicardial vessels
that bring blood deep. [Sbobine 2017/2018]
Coronary reserve
The maximum vasodilatation capacity secondary to a metabolic stimulus is called Coronary Reserve.
• Epicardial arteries: 5% of total vascular resistance
• Intramyocardial arterioles are responsible for coronary resistance:
o Diameter <300 μm: 95% of the resistance o Diameter <100 μm more than 50% of the resistance
Modifications of the microcirculation can lead to changes in the flow and coronary reserve with consequent ischemia [Slide]
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It has been said that the pressure entering the coronary system is about 100mmHg, at the end of the epicardial resistance vessels it is about 60mmHg and, once
crossed the muscle wall it is about 20-30mmHg. For example, if there was a stenosis shortly after the onset of the coronary artery, there would be a post-stenotic
pressure drop which would cause a reduction in the flow. In reality this does not happen because the resistance vessels dilate making sure that the pressure
downstream of the stenosis is reduced, thus allowing the ΔP to be maintained .
For example, if the pressure at the level of the stenosis is reduced to 80mmHg, the resistance vessels would expand bringing the pressure around 40mmHg, thus
maintaining the ΔP of about 40mmHg. The same would happen at the level of the subendocardium, in which the resistance vessels, dilating, would bring the
pressure around 10mmHg, thus keeping the ΔP more or less constant. This determines an almost total use of the coronary reserve at rest, so in case of physical
effort the vessels could not be further dilated, thus preventing correct oxygenation. In fact, during exercise, in physiological conditions, the pressure increases a lot
to ensure correct perfusion. However, if the coronary reserve is exhausted, there is not an increase in pressure sufficient to allow correct oxygenation, since the
resistance vessels are fully dilated.
Reverse Robin Hood phenomenon [Sbobine 2017/2018]
If vasodilators are administered for resistance vessels (amlodipine, nifedipine, verapamil, adenosine) their pressure drops from 40 to 0 mmHg, the ΔP rises from 40
to 80 mmHg, consequently the flow increases (Bernulli's law) but does not enter the endocardium ( coronary theft ), the patient has pain.
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Myocardial scintigraphy is based on this principle, adenosine is used to create theft, adenosine does not tachycardise. This system works for large stenoses where
the coronary reserve is very compromised, for medium situations it does not work, adenosine manages to create theft and ischemia detectable by the scintigraphic
method, with adenosine a less sick population is selected than that detectable with an exercise test. If the scintigraphic operator does not specifically ask for the
stress test he will do adenosine.
Concepts to remember: heart attack affects men more than women (ratio of 5: 1), but mortality is higher in women for two reasons: delay in hospitalizations and atypical infarct
pains (left precordial area or breast and epigastric area) .
It should be remembered that acute events mean NSTEMI, STEMI, unstable angina and sudden death.
CAUSES OF MYOCARDIC ISCHEMIA :
• Coronary stenosis : development of stenosis in epicardial vessels due to the presence of atheromatous plaques. However, it must be remembered that stenoses in themselves
do not justify the acute event. When you have patients with valvulopathies, what you do in medical practice is also to look at the coronaries and it can happen that however injured,
the patient may never have had a heart attack. This is due to the mechanism put in place by the heart that compensates by going to take advantage of the coronary reserve. So it
must be remembered that stenosis is certainly important, but alone is not enough. From the years '95 -'96 the idea that the main pathologies are connected to atherothrombosis
takes hold. From this we deduce that even a plaque that occludes by 50%, like one that occludes by 90%, can give thrombosis.
• Coronary thrombosis : thrombus in the epicardial branch and subsequent occlusion in the vessel lumen due to plaque rupture. Various therapies have been implemented for
coronary thrombosis, first of all thrombolysis (drugs in the vein to dissolve the thrombus). You will see below what the condition is for thrombolysis, when choosing angioplasty and
when doing both.
• Dysfunction of the coronary microcirculation : structural and / or functional alterations of the resistance vessels which alter their vasodilatation capacity, with consequent
reduction of the coronary reserve even in the absence of stenosis of the epicardial vessels. Today it is constantly talked about and it is a condition to keep in mind because it is
there but you cannot see:
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from coronary angiography (with a catheter one puts contrast medium in the coronaries) only the epicardial vessels are seen and not the microcirculation and every time a person
has a heart attack, even young, he can have normal coronaries. In fact, if angiography is done and nothing is seen by exclusion, it can be deduced that microcirculation is the
cause of the problem, but it cannot be demonstrated. It could also be spasm, but in that case you should take a test that can rule it out or not.
There is a phenomenon called " no reflow ": a patient arrives who has a stenosis but, although it is removed, the blood does not flow and the patient dies despite being given as
many drugs as possible. If the blood does not progress, whatever the cause (which can be multiple), there is something that in the microcirculation does not work. We do not know
what can determine it but we go by deduction because we do not see anything in the coronaries. It is not known how much this phenomenon impacts in the current clinic. For
example, women have a more insufficient microcirculation (and perhaps this may explain why they die more than men for the same heart attack). So it must be remembered as the
cause of ischemia.
• Coronary artery spasm : vasoconstriction of a segment of one or more epicardial coronary vessels and subsequent total or subtotal occlusion of the vessel lumen. The first to
hypothesize it was Dr. Prinzmetal in 1959, who described the variant or Prinzemetal angina. Until 1959 there was a clear idea: patients who underdeveloped had angina (there was
no troponin or markers), if instead they overdeveloped it was heart attack. Prinzmetal, however, described a series of short-lived angina (especially at night and in the early hours of
awakening) which, in conjunction with the pain, overturned. He then described it as a variant of angina and hypothesized that it could be due to a coronary spasm that closes the
coronary artery and then reopens. Coronary angiography is introduced after about 16 years (1975) and is done on patients who have been diagnosed with Prinzmetal's angina.
These individuals had coronary artery spasm during the examination and in fact showed coronary artery which suddenly closed and coronary artery spasm was confirmed. Today,
however, it is known that if a person suffers from Prinzmetal's angina, he may not have spasm during the examination, therefore after describing the symptoms, the doctor could
test the provocation: give a vasoconstrictive substance that goes to provoke him that in the past it was ergonovine (which was given during childbirth to reduce uterine bleeding at
increasing doses), today acetylcholine is given which acts with a single dose. In general, however, unfortunately these tests are not done or are done badly, either for a short time,
or for fear. It is very wrong because if a spasm is diagnosed, it can be treated with a Ca-antagonist drug.
Example of plaque occluding 30% of the vessel.
Glagov's Coronary Remodeling Hypothesis
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Until the 1980s, atherosclerosis was thought to be a progressive phenomenon and it was thought that there was no atherothrombosis. So there was the idea that the plaque
progressively grew to completely occlude the lumen of the vessel and then triggered the heart attack. Today it is known that this is not the case, because there are collaterals that
grow progressively to hypoxia.
Thus a gradual occlusion is thus compensated with the neoangiogenesis that forms the collaterals. Precisely for this reason, studies were carried out in which it was thought
possible to create products that induced neoangiogenesis to reduce mortality, but they were blocked because complications such as prostate cancer had appeared.
In fact, anti-angiogenetics are used today to block tumor metastasis and therefore are used for cancer therapy. Therefore, a sudden occlusion can lead to a heart attack, while a
progressive occlusion can be paradoxically better.
Atherosclerosis does not necessarily occlude the lumen, but expands towards the adventitia and when it is completely extended and there can no longer be any positive
remodeling towards the adventitia, the occlusion of the vessel begins.
Through a catheter and the echo one can notice atherosclerosis in which the atheroma does not grow towards the lumen but towards the adventitia.
Comparing the images of the coronary artery it can be seen how this is normal at angiography while the adventitia thickening is evident on intravascular ultrasound, while the lumen
will not be narrowed.
VULNERABLE PLATE
In the years '95 -'98 the term vulnerable plaque was introduced and Valentine Fuster was one of the pioneers.
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Plaques are present in most individuals that are not as likely to break.
If an angiography is performed to evaluate aortic stenosis, coronary arteries are also observed.
When replacing the valve with a catheter it is important to make sure that there are no plates otherwise after having replaced it with TAVI (transcatheter portico valvular implant), in
the event that an accident occurs at the coronaries it would be difficult to pass the mesh of the implant.
Plaque composition is important but also stressful factors and positive modernization.
From the diagram it can be seen that most of the infarcts occur for stenoses of less than 50% but this is not strange because it is important to evaluate the evolution of the plaque.
The pimple is an example. When there is a pimple at the beginning it hurts, it burns and if it is stressed the pus comes out, but after two or three days, which in the case of plaque
also equate to years, if it does not break it becomes harder and even if it is stressed it does not break.
If the plaque thickens and the lipid core comes out, the platelets are activated immediately which will subsequently lead to the formation of the thrombus and occlusion.
Determinants of plaque rupture:

- Atheromatous core size - Thickness of the fibrous cap - Inflammation and remodeling of the plaque
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Källtextthat the plaque has reduced and
In this image it can be seen how the lumen of the coronary artery one year after heart transplantation has increased. From this it can be deduced
that atherosclerosis is not an irreversible phenomenon. Until 2001 it was thought that arteriosclerosis could only slow down and stop but that Dal
it could not regress.
diagramma si può notare come la m
abbiano per stenosi inferiori al 50% ma
importante valutare l’evoluzione della pla
Bidra med en bättre översättning

Nissen through this simple experiment shows that by changing the host the atheroma can decrease.
In addition to the reduction of atheroma, an increase in echogenicity can be seen in the second image, which is due to the reduction in the amount of cholesterol in the plaque.
Statins allow the reduction of cholesterol and the hardening of the plaque, decreasing the probability that it will go to break.
Plaque cap
It is essential to consider the plate cap that gives stability. A thin hooded plaque is vulnerable. The amount of cholesterol in the plaque is also important but the cap is even more
so. However, the amount of cholesterol present can be reduced. but it has been a failure. These are difficult to locate
We have tried to intervene only on vulnerable plaques
also because the images are not always clean and there are difficulties of interpretation. Fundamental was the introduction of statins that allowed to make plaques passive.
The first image indicates a stable plaque: the fibrous cap is thick and the amount of cholesterol is minimal; in the second
image you can see a thin cap, a significant presence of cholesterol and the breaking point of the plaque that leads to acute
coronary syndrome is also visible.
To highlight this vulnerable plaque, OCT (computerized optical tomography) was used. In these cases it is possible to intervene through angioplasty or by applying a stent.
The stent, however, does not always solve the situation: stent disease can occur as these iron appliances stimulate the proliferation of the intimate.
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OCT by ophthalmologists can be used easily to perform operations on the retina.

The CT scan enlarges up to 250 microns, the intravascular ultrasound up to 100 microns while the OCT up to 10 microns: it is like using a microscope.
For the ophthalmologist, the use is simpler because the device goes into the aqueous humor. Inside the vessels, on the other hand, there are red blood cells that if they are
affected by infrared rays, nothing can be seen. A balloon is inserted into the vessel which is inflated to the point of preventing the passage of the red blood cell, after a splash of
water the image is taken and the vessel can be clearly seen.
It is used in Japan very often especially to see the initial proliferation of stents so that it can be blocked
There are many limitations in this technique. The plaque cannot be totally visualized as in the intravascular ultrasound, with this technique it can be deepened to a maximum of 2
microns and in most cases only the cap of the plaque can be seen.
Intravascular ultrasound
It is a more specific exam, the use of which is however highly selective because of the times (twice the time is necessary) and the costs. IVUS is an intravascular ultrasound
method that is carried out using a special microcatheter inserted in the coronary object under study. It allows to measure the residual coronary lumen, and therefore to confirm the
criticality of a stenosis highlighted at angiography, to perform a tissue characterization of the plate and to accurately measure the dimensions of the vessel, so as not to
underestimate or not to overestimate the dimensions of the stent to be implanted.
Vulnerability of the patient
A vulnerable plaque is often associated with patient vulnerability factors:
- familiarity: a patient who is familiar is by definition vulnerable; - hypercoagulability: it is not easily identifiable, it is a big problem not so much in determining the probability of
heart attack but how much in the cure; - stress: not calculable but of great importance. The relevance of this factor can be highlighted
through a study conducted about 15 years ago on the diet / heart attack relationship.
With an incidence of heart attack in the USA of 300/100000 inhabitants, in France and Italy of 150/100000 inhabitants and in England of 250/100000 inhabitants, there is a clear
discrepancy between countries with a balanced (Mediterranean) diet and countries with a incorrect feeding. However, it is also evident that, with the same incorrect diet, the
incidence of heart attack in England is much lower than that of the USA, therefore the stress factor must be taken into consideration.
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BLOOD PRESSURE
The American guidelines have set the reference values at 120 on 80 mmHg, which means that almost all of us are hypertensive. Why was it done? There are those who say that
there has been pressure from the pharmaceutical industries, others say that there are scientific data that show that the lower the P values, the more the cardiovascular risk is
reduced, there is much confusion about it.
In Italy a person is defined as hypertensive if he has blood pressure values equal to or greater than 140/90 mmHg.
When measuring the pressure to a patient in the clinic it is good to take the measurement at least 3 times at a distance of 5 minutes, as higher than normal values could be
detected (which are transient) due to the emotion of the subject. At the limit, the pressure holter is recommended, an instrument that takes the pressure every 10 minutes: with
more than 40% of abnormal pressure values, the patient is hypertensive.
The values between 140 and 149 are borderline, it is necessary to evaluate how to proceed according to the patient (e.g. ACE inhibitor therapy in an elderly person who has
vessels with a stiffened wall per se leads to an increase in differential pressure, with normal diastolic and a slightly increased systolic).
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DIABETES MELLITUS
Diabetes is referred to if fasting blood glucose is equal to or greater than 126 mg / dl or with glycated hemoglobin equal to or greater than 6.5%.
Diabetes mellitus has been defined as "Coronary Arthery Disease Equivalent", this means that 100% of diabetics have coronary artery disease, of which 65% die from
cardiovascular disease.
It follows that diabetic subjects should be treated as patients with coronary artery disease.
The first goal is to bring the glycated hemoglobin below 7% and keep the blood sugar normal.
For the primary prevention of coronary artery disease, statins are used (they have a powerful anti-inflammatory effect, preventing the development of coronary artery disease,
however they have side effects especially at the muscle level due to their action on the mitochondria) and aspirin.
Studies of recent years, however, have shown that aspirin does not work in diabetics (no reason is known), therefore these subjects should not be given this drug, since they would
risk having side effects unnecessarily.
Aspirin, statins, Ace inhibitors and beta blockers are the drugs to be administered for therapeutic purposes.
LDL CHOLESTEROL
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In a normal person it should be <160 mg / dl. The LDL cholesterol value is taken into account rather than the LDL / HDl ratio, as HDLs, however high they are, cannot compensate
for high LDL levels.
In subjects with high cardiovascular risk (for example who have had a heart attack or diabetics) it must be <100 mg / dl.
In patients with very high cardiovascular risk (unstable angina, NSTEM, STEMI) it must be <70 mg / dl.
INFLUENCE
Influenza is certainly a triggering event for coronary artery disease, therefore the flu vaccine is recommended, especially for subjects over the age of 65 or who work in a hospital
setting.
The risk of AMI and stroke increased approximately 4 times after a respiratory tract infection, with higher risk in the first 3 days.
Annual influenza vaccination is recommended in patients with documented cardiovascular disease
ECG, Stress Test and SPECT

In the initial speech, the professor explains how he makes himself available for extra activities (cardiac ultrasound, ward visits, electrocardiography
lessons), by writing an email in advance so that it can be organized (which our representatives will think of with surveys, coordinating with channel B
and avoiding a myriad of emails). ECG
When you look at an ECG you have to look at it all, because we are always attracted to the thing that we believe is most important (for example, if
there is an elevation of the ST section, you only look at that and you think it had a STEMI, but maybe there is even a third degree atrioventricular
block and the patient dies of heart failure instead of a heart attack, because the block stops
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the transmission). We start from P, then PQ, QRS, ST and T (the U if there is or is not there does not
change, we remember that there can be), then we look at the transmission speed, that is, the heart rate
. Wave P.
It is the wave of atrial depolarization. A non-normal P can only be of 2 types:

● Pulmonary P from right atrial overload;
● P "double hump" from left atrial overload.
The most classic example in which you can have a P from right atrial overload is pulmonary embolism: an embolus starts from a deep vein
thrombosis in a bedridden person after 55 years (very frequent condition, perhaps after a hip surgery ), the embolus goes into the veins and reaches
the lungs; if the embolism is massive you can die (mortality higher than the heart attack but lower incidence). The right atrium is overloaded and the P
becomes sharp (pointed) and high (more than 2 squares, that is more than 2 millimeters). The most classic example of left atrial overload is mitral
stenosis (more common in rheumatic disease that is now disappearing). This stenosis closes the mitral ring, therefore the blood from the left atrium
does not go easily to the ventricle and stagnates in the left atrium giving overload. The most typically described P is "double-humped" or biphasic
(camel), because by overloading the left atrial component, there is no more contemporaneousness of left and right atrial contraction and therefore a
dissociation between the 2 atria comes out. The question would also be when overloading to the right you should have the same thing; in that case
first we have the left atrium, that is the abbreviation (which we will then find in the paradoxical wrist and in many other things) is AP, first closes the
aorta and then the pulmonary; if it becomes PA, the question is crossed. With AP the aorta has overloaded so it is seen first (we are talking about
closing the aortic valve but the whole system works like this) then with the single pulmonary P because with its height it incorporates the other and
becomes unique. (note from the reviewer: this is the speech he gave in class, I think it meant that we do not have the double hump in the right atrial
overload, because the greater amplitude is as if it "hides" the dissociation of the contraction of the two atria, but only he knows what he said) . Very
easy to see the heart attack and at the same time a left atrial overload because the heart has collapsed. All this however, is seen in all derivations, it
is not relative to one; in one derivation you can see well, in another less, but you will always find a point where you see well. PQ
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The PQ interval must be between 0.12 and 0.20s (3 to 5 squares). If it goes beyond 0.20 (over 6 squares) there is a first degree ventricular atrium
block and it is already not normal. If, on the other hand, it is too short, like 0.8s (2 squares), there is a ventricular pre-excitation. It often happens in
young people whose tachycardias start and end suddenly, especially in the female sex. ST This in heart attack. Here it is
is the trait mentioned
isoelectric, i.e. by pulling a line, it is noted that PQ is at the same height as ST. If it goes down, there is a sub-leveling, a sign of myocardial ischemia;
if it goes up it is a sign of subepicardial or transmural ischemia (elevation). Wave T
The T indicates ventricular repolarization, which is normally, except in aVR (as well as the P wave), positive; in some cases it is negative, it can be,
but not always, a sign of ischemia, pulmonary embolism, stroke or other diseases. So an abnormal T suggests something . QRS
The QRS must be 0.08 seconds, if it spreads there is something: left bundle branch block, Wolff-Parkinson-White pathology.
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On precordial derivations, as the heart "shows" its left side, V1 and V2 manage to look a little to the right, therefore they have a negative deflection.
The electrode lets itself be influenced by the vector: if it "sees" the vector going towards it, it goes up making the R, if it sees the vector moving away,
it makes a Q. The vectors are 2 because they depolarize the left and right ventricle, therefore the the electrode gives the signal of what it sees most;
the left ventricle is large, the right ventricle is small, one vector will be 5 centimeters maximum, the other 2.5, the vector that influences it the most is
the left, unless its position is no longer addressed to right than left, at this point it is influenced more by the vector that comes towards it, more
inferential towards the right. On V1 and V2 that let themselves be influenced more by the vector that goes to the right, the difference is more to the
right than to the left, so much so that you see more of the S than the R. As you move in the precordial ones up to V6, the left ventricle is seen more,
there is only a small part that will concern the right ventricle and therefore in this case QR has a nice big R. The negative deflection if it falls before it
is called Q, if it falls after it is called S.
For the limbs there are D1, D2, D3, aVR, aVL, aVF. In the AVR it must be with a negative deflection; the only pathological condition that can justify a
positive one is ischaemia of the common trunk (but the patient is dying because it is a deadly thing). D1 and D2 are mostly positive R, D3 too,
however it can be influenced by the electrical position of the heart, that is, if the diaphragm rises a lot, the heart becomes more horizontal and
changes as the electrodes of the feet "see", which they see plus the face behind. The aVF is that of the feet: it normally sees the left ventricle very
well. If the diaphragm rises to a horizontal position, the heart moves by rotating and changes its position, therefore from the feet, the right ventricle is
seen and has a negative deflection. So a D1, D2 with R and a D3 with an RS that is not Q, when there is Q there is something wrong, a big mess is
coming, like a heart attack. ( reviewer's note: I leave the interpretations of this speech to you, he said it would explain better in the extra lesson on
electrocardiography) . The R therefore in aVR is negative, aVL and aVF are usually positive, but sometimes aVF is negative, the same goes for D3,
however R is always there, because if you do not see the R, we are facing something serious, or a heart attack (if there is no elevation, it is prior).
Heart rate
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It is easily calculated with the quadratons, with 5 quadratons it is already at 60 beats per minute. This allows a very easy and quick reading of the
track, which is very important when there is an emergency in which it does not matter to be precise. The 2 pathologies related to altered frequency
are tachycardia and bradycardia. The normal resting frequency is between 60 and 100. If the heart beats at 99, it beats strongly but is not sinus
tachycardia. An athlete can also go to 42, in this case it is not synonymous with bradycardia. There are famous personalities from the past such as a
famous French cyclist who had a frequency of 42 at full ascent in the Alps, so it is clear that many factors can play a role in frequency. It is necessary
to have points of reference to carry out studies to understand if the patient is in bradycardia or sinus tachycardia; studies must always be done,
although in the end it could be concluded that this patient is too nervous. Medical art is needed when something goes outside the box, the computer
is useful, but it cannot make a diagnosis. Rhythm (says he has already mentioned it)
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Cardiac axis (read the slide)
The right axial deviation can be due to right ventricular hypertrophy, the left one to left ventricular
hypertrophy, but also to aortic stenosis: by closing the aortic valve the heart has difficulty pumping and
hypertrophy.
We will see the axial deviations on the field.
Normal basal ECG
You have to look at everything from the P wave. Is there a more horizontal deviation (when the diaphragm comes up), because D3 has a small R (but
there is!) And a Q ? (note from the reviewer: I would say S, but here too, I leave your interpretations) much more marked. FP measures 4 squares
then 0.16. We start counting from the beginning of the P wave. The R rises more and more from V1 to V6 and the intermediate elements V3, V4 are
transitional, that is balanced between R and S. It is very important, because when they are found flattened, where there is no transition anymore, it
means that there has been a heart attack.
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Stress test
It is done in young people in the case of competitive sports and should be indicated in the suspicion of coronary heart disease, that is, typical or
atypical chest pain (not if there is a heart attack in progress). When there is a doubt, one must always check. Many old general practitioners do not
ask for the stress test, but continually ask for ultrasound: if the coronary artery has not closed, nothing can be seen with the ultrasound. When faced
with the suspicion of angina, the first test to be done is the stress test. By asking for an ultrasound you only end up clogging the waiting lists (at
Sant'Orsola the waiting list is 11 months). Heart failure derives from heart attack most of the time, heart failure that does not depend on heart attacks
is yes and no 10% (an example is dilated heart disease). The more infarcts not treated immediately, the more there will be decompensations, there
will therefore be an increase in this reflex pathology which will then lead to an excursus of 5 years on average. When the stress test request is made,
civil and criminal liability is assumed together with the operator who performs it. If a person has ischemia, it can happen in one case out of many, that
goes to ventricular fibrillation, falls from the cycle ergometer and can also go against death if you do not intervene immediately with the defibrillator
and when the investigation starts, the public prosecutor's office he also calls those who made the request, for this reason many doctors are afraid to
request this test, but it is essential to act as quickly as possible. Exercise testing is therefore very important, because it is one of the ways to find out
that there is ischemic heart disease. If you see a ST segment sub-leveling with chest pain (sometimes even sub-leveling), you understand that the
coronary arteries are ill and refer the patient to angiography immediately, in order to identify the problem. Clinical indications
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Some indications are quite obvious. Angiography is done to a patient with suspicion of angina who is positive for the stress test. Post-IMA (acute
myocardial infarction): what happens? Will they do primary angioplasty at all? Not all of them arrive on time, there is a 12-hour limit and 30% of the
sick arrive after this limit. After 12 hours there is the blockage to be able to carry out both thrombolysis and angioplasty. What remains possible is to
calm the patient, put him to bed and treat him with supportive drugs. The severity of the heart attack, whether it deserves intervention or not, is judged
by a stress test before discharge. This is especially true for non-STEMI heart attacks, about which literature is still debating whether to do the surgery
or not. Instead as regards the stable angina ("the subject does 100 meters then feels pain and stops, then starts again and does another 100 meters
before stopping again etc ...") you want to avoid doing the surgery: it is the patient with the medicines and to verify that these have had a positive
effect is done the stress test, comparing the results with those before the treatment. The professor loves the ergometric test by bicycle.
Stress test for preventive purposes An effort test is made every year after a certain age, if you are overweight, if you are diabetic, if, in
general, the risk factors occur. It doesn't have to be screening: about 20 years ago there was an attempt to use it as a screening, but the cost was
enormous. The test was for all men> 45 years old and women> 55 years old. However if you have 2-3 risk factors (smoker, hypercholesterolemic,
hypertensive ...) or familiarity (death of my father from a heart attack) you should undergo the effort test.
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Contraindications
There are contraindications to ergometric tests, among which some must be highlighted, although they may seem very obvious:
● TWO DAYS AFTER AN INFARCTION (Obviously the stress test immediately after heart damage is not recommended, if the subject is diabetic,
therefore equivalent to one with coronary heart disease, the stress test should not be done after 48 hours but after 3 days that it is completely
asymptomatic (as indicated by the American guidelines drawn from the studies of?); the diabetic must be treated with suspicion. The same is true for
the man over 75 years, who must be very stable. In these two cases the precaution must be greater than 48 hours. This is the doctor who has to say
it, not the executor)
● UNSTABLE HIGH RISK ANGLE (The first fundamental rule, as mentioned before, is never to send a patient to do an exercise test if he has had a
form of ailment such as dyspnea, suspicious pain in the last 48 hours (in hospital protocols he is often mistaken : when a person has pain and has
negative troponin, one can immediately think that he does not have a heart attack and to be sure the stress test can be requested after 12 hours, but
fortunately it cannot be done if not waiting at least a week; if the troponin did not rise could be unstable angina, therefore after 12 hours, provoking a
discharge of catecholamines as the stress test does, on an ischemic lesion means putting the subject in conditions of having ventricular fibrillation).
● MAJOR ARRHYTHMIA (In fact, a person with ventricular fibrillation "resurrected with a good defibrillator stroke" cannot be sent for the stress test)
● HEMODYNAMIC COMPROMISSION (such as after acute pulmonary edema)
● SEVERE AORTIC STENOSIS
● HEART RATE
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● SUSPECTED HEART TUMORS (So rare as to be unsuspected, but masses can be noticed by doing routine ultrasound)
● DISEASES: MYOCARDITIS, PERICARDITIS AND ENDOCARDITIS
● PULMONARY EMBOLIA AORTIC DISSECTION (When talking about the diagnosis of chest pain we will focus on the differential diagnosis
of the dissecting aneurysm of the thoracic aorta, we will analyze it with the eye of the cardiologist, taking into account that if a patient has a
spontaneous aortic dissection every hour that there is a 10% less chance of survival due to the failure to carry out plastic reconstruction of the aorta,
which means that after 10 hours we can speak of walking dead). Techniques
There are 2 of them:

● Treadmill, treadmill, in which the "Bruce protocol" is followed, which is of different types according to the number of phases;
● Cycle ergometer, with workload that increases by 25 watts every 2 minutes.
In Italy the treadmill is most used ( the professor prefers the cycle ergometer but has both). There are now 7 speed levels in the treadmill. The risk is
that 75-year-olds fall from one level to another because the effort is not well built. In the cycle ergometer you get tired after a while, but there are no
trauma problems.
The test is done for diagnosis and should be done again to see if the therapy is working, whether you have given medicine, or if you have put a stent:
after 6 months you want to see if the ischemia has dropped (for example if before it did 100 watts on the cycle ergometer, now it does 150). When
someone knows they have heart disease followed by an intervention, they diet, then lose weight. On the treadmill, the effort is proportional to the
weight: thin and young people are quick because they weigh less, so the effort is less. On the cycle ergometer this problem is mitigated, you are
sitting and only the legs move. The reason why according to the prof is preferable to the test by cycle ergometer is that if you take a patient who has
had a heart attack, you treat him with medicines and you want to monitor him through the stress test, usually after 1-2 months , this man in the
meantime will probably have lost a lot of weight: if he was obese before the heart attack he will now lose weight and for fear and paranoia he may
have lost up to 20-30 kg. This difference in weight greatly influences the effort made by running, while it affects much less, being muffled by the fact
that you are sitting, in the effort to the exercise bike.
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Parameters to be evaluated
They will also tell us when the stress test is to be stopped. There are some standard parameters to always monitor during the stress test: we must follow the
ECG, the HEART RATE, the ARTERIAL PRESSURE, the SIGNS AND CLINICAL SYMPTOMS: it is important to remember that it is not enough to monitor only the
ECG.
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In theory, a subject doing the stress test should be pedaled, up to the theoretical maximum frequency that corresponds to 220 minus the age (for
example, a 60-year-old man should reach the maximum frequency of 160). However, a frequency of 140 can also be satisfied ( The theoretical
FCmax is a useful measure to estimate the adequacy of the test to evoke an inducible ischemia: the achievement of 80% of the theoretical FCmax is
considered a good diagnostic result and the achievement of 90% of the theoretical FCmax is considered an excellent diagnostic result ). If the doctor
who requested the stress test reads "negative" the first thing to do is to check the frequency: if it is 90 beats per minute, it means that the subject has
stopped running immediately, the test is unreliable, it must be remade; if you read negative you are influenced to think that he is fine. It is practically
impossible for someone to go into ischemia at even 80 bpm: that patient could still have large occlusions. But many stop without checking the
frequency again. One must know how to distinguish true negatives from possible false negatives because the results were not significant. The ceiling
is of little importance when in any case such a target heart rate is reached (oxygen consumption is not given by the pressure, but by the frequency),
at 140 you can already see something. We must therefore be wary of the word "negative stress test"; it cannot be declared negative when the subject
has not reached an acceptable frequency or to be perfect, maximum, with respect to his age.
Another key point is chest pain. The pain itself, regardless of an electrocardiographic sign of sub-leveling, is a reason for interrupting the stress test
which will therefore be positive. If there is a global ischemia, the electrocardiograph does not see it. The largest possible occlusion is that of the
common trunk (often causing death) which gives ischemia on everything; it is therefore very probable, not certain, that if a subject experiencing pain
during the stress test, not associated with any electrocardiographic sign, could have a common ischemia of the trunk . We have already talked about the
AVR saying that it must always be negative and that if it goes up there are two possibilities: inverted electrodes or occluded common trunk (the one from which the
circumflex and the interventricular (or anterior descendant) start. We also said that all ECG alterations are the result of the comparison between healthy tissue and
ischemic tissue, that is, they reflect an imbalance. But if the ischemia is very large there is no such imbalance: with not total occlusion of the common trunk, that is
up to about 80%, we may not see any changes in the ECG, even if the patient feels pain.
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Silent ischemia is therefore not uncommon. Someone feels something before the heart attack, about 4 out of 10. You can start to see that the ST tract
goes down even if the subject is well. In this case, we stop immediately, as per the guideline, because there is an ischemia and one should not want
too much when the proof of positivity has already been obtained . Therefore another interruption parameter is a frank ischemia of 2 millimeters visible
with the electrocardiogram.
Interruption is also important for blood pressure for several reasons:
1. In order not to cause damage to the patient's brain: if the systolic pressure exceeds 220 mmHg, as the cerebral arteries are tense, it is better to
stop; the rule for the interruption is actually 250, but it can already be stopped at 220 being a good level of intracranial pressure; 2. Whenever a
passage is made (such as from 25 to 50 watts) during the stress test, the pressure, not only the frequency, increases progressively; if the pressure
falls it is because it is going into ischemia, then the heart begins to lose strength with the systolic range and clearly the pressure no longer rises. If
the pressure drops, the stress test must be stopped because the patient is going insufficient, it is a sign of silent myocardial ischemia, also not
visible with the electrocardiogram.
When you do the stress test on patients you will always be two: one checks the pressure, the other the ECG trace on the monitor. You need to know
when the stress test should be stopped and why.
If a cardiac arrhythmia appears during an exercise test, be it a trivial atrial fibrillation or a ventricular tachycardia for which you can die, you must stop.
The situation can have a negative prognosis and you risk death shortly thereafter, or you must give him a defibrillator discharge . The DOUBLE
PRODUCT, included among the hemodynamic parameters to be evaluated , has been an almost abandoned invention. We wanted to calculate
oxygen consumption by multiplying heart rate by blood pressure. In reality, it serves almost nothing, because the real oxygen consumption is basically
given by the increase in heart rate. As already mentioned, along with blood pressure, perfusion also increases, and this is a positive effect, but there
is also a certain risk of overload (negative effect), called "heart afterload".
You should never ask patients to put too much effort: if the subject complains, even if not because of chest pain, when he says "I can't take it
anymore" you have to stop. You should never put a person to the limit of his physical condition because he puts him at risk. Discontinuation criteria
include lower limb cramps and claudication. Others are bundle branch block or BAV (atrioventricular block). Sub-leveling of the ST section
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There are three types of alterations:
● Downsloping, go down;
● Horizontal;
● Upsloping.
The possible different forms of the st tract in the ECG tracing are:
● NORMAL
● QUICK ASCENT (Not too different from the isometric)
● HORIZONTAL
● SLOW ASCENT (Upsloping which remains underdeveloped anyway)
● DOWNSLOPING (In this case the patient is immediately sent to angiography because it is useless to wait when the situation is critical. When there
are strong downsloping, of 3-4 mm, perhaps for efforts associated with a heart rate of 150 bpm, you must immediately send in angiography).
When the ST segment is downsloping or horizontal it is a very serious, very severe ischemia, an angiography must be done immediately. The
problem is upsloping: when going to a high frequency it tends to form an under-leveling and must be measured from point J which is 2 squares that is
0.8 from the fall of the QRS. The guidelines indicate sub-leveling already at 0.5, at 1 it is certain.
It is difficult to do the stress test well. The British have a particular system, they just want a certain type of product from abroad, they don't need to hire
people from abroad; the first year they lock you in a room because they want to see your brain: to create a brain that can do research. By staying in
the clinic for 4 months to do ultrasound you learn to read it because it is technical, developing a brain is much more complex. After that year, you start
with the unique exercises, for example, doing only stress tests. Once there were no computers so there was a lot of interference on the tracks and
you couldn't see anything. Then came the computers that go to clean the interference if they are decent and a well-made drawing comes out, but if
the track below is not done well, the computer does not recognize anything. From here we understood the need to thoroughly clean the area where
the electrodes are positioned, remove all hair; in women there is a strong anatomical difficulty in placing the electrodes which makes everything more
difficult, a retina is put to make sure that while running the electrodes remain stuck. It is important to know how to put on the exercise electrodes
otherwise you will not see anything. In women, therefore, it is more complicated, therefore it is necessary to decide what to do to a woman with the
suspicion of angina: it is better to go directly to the scintigraphy without going through the stress test, so much the sensitivity and specificity of the
stress test in a woman is of the 50%; in men it reaches 65/70%; with scintigraphy we are around 90%. Scintigraphy cannot always be done directly
because it costs money. In all systems, not only the Italian one, it is preferred to pass, apart from the case of women, for the stress test.
When you have an ascendant, the doubt can remain if it is not clear, therefore whether it is a man or a woman, it is better to do the scintigraphy as a
second investigation because the path is suspect but not definitive. The difficulties are to understand if and how much the st tract remains
underdeveloped: sometimes the underdevelopment is minimal and it is not known if it is only an artifact or the patient is really ischemic. If the fact that
the patient has felt pain is associated with the upsloping ECG then he is ischemic, but if he has not felt anything, the result cannot be judged and the
scintigraphy must be requested.
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In the concept of stress test there should be no elevation, but the inventor of the Prinzmetal variant angina identified it by doing these things,
identified it by doing these tests , at that time there was no angiography and saw that instead of having an under-elevation, it had an over-elevation,
the coronary spasm with effort, therefore giving an over-elevation. (I report also how the professor explained it: “at that time there was no angiography
and instead of having the sub-leveling it had the leveling, so in fact they are the ones we trigger that are rare, it is the coronary artery spasm that
makes the leveling "). The possible ALTERATIONS OF THE ST SECTION are above all sub-levelings, since the "poor" state, the subendocardium,
always suffers first. So a transmural infarction with elevation is very rare and do not observe it unless you whip the patient to continue pedaling
beyond his ability or unless you have pushed to continue, even if not under excessive effort, a vasospastic patient with Prinzmetal's angina (variant
angina). In this case stop the test, treat the patient with nitrates and "everything passes".
We investigate the case of the patient who suddenly appears an elevation of the st tract. This happens because an angina variant of Prinzmetal has
"started", even if it is not the preferred stimulus. The main stimulus to artificially "start" it, therefore not spontaneously, is to inject methylergometrine or
acetylcholine (vasoconstrictors), while another possible stimulus, if the patient has already been sick a few days before, is hyperventilation, for about
5 minutes, with the elevation and pain appearing after the patient has stopped hyperventilating. For this to happen during the stress test you need to
be very sensitive. Furthermore, the variant angina of Prinzmetal also has ethnic characteristics: it mainly affects the black population. When you make
the transition from 25 to 50 watts, for example, there is a button that allows you to see the real track, so you see what the computer is seeing,
because if you see the alteration in the real track, there must be three beats consecutive underslung well, it is clear, you have the real diagnosis in
your hand. The computer does what we would do faster. If we are shown an illegible trace for the excess of artifacts, the computer tries to read it
anyway but the result will be delusional. If you don't pay enough attention, computers can trick you. When we are subjecting a patient to the cycle
ergometer test there is the possibility of pressing a button to start the ECG tracing "live" and continuously for 30 seconds. If we realize that in the ECG
tracing we do not understand anything, it means that the electrodes have been badly put, then we stop everything and reposition the electrodes.
Different factors of imprecision must always be considered: the stress test is much more specific in women than in men for reasons
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anatomical, sweat can detach the suction cups of the electrodes, etc ... So it takes some attention and a lot of practice to get a well-made track, so
that at this point the computer performs its function optimally. There is a rule for evaluating the track: if you see 3 consecutive sub-leveled complexes,
then the stress test is positive.
Arrhythmias necessarily have negative prognoses. Modifications of the t wave
The modification of the t wave may or may not be related to myocardial ischemia. It appears with many and different pathologies, such as pulmonary
embolism (many times there are inverted t waves) or electrolyte alterations, such as increased potassium. The t wave is influenced by age and
hyperventilation: this reduces the level of reliability. However, there are two modifications that can be given some clinical significance. The first is the
PSEUDO-NORMALIZATION OF THE T-WAVE, possible when the patient arrives and already has the inverted t, perhaps for pathological reasons
(such as for example a small heart attack in which the vessel was then reopened via stent), is subjected to a control, pedal and overslide the t wave
that was previously inverted: all this is a sign of possible ischemia. The second is the appearance of NEGATIVE T WAVES DURING RECOVERY:
after nothing is visible during exertion, during recovery, which must be recorded for at least 5 minutes, inverted t waves begin to appear. This is a sign
of possible ischemia. Why does it happen during recovery? Because these are particularly vasospastic patients. An example can be when a patient
does not take a heart attack during an expensive sport but afterwards, when he enters the locker room, then at the bottom there is a vasospastic
component. Our body is made of rebounds between the sympathetic and the parasympathetic and we must know how to cushion them. One problem
with aging is that this system of cushioning fails. The one who cushions is dopamine and if there is a dopamine depletion the balance is lost, you can
go from extreme excitement to extreme depression and therefore probably these vasospastic people have an altered autonomic neurormonal system,
so in the moment of rest there is this rebound. After a vasotonic fall there is always an even higher vasoconstrictive rebound and one becomes
tachycardic as a sign of the activation of the sympathetic nervous system. Most common example: have you ever seen someone who fell on the
ground while eating with a vasovagal reflex? It should be borne in mind that vagal syncope is characterized by fainting of the subject. In summary, the
vagal reflex is common after large binges and many times if you check the radial pulse you feel nothing, while the carotid pulse is slightly felt. So the
negative t wave during recovery means possible ischemia, and certainly the patient will have stenosis, but it can also be on a vasospastic basis.
Factors interfering with the interpretation (this year the prof did not mention this
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slide, he only mentioned the case of the woman in the previous speech)
What are the factors that interfere with the interpretation of the ergometric test?
● FEMALE SEX, about which there is another variant to consider: women have atypical pain compared to that of men in 70% of cases. The typical
ischemic pain of man is retrosternal and radiating to the neck, up to the jaw. But the woman has precordial pain much more often and this is
something that until a few years ago we didn't even think about, until in 1993 a woman became director of the NIH she gets angry rightly because
there is a disparity in frightening treatment towards of women and wrote an editorial called The Yentl Syndrome and had a considerable weight, with
many positive consequences, in particular it blocked every industry from doing trials if there was not enough representativeness of women inside
(30%). This was later extended to various minorities (Hispanics, blacks ...), who must be represented at least 10%. So we started to find out that
women told things differently. So the description of chest pain that came from Heberden, the one who described angina in the eighteenth century,
was not reliable even for women. The reliability of the ergometric test for women is low both because the ECG can be bad (50% specificity) and
because the patient can say she has pain somewhere else. “Clinical advice”: the woman is different in attitudes and much more talkative when she
has to give definitions and explanations, which you as doctors must be careful of. So apart from the ECG in the female sex, it must be taken into
account that the pain is accompanied by dizziness and is localized in different points. However, the system must be stopped because the patient
cannot be said not to be cardiochemic. The prof often ends up sending women directly in scintigraphy because the results of the ECG are very
confusing.
● ANATOMICAL CONDITIONS: obviously if one has kyphoscoliosis the positioning of the electrodes is very complicated.
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● Important: If a patient already has arterial hypertension, you can suspect that he has cardiac hypertrophy. You send him to do an ultrasound and
check. In any case, the professor is not in favor of asking for ultrasounds for everyone, as we often tend to do now, because otherwise there are very
long waiting lists and patients with greater urgency, such as those decompensated following a heart attack, are forced to wait a lot before I can take
the exam. Clearly if a patient has hypertrophy, the oxygen discrepancy is greater, so it is easy for a sub-leveling to be visible, but this is a sign of
hypertrophy, it does not prove that that patient is cardioischemic
Duke Treadmill Score
Americans still use it, but less and less; there is still in the guidelines. In the United States they are more conservative, in Europe coronary
angiography is performed but an angiography has risks, it takes a scale of interventions until it is decided that it must be done. The Americans wanted
a patient to hit -11 by doing an account they called Duke Treadmill Score from the Duke Center in Virginia, a hospital famous for statistical clinic
studies. If it reached -11, that is high risk with 5.25% mortality per year, coronary angiography could be done otherwise. This -11 was calculated using
the formula ( top of the slide ). For example one did 2 minutes, then 5x2 = 10 so he didn't do 11 but if you have pain it is -4 more then with that -4 all
the other accounts
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they always come back. Not much is used in Europe. In America they are more conservative, they make fewer interventions because they end up in
jail if inappropriate interventions are made.
It takes a defibrillator in all rooms where stress tests are done. Everyone should know how to use a defibrillator, in other European countries there are
many. When a subject is sick, one must understand it by feeling the carotid artery: if he does not beat, the patient will die within 15 minutes. If the
subject has an atrioventricular block that led to his arrest, defibrillation is useless, but you cannot know without electrocardiography, therefore it is
better to always try to defibrillate, because if, on the other hand, he is in fibrillation, he can be saved. If a patient has sustained ventricular
tachycardia, one should defibrillate in synchrony by shooting on R; there is a button next to it that says "sign syncrone". With a ventricular tachycardia
the carotid pulse is felt. When you no longer feel your ventricular pulse, you are either in cardiac arrest from atrioventricular block or in ventricular
fibrillation.
The defibrillator is made up of the plates, a mostly red button with the word open to turn it on; then there is a knob that says 100, 200, 300 joules. If
you have a person who is dying in front of you, it is better to put 300 joules immediately, at most he will have burns in the following days. The plates
are placed and the blow starts. While using the defibrillator, you must avoid keeping your feet in the water or keeping an iron object next to you in
order not to "self-discharge". You can't hurt a person who is in cardiac arrest, at best you don't do him any good, but it's always better to try.
Myocardial perfusion scan
Referring to the image in the slide: at a certain point during the stress a hole is objectively visible. At rest it is lit everywhere, the "circle" is complete,
while under stress the circle is incomplete. If under strain it does not pick up and at rest it picks up we can deduce that the patient has either stenosis
or problems in microcirculation, then he will undergo angiography to check clearly. Radionuclide is given, there are various tracers including thallium,
an analogue of potassium; the heart "eats" ( capta ) potassium, therefore at rest giving the radionuclide the heart eats it. If you give it instead
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the radionuclide during an effort and a coronary artery has a stenosis you can see a hole: everything else around "is eating", that part is not. It is
therefore much more specific and sensitive than the electrocardiogram. When the test is repeated at rest, the heart "eats" all the radionuclide and
there is no longer a hole; this is called reversible stress hypoperfusion, an unequivocal sign of ongoing ischemia; when there is an irreversible
hypoperfusion, the hole is seen during exertion and even at rest, it means that that area is infarcted, it will never "eat" again.
Effort can also be induced pharmacologically with adenosine ( " Patients with severe motor difficulties are obviously in difficulty in performing an
exercise test with a cycle ergometer or treadmill. In these patients it is possible to resort to pharmacological stimulation tests using substances
vasodilators such as dipyridamole or adenosine "-Wikipedia) . With intravenous adenosine a frequency of 90 beats per minute is induced; the
mechanism is reverse "Robin Hood" or "I steal from the poor to give to the rich". Example:
Inlet coronary pressure = 100 mmHg Let's say there is a stenosis.
Post stenotic pressure = 60 mmHg Pressure in sub-epicardial resistance vessels = 10 mmHg
Pressure in the sub-endocardial resistance vessels = 0 mmHg
With P the blood goes on, there is no ischemia. Adenosine arrives, a powerful vasodilator of resistance vessels: Coronary pressure = 100mmHg
Post stenotic pressure = 60mmHg
The resistance vessels dilate completely so the sub-epicardials go to 0. The sub-epicardial dapressure from 50 has gone to 60 so the flow increases
(Bernoulli's law) in the epicardium (I gave to the rich) but from the epicardium at the endocardium is 0, the flow is not there (I stole from the poor,
coronary theft ). It should be known how it works because millions of adenosine scans are requested every day. Adenosine is injected and if the
patient has severe stenosis he goes into ischemia. Then use the theft mechanism.
Myocardial scintigraphy is based on this principle, adenosine is used to create theft, adenosine does not tachycardise. This system works for large
stenoses where the coronary reserve is very compromised, for medium situations it does not work, adenosine manages to create theft and ischemia
detectable by the scintigraphic method, with adenosine a less sick population is selected than that detectable with an exercise test.
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Dihydropyridine drugs cannot be applied alone in myocardial ischaemia, demonstrated after a Dutch trial in which the candidates who took them died
because these drugs "led to theft"; therefore it is necessary to use other drugs such as calcium channel blockers, verapamil but not amlodipine,
felodipine which are poorer relatives of adenosine which does this more markedly .
Stable coronary artery disease (SCAD)

Revision note: I know that some lists may seem to you without any logical sense, but I have integrated the lesson following the guidelines so dear to our professor, and these lists have been copied
evenly from these lines. =)
(The teacher starts the lesson by talking about the Cardio exercises that will be held in the department in small groups. In addition, he puts some interest in the
evaluation questionnaires of the course held by the teachers, which will be held at the end of the lessons).
STABLE ANGINA Chronic ischemic heart disease is all in all the most benign of forms. The problem of chronic ischemic heart disease is what will happen next; if
we stop to think about a person who does about 600m, who gets pain, he stops and after about 2 min the pain stops. The problem, in reality, is that sooner or later
angina will no longer be stable; so the disease is stable, but sooner or later it will destabilize, so I will still have a heart attack. Meeting it as stable angina, however,
it must be treated, treated and diagnosed as such.
Precipitating factors:
• Physical effort: in the previous lessons we have already talked about the stress tests, the scintigraphy etc ... It is clear that it is not so much the stress test, but
the tachycardia.
• Emotions : emotions too can cause the heart to go to 120-140, thus leading to sudden tachycardization; emotions of all types based on the characteristics of the
pc. This in the doctor, if he does not investigate well, can make the diagnosis wrong. So before making a diagnosis of unstable angina, the doctor must understand
if emotions have appeared. A tachycardization is no more or less equivalent to an effort, therefore it is a false axiom to say that among the precipitating factors
there is only the effort.
• Same thing as stress , which can act by linking it to emotions (stress = negative emotions). (The professor says that between emotion and stress there is not a
very big difference; stress as well as an emotion can be negative).
• Among the precipitating factors there are also spontaneous factors, apparently spontaneous, difficult to identify; a "chronic stable angina" does not always
manifest itself only through physical exertion.
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• Transient chest pain: we have already talked about it in the last lessons. The typical pain is retrosternal, which radiates to the shoulder ..., but it can also be,
especially for women, atypical pain.
Stable angina is a stabilization after an acute coronary syndrome (SCA). A subject born and raised with a stable angina ( The professor does not end the sentence
) ... The plaque, as we have already mentioned, is more vulnerable than the one full of cholesterol. When you have many subocclusions, in Cardiology, you will
have a NSTEMI infarction, but if we go on for many years, they can for intermediate positions give life to stable situations. But the most frequent is after an acute
event.
QUESTION : But what if we go inside with the catheter to remove the strictures? Well, in the meantime we cannot see all the stenoses, because if a patient arrives
late, after 12h from the event, it does not require any intervention; after about 15 days the patient becomes stabilized by definition and, therefore, when he moves
he can have stable angina. This is the most frequent situation. The stable form is rare, while after an acute coronary syndrome it can be frequent: the stent does
not solve everything, in fact, stent stenosis exists. In fact, if the latter were not there, all of us after 50 years, prophylactically, we have stents. But it is not so.
CLINICAL PRESENTATIONS:
• Exercise angina caused by :
o Stenosis of epicardial vessels. o Microvascular dysfunction: example of microvascular dysfunction, which causes mortality, is the phenomenon of no-
reflow. If the stenosis has opened but the blood does not flow, the blockage must be in something that is not seen with angiography and therefore is at the
level of microcirculation. Why do you have angina? Is it microcirculation? It is said yes but it is an assumption because we cannot see it. What cannot be
documented in the epicardial vessel is translated into the resistance vessel, but it is an assumption. o Vasoconstriction at the dynamic stenosis site o
Combination of all the above.
• Angina at rest :
o Vasospasm :
▪ Epicardial focal
▪ Widespread epicardial
▪ Microvascular
▪ Combination of the previous ones The incidence and the number of heart attacks is much lower. The danger is actually much less. The jar reopens more
easily. Attacks of vasospastic angina can occur without anything happening. If a person has plaques and will have angina and we discharge him after 6
months he will have a heart attack. Prinzmetal's angina, the focal spasm, not the diffuse vasotonic spasm, is a feature that no one has ever understood.
The attack on the patient comes at night; this wakes up with pain in the early hours of dawn, completely at rest. Rest angina is most often identified with
vasospasm which can be spread. There is vasotonic angina, Prinzmetal's angina, focal. Japanese terminology unified (wrongly says the prof) the
different types, defining them "vasospastic".
• Asymptomatic: many patients come to the ward, saying they have difficulty breathing. We visit it and feel no sign of pulmonary edema. The cardiologist also
sees the ejection fraction
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perfect, therefore the question is: it can be a transient phenomenon that appears and then disappears. In a transient ischemic crisis if we mounted an ECG
holter (which records 24 ECGs), we would see most people recording a heart attack without ever having felt pain in their life; we will see the ST section that
makes ischemic crises. We understand that such a primary prevention system is not feasible. "Transient ischemic crisis: the heart as soon as you touch it with
ischemia goes down!". If there is an ulceration of a plaque, the platelets "want to close" to make thrombosis, but we have the endogenous fibrinolytic system
and therefore I can reopen the vessel. (the professor explains himself very badly) So it is necessary to evaluate well the case of each patient regarding this
condition.
• Ischemic cardiomyopathy
The professor did not mention it.
(The professor says that his Master is the one who detected the spasm in England. He also speaks of a 27-year-old girl who had a heart attack, spasm; entering
the room they saw the anterior descendant occluded. With nitrate it was reopened and there was no stenosis).
PREVALENCE:
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We have already said that the incidence is higher in humans. We are not talking about mortality but about clinical presentation, in this case for stable angina.
QUESTION: Why is prevalence higher in women than men between 40-59 years? PROF. ANSWER: In women we are in a period close to menopause (hot flashes
etc ...). Hence, there are currently a number of studies in which women are more sensitive in this age group. INCIDENCE more than the prevalence is affected by
the total number. And therefore men are always at the forefront. Age of frailty: after 65; we talk about general rules and percentages. After 75, fragility is given by
the lack of self-sufficiency.
PROGNOSIS:
The prognosis for stable angina is much better than that of an acute coronary syndrome, especially of its most frightening and dramatic manifestation of myocardial
infarction with ST level, transmural infarction. Mortality: 1-2% of mortality per year.
SIGNS AND SYMPTOMS: The professor underlines point 4 of the slide: "Remission after max 10 min".
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One patient reports potentially dangerous pain. Even before proceeding to hospitalization, it is necessary to establish whether or not this pain passes. In all the
books we find written that remission passes after 10 min or after sublingual administration of nitrates. But if everything lingers on making an effort and therefore
exceeds the limit of oxygen consumption, after which the discrepancy between demand and supply is formed. I stop and should go alone. So if we examine a
patient who has had a heart attack and has nitrates with him that we administer sublingually and the pain ceases after 10 minutes, I doubt that he will have more
than an exercise angina (exercise angina: I do tot meters and I stop).
DIAGNOSIS:
We have already spoken in the last lessons of scintigraphers and stress tests. How specific is the stress test? 70 in men and 50 in women.
• Blood-chemical tests : everyone does them nowadays, but nothing is seen. Once in a while you can see an increase in PCR, which can lead to suspicion of
angina. PCR is not related to the acute event, but to the amount of (chronic) atherosclerosis. So if the patient has had pain + has elevated PCR + has a normal
ESR (most important inflammatory index): sign of atherosclerosis (differential diagnosis with an abscess for example, which would also have an increased ESR).
• ECG: the basal ECG , which is usually not diagnostic, is self-evident. In order for the patient to be diagnostic, the patient must feel pain at the moment of the
examination: total uselessness before a major surgery to do a basic ECG. So it is a waste of time, it must be understood that doing a useless thing will never say
anything in a patient with transient ischemic crisis; a sub-leveling (holter) can be seen in 24 hours. If a patient has severe chest pain, something more must clearly
be done. It is after the heart attack that ECG is altered. Therefore, other tools must be used.
• Stress test if the suspicion is clearly greater.
• ECHOCARDIOGRAPHY: something more refined. The echo shows us if there was a heart attack.
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Eco-stress : invented at the CNR of Pisa. Use of dobutamine, which accelerates the heart rate, similarly to an exercise test, and instead of looking at the
results with the scintigraphy, we analyze them the ECO, with which we spend less. Dobutamine accelerates the heartbeat by simulating a high frequency
(sympathetic mimetic and vasoconstrictor) and with the ECO it is seen if there is hypokinesia. The limit, like all ECHOs, is that it is a very operator-dependent
examination: microscopic hypokinesia is really very difficult to see. Scintigraphy is less operator dependent.
• CT of the coronary arteries: we talked about negative predictive problem and positive predictive power. Negative predictive power: does it mean "if I see
nothing, can I be sure there is nothing?". If I see a stenosis (positive predictive power). QUESTION: What is the resolving power of OCT? 10. For IVUS 150-200
microns
• SCINTIGRAFIA
• ANGIOGRAPHY
QUESTION: If a patient with stable angina presents, what is the first test to be performed? PROF: the first, also from an economic point of view, is the stress test .
We are talking about a stable shape and therefore I can afford the luxury of a few days. Then I move on to a scintigraphy (if I have doubts). You do the CT scan, for
example, if they have stents 6 months apart.
CCS CLASSIFICATION: CCS severity classification (Canadian cardiovascular society), exactly the same classification that you have for heart failure and dyspnea:
one made by the Canadians (angina) and the other by the Americans (dyspnea).
What is it for? The classification is used to see if the therapeutic measure we performed had a result or not. If drugs are given, as for the stress test, and these
work, if the patient belonged to a given class, it goes back to the previous class.
4 classes which are therefore extremely important clinically (similarly for heart failure):
• Class 1: ordinary physical activity does nothing. Angina appears in intense and long-lasting efforts. All that is out of the ordinary is class 1: if you climb the Asinelli
tower, not being a normal but exceptional effort, you return to class 1 because it is something that can happen.
• Class 4: (class 2 and 3 are difficult). It is the most disastrous, inability to conduct any physical activity without anginal pain, with presentation even at rest. It is
almost astride the unstable angina, which presents itself with minimal physical activity. A class 4 subject must make an angiography on the fly, and the situation is
already critical to intervene.
• Class 2 and class 3 are divided on the basis of the number of blocks to be covered to feel pain; a block or two (one block corresponds to about 100m). This is
very important because with a suitable medical treatment it is possible to pass from class 3 to 2, improving the quality of life of the patient.
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After a heart attack the prognosis is not only dictated by stenosis but is also dictated by your heart; there are stent or bypass subjects who have the ejection
fraction as previous to the event. It is only when the heart loses functionality that one risks the arrhythmia, the complications. Those who have a preserved ejection
fraction have 73% at 12 years; 54% those who have it under 50%, up to 35%, which would be those with an abnormal function, finally 21%, those under 35%. To
remember : 35% because the new conditions of the use of the implantable defibrillator has been increased to 35%. Normal is above 50%, abnormal is below 35%.
Severely compromised is below 35%.
DIFFERENTIAL DIAGNOSIS FOR THORACIC PAIN FROM ISCHEMIA:

• Pericardial pain , very common: we notice it on the patient asking him to go up and down and move up and left with his body and telling him if the intensity of the
pain changes. If the pain changes with pressure it is pericardial and if it is better sitting forward ( Blechman position ). So we detach the pericardial sac more from
rubbing, so we feel less pain. In a pericarditis, unlike a neuromuscular pain, it doesn't matter if you go against it. Exhalation and deep inspiration also determines
pain modification, because in inspiration we have an increased venous return and therefore we increase the heart more and stretch the pericardium more,
therefore more pain in inspiration. Clinically it is possible to find a ST elevation which is diffuse, not convex. While the heart attack closes a coronary artery and we
find it in a region. Here (in the pericardium) instead it is widespread.
• Dissecting thoracic aortic aneurysm : those who have it will have 10% less chance of surviving every hour that passes. It means that if we do not have surgery
in 10 h, we will die 100%. Pain is similar. We can have a fortune: retrosternal pain that can radiate at the interscapular level . In this case it is highly specific for
aortic dissecting aneurysm.
• Pulmonary embolisms also cause chest pain (especially massive ones).
• Non-cardiac causes , including epigastric pain (we said woman's atypical), but sometimes it can be a little higher. Epigastric pain is not only typical of
gastroesophageal reflux. Esophageal spasm sometimes anticipates coronary artery spasm. Esophageal pathology is sometimes not easily distinguished from
coronary artery disease. Chest pain, where pain increases at acupressure.
TREATMENT:
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2. behavioral therapy: that is, the lifestyle; do not smoke, walk 20 min a day, eat
well etc ... 2. drug treatment; 2. interventional or surgical revascularization.
NB: - important LDL - PA: 130-139 / 80-85 mmHg - physical activity - nutrition is also important (it is an example of a patient who eats salad with anchovies, which
has HDL equal to 95 mg / dL).
The pharmacological MANAGEMENT STRATEGY is based on 2 cornerstones:
1- angina relief :
THE FIRST LINE is nitrate which must be given sublingually and when needed. The patient must lie down because the patient often has a pressure drop. If
you get a syncope, you fall down and hit your head you can get damaged. (The professor says that nitrates in the form of transdermal patches are useless).
Nitrates have a problem: after 24h metabolites are formed from the liver which are completely inactivated. So even in acute, after 24 h have no effect. Orally
administered nitrates are of no use. After 12 h its effect wears off, so chronic nitrate is useless and should be administered sublingually.
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Here we are talking about a prompt intervention, the real therapy is made by these 2 classes of drugs: Beta-blockers or Ca2 + antagonists : first beta-
blockers are used, but if I can't I will use the Ca2 + antagonist. So they are not on an equal footing, but it is a failure. Why beta blockers? A subject is beta-
blocked by definition when his resting baseline HR is <60 bmp (sinus bradycardia). Stress, however, by definition <90bmp. This is a beta-blocked product,
otherwise we are administering drugs without beta-blocking it. I am a beta blocker doctor, but I give him such a low fee that he does nothing. So the beta
blocker is the first drug that must be given absolutely. When it cannot be given, the second one is used:
• Some time ago it was a blasphemy to give beta-blocker in patients with severe COPD.
• Beta-blockade is absolutely contraindicated in peripheral diseases of the lower limbs , because if we block beta it will be stronger alpha (the pz has
arteriopathies) and therefore we can send the pz in gangrene, to an amputation.
Other first-line drugs are calcium channel blockers , to be considered the dihydropyridine Ca2 + antagonist if FC is low or beta-blocker contraindication /
intolerance. Dihydropyridines can be associated with beta blockers; this may seem like a paradox, but I have to take into account concomitant diseases; if a
person is hypertensive and I give him a beta-blocker, but after some time I still find him hypertensive it means that I will also give him a Ca-antagonist, a
diipropyridine, because if associated with the beta-blocker it does not hurt. But if I have a patient to whom I cannot administer a beta-block, I must turn to the
other Ca2 + - antagonists, those of the second genus such as diltiazem and verapavil. Why do I use the latter? The dihydropyridine acts as if it were a small
adenosine we speak of coronary theft; therefore dihydropyridine cannot be given alone because it would lead to coronary theft.
The biggest problem, ergo, we find it when a patient has both hypertension and stable angina, however if the patient does not have problems taking beta blockers,
dihydropyridinics can also be associated.
The standard dose of calcium channel blockers is 60 mg 3 times of diltiazem and 120 mg 3 times of verapavil.
Calcium antagonists paralyze all the muscles they find, even those of the organs, therefore patients will become constipated ; obviously the patient is already
aware of all this because he has read the leaflet therefore as good doctors the only thing that can be done will be to calm him down and invite him to take the
pills anyway.
2. EVENT PREVENTION: aspirin and statins. Aspirin as a secondary prevention. Statins are revolutionary drugs, they also partially reverse the atherosclerotic
plaque and passivate it: cholesterol dries up. They are life-saving medicines.
We also have a very strong second line (it doesn't mean that I put it in the first line, but I add these drugs to the ones mentioned above) consisting of the use of
drugs such as ivabradine, nicoradil and ranolazine. These drugs are Na + and K + channel blockers. These drugs are used in addition to or in place of those of the
first line. Most often these drugs are not used because the use of first-line drugs is sufficient. You will never break through the first line complete with beta blocker
and calcium channel blockers. (the professor reports that he never personally gives them).
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COURAGE STUDIO: It is the most famous study of the last 10 years on about 3000 patients with stable angina, almost all post-infarction with medical
treatment or medical treatment + stent surgery with angioplasty. Everyone thought that an angioplasty intervention was better, but as you can see from the graphs
shown here, the curves of all the end-points at 5 years of follow-up no difference between the different treatments. Therefore, discussions began as to whether it
was right or not to do this. The European Society is oriented differently in this regard, recognizing that mortality does not change. (A new study entitled
"COURAGE" was conducted in 2007 that compares revascularization with medical therapy. This study has defeated public opinion, especially in America, a country
with a strong sensitivity towards the patient. America when there is a congress they want doctors and patients to speak so that there is debate and awareness on
both sides. Through this study it was understood that there was absolutely no difference between revascularization and medical therapy, essentially this study says
that putting a stent is useless. All this has led to a gigantic control of the implantation of the stents and has led to a revision of the guidelines for the implantation of
the latter, in the American guidelines a stenosis is critical when it exceeds 70%.) Another study has been done in Europe: the "FAME2", through which scholars
have deduced that in some cases the stent and axis set. The difference between COURAGE and FAME2 lies in the end-point, or in the end; in FAME2 there was
also a return to hospital revascularization. .
(It is on the basis of this study, which lasted only 12 months, that the European guidelines were made. The guidelines in Europe are different from the American
ones, they say a series of very reasonable but all very interventionist things; they are guidelines that foresee the interaction of several doctors, are multidisciplinary
because they involve collaboration between the patient, the doctors, the patient's family. It is therefore necessary, as far as possible, to involve everyone and
discuss the various possibilities. Very important therefore is the information that thus leads to conscious choice, some patients will make choices that cannot be
shared, however if these follow the information we cannot oppose).
The death toll is important to remember that it doesn't change. The professor says he is in favor of European society, because quality of life is important to him, a
factor that should not be underestimated.
ACUTE CORONARY SYNDROMES

Acute coronary syndromes (SCA) are responsible for 270,000 deaths per year. There is a 1-2% mortality for a subsequent advent of an acute
coronary syndrome and 4-12% in the following 30 days, depending on whether primary angioplasty or thrombolysis are performed. These data are
actually subject to bias, as only patients who arrived in hospital on time are taken into account, without considering those who do not survive. It is
considered the epidemic of the twentieth century, while mortality has been significantly reduced in the current century thanks to advances in diagnosis
and therapy. On the other hand this has increased the cases of decompensation that occurs in 70-90% of the survivors of an SCA, with an
accumulation of deaths due to
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distance of about 5 years. (this is an average estimate, the survivors can live for more or less years).
The acute coronary syndromes are divided into: - Angina Unstable - Myocardial infarction - subendocardial ( NSTEMI ) - transmural ( STEMI ) -
Sudden Death
As reported by the 2007 Heart Disease and Stroke Statistics (conducted in the United States but reflecting the western European world, although the
incidence is lower in the latter), the number of hospitalizations per year is 1.57 million. This has a great weight on hospital structures which are largely
insufficient.
(The thing that emerges is that NSTEMI are 1.24 million or four times as many as STEMI. In the register of acute coronary syndromes of the Eastern
countries there are much more STEMI than NSTEMI. Based on these data it would therefore seem that the country of birth influences the onset of
STEMI or NSTEMI. Actually we must consider age . Everything is linked to age (...) adjusting mortality for age there are no differences. In Western
countries where expectations are increasing of life, NSTEMI is prevalent. In all Eastern European countries STEMI prevail. The reason is to be found
in old age, because the older you are the more the stenosis increases, and although doing the collateral circles, maybe they do not do enough and
therefore a prolonged ischemia of the subendocardium occurs which becomes NSTEMI. Sbobina 2017/2018)
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Spectrum of Acute Coronary Syndromes The patient reports chest pain, a primary symptom that should lead to suspicion of SCA. It is
important to make a differential diagnosis with other pathologies that give chest pain, such as aortic aneurysm, for which a rapid diagnosis is
necessary since for every hour that passes there is a 10% increase in mortality. In addition, aneurysm rupture and subclavian (most frequent site) or
coronary dissection may occur, generating ischemic damage of the myocardium. A factor that allows to discriminate the chest pain due to the
aneurysm is the retro-scapular irradiation. The diagnosis is made at the entrance with ECG and biomarkers. - In the case of STEMI I will have - ST
level elevation - troponin increase - chest pain (not always present) - In the case of NSTEMI I will have - troponin increase - level elevation not
present - In the case of Angina Unstable the levels of troponin, index of necrosis, will be normal.
Between NSTEMI and unstable angina the difference is troponin, which is an index of necrosis . But this border is hypocritical: if you dose
troponin in the coronary sinus (venous, which discharges the arteries) it is always positive because a minimum of cell breakage is always there.
Troponin high sensitivity has been introduced for four years . This led to the almost disappearance of unstable angina because they are all positive,
even those who have nothing, even patients on statin therapy (because statins cause myopathy). However, these will not show the classic troponin
curve following the ischemic crisis. Many who take statins are positive because the concept of specificity does not apply to troponin or to drugs in
general. Uncoil 2017/2018)
When in the past the biomarker analyzed was CK, a massive necrosis of the myocardial tissue was necessary to increase its blood values. The
introduction of high sensitivity troponin has caused loss of diagnostic power ( ISOLATED increase in troponin is NOT a sufficient criterion for the
diagnosis of myocardial infarction) and prognostic that biomarkers had in the past. To discriminate between cases of asymptomatic or nuanced heart
attack and increase in non-heart attack troponin (e.g. for statin-induced rhabdomyolysis or acute pulmonary edema), reference is made to the
troponin curve.
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The classification arises from the need to allow the clinician to diagnose transmural via STEMI. This is important because in these cases the more
you waste time the more the risk of dying for the patient increases (we repeat, TIME IS MUSCLE!). In the case of NSTEMI, however, there is not so
much urgency because there is no complete occlusion. In these cases, in fact, there is a strong debate on the most appropriate treatment, in
particular whether to do the surgery or not to do it. (Unroll 2017/2018)
Fourth definition of myocardial infarction

Criteria for myocardial damage Evidence of increased cardiac troponins of high sensitivity (cTn) with at least one value above the 99th percentile of
the upper reference limit. Myocardial damage is considered acute in the event of an increase and / or decrease in cTn values. Criteria for the
definition of Acute Myocardial Infarction (type 1, 2, and 3 AMI ) Evidence of acute myocardial damage with associated clinical evidence of acute
myocardial ischemia and with evidence of an increase and / or decrease in cTn values with at least a value above the 99th percentile of the upper
reference limit associated with at least one of the following:
• Symptoms of ischemia
• ECG changes indicative of new ischemia (new ST-T anomalies or new left bundle branch block at 12-lead ECG) ST anomalies are an indication
of an ongoing heart attack
• Appearance of pathological Q waves on the ECG In cases of a transmural infarction the pathological Q wave is characteristic : where before there
was an R now there is a Q in V1, V2, V3 and V4. This phenomenon is due to the sum of the heart vectors: the electrode no longer sees the tip of the
left ventricle (responsible for the positive deflection) due to the area of necrosis generated, but only sees the tail of the right ventricle vector
(responsible negative deflection) Given the presence of the pathological Q wave, in the past transmural infarction was also called Q wave , the
subendocardial non-Q wave because it did not affect the entire wall. Pathological Q wave is an index of past, not in progress, heart attack. The
replacement of the definition Q-non Q with STEMI-NSTEMI arises precisely by virtue of the possibility of being able to promptly establish the need for
intervention.
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• Feedback with imaging techniques of a new viable myocardial loss or of new alterations of the regional Chinese parietal (hypokinesias)
• Coronographic or autoptic finding of intra-coronary thrombosis
(Digression on possible causes of sudden death of young boys: - dysplastic arrhythmogenic disease of the right ventricle (serious anomaly that leads
to ventricular fibrillation), - Brugada syndrome (often asks for examination) - Heart attack as can be seen are all causes of relevance cardiac)
Clinical classification of the different types of myocardial infarction Type 1: Spontaneous myocardial infarction Erosion and / or rupture,
ulceration, fixation or dissection of the atherosclerotic plaque with consequent intracoronary (intraluminal) thrombosis in 1 or more coronary arteries
which causes a reduction in myocardial flow resulting in myocardial necrosis.
▪ Generally unstable atherosclerotic plaque is obstructive
▪ 5-20% of patients show non-obstructive unstable lesions or "absent" underlying coronary artery disease
Type 2: Myocardial infarction secondary to ischemia due to an ischemic imbalance Imbalance between oxygen supply and demand (e.g.
endothelial dysfunction, coronary artery spasm, tachyarrhythmias, bradyarrhythmias, severe anemia, severe hypertension, hypotension, respiratory
failure, hypotension / shock etc)
For example, the tricoronary patient (three-phase coronary artery disease) with 90% stenosis, with ischemia obliges us to stop the stress test. In this
type of patient, troponin is naturally high. This represents the limit of the exact definition: if a cell breaks or
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if they break a million it is always necrosis and therefore a heart attack. With this definition we come to diagnose a heart attack to a large number of
patients who long ago would have been defined as suffering from coronary artery disease. This can be confusing especially from the prognostic point
of view. While before there were many unstable angina, now with the new definition and with the high sensitivity troponin, they are hardly found
anymore. Before, he differentiated, based on troponin, in high-risk, low-risk unstable angina to decide whether to do the surgery with catheterization
and stent, based on troponin. Now all patients are almost all positive, so they are all similar. They overwhelmed a prognostic-therapeutic paradigm.
(Sbobine 2018/2019)
Type 3: Myocardial infarction resulting in death when cardiac biochemical marker levels were not yet detectable. Sudden cardiac death,
accompanied by symptoms suggestive of myocardial ischemia, likely associated with new ST-segment deviations, or new left bundle branch block. In
any case, death occurred before blood sampling or when levels of cardiac biochemical markers were not yet detectable. The report is therefore
autoptic.
Type 4 is in turn divided into

• Type 4a: Percutaneous coronary intervention (PCI) -related myocardial infarction Raising cTn values> 5 times the 99th percentile of the upper
reference limit or raising cTn values> 20% if the baseline values are high but stable o are decreasing with symptoms suggestive of myocardial
infarction in addition to: (1) new pathological Q waves. In practice, a heart attack subject, who therefore has elevated troponin, and to whom a
primary stent is immediately placed, if in the following 4 hours the troponin levels rise further it means that something went wrong: the patient had a
heart attack called periprocedural , that is, due to the surgical procedure. Another coronary branch must have occluded. This happens for example
at the level of the bifurcations, as can be the one between the anterior and diagonal descendant, where kissing baloon is necessary. While the stent
opens the anterior descendant, it closes the diagonal causing damage to the myocardium. Often the doctor can "find himself forced" to intervene in
this way because the patient is in danger of life for example for acute pulmonary edema. A periprocedural infarction can occur even if coronary artery
dissection occurs during surgery.
• Type 4b: Myocardial infarction related to stent thrombosis. The first 24-48 hours after stent insertion, the patient is kept in hospital because
thrombosis of the same stent may occur. In the past, POBA (plain old baloon angioplasty) was used, which however gave 25% of stenosis years
later. Today there are two types of stents: -The Bare Metal Stent with 10% re-inclusions - The DES (Drug Eluting Stent) releases anticoagulant
substances that should have been reduced
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re-occlusions and so it was, bringing the percentage to 7%. However, with the first generation DES, there was a big scandal. These released
clopidogrel , an anti-aggregant much more potent than aspirin. When it was necessary to interrupt therapy, for example to go to the dentist,
acute thrombosis of the stent and myocardial infarction were generated. Furthermore, the release by the stent of coagulation inhibitors can be
recognized as a foreign phenomenon by our body, triggering activation of the fibrinogenetic system and therefore thrombosis. Second generation
DESs were therefore developed which do not generate this type of problem.
• Type 4c: Myocardial infarction related to restenosis Myocardial infarction associated with angiographic or autoptic findings in a clinical setting of
myocardial ischemia associated with raising / lowering levels of cardiac biomarkers with at least a value above the 99th percentile of the upper
reference limit . In this case, restenosis is not a stent. Example: The patient has a major occlusion and other sub occlusions. The major occlusion is
removed, but what to do with the two sub occlusions? There is a great debate in this regard between those who support the need to remove the two
subocclusions and those who believe that the risk of removing them in a person in shock is so high as to require a second intervention in the
following days and not immediately. A solution has not been reached, one can choose either, and most doctors choose the second alternative. In this
way, however, there is a risk that untreated subocclusion gives a myocardial infarction related to restenosis.
Type 5: Coronary artery bypass surgery (CABG) related myocardial infarction Increased cardiac biomarker values> 10 times above the 99th
percentile of the upper limit of reference in patients with baseline normal cTn levels in addition to: (1) new pathological Q waves or new BBS or (2)
angiographic finding of graft occlusion or of a native coronary or (3) finding to diagnostic imaging of a new viable myocardial loss or new alterations of
the regional Chinese parietal. In these cases, injuries can occur as a result of the surgery, which can then lead to a heart attack. There are situations
of different severity, but it is preferable to risk creating a small infarction with the scalpel during surgery rather than leaving the coronary artery semi-
occluded
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The professor underlines that circulating levels of high sensitivity troponin are also found in healthy subjects and that there are levels in the "gray
zone", that is a little higher than normal but not heart attack indicators, for which I will refer to the curve of troponin. This curve shows me that in the
first two hours the troponin levels reach the maximum peak and then decline. The troponin dosage becomes important and is always done in and out
of the PS where there is a suspicion of heart attack, even with normal ECG. Other markers such as CK and LDH are also shown in the graph, but
currently only troponin is used for heart attack. CK is still used as an indicator of muscle damage in treatment with statins; if CK levels are elevated,
dose reduction or discontinuation of therapy will be required. (Prof cites the scandal relating to the death from kidney failure generated by the
coupling of fibrates and cervastatin, withdrawn from the trade)
Causes of elevation of cardiac troponins other than myocardial infarction Damage related to secondary myocardial ischemia
• Tachi or bradyarrhythmias
• Aortic dissection and severe aortic valve disease
• Hypotension, hypertension, hemorrhagic shock, hypertensive emergency
• Acute and chronic heart failure, without significant concomitant coronary heart disease
• Hypertrophic cardiomyopathy (from discrepancy, in this case not due to stenosis but to thickening
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ventricular wall without parallel circulation development)
• Vasculitis, eg. systemic lupus erythematosus, Kawasaki sdr
• Endothelial coronary dysfunction without significant ischemic heart disease Damage not related to myocardial ischemia
Cardiac contusion (for example in the event of a road accident in which there is a direct impact on the chest)
• Cardiac incisions produced by surgery
• Radio frequency or cryablation therapy (cytotoxicity due to radiotherapy)
• Rhabdomyolysis with cardiac involvement
Myocarditis
• Cardiotoxic agents, eg. anthracyclines, hercepetin, CO poisoning
• Severe burns involving> 30% of the skin surface
Indeterminate or multifactorial group

• Tako-Tsubo syndrome
• Severe pulmonary embolism or severe pulmonary hypertension
• Cardiomyopathy of the peripartum
• Kidney failure
• acute and severe neurological diseases (eg stroke, trauma)
• Infiltrative diseases (amyloidosis, sarcoidosis)
• Intense physical efforts
• Sepsis
• Acute respiratory failure
• Frequent defibrillation shocks
Diagnosis
Chest pain :
• Retrosternal
• Perceived as a feeling of compression
• Irradiated to the left arm, both arms or right arm, neck or jaw
▪ Objective exam :
• Mostly normal
• Signs of heart failure
• Signs of hemodynamic instability
• Signs of electrical instability
▪ Perform ECG within 10 min from the first medical contact. This guideline is actually almost impossible to follow, because the time that
passes between becoming aware of the malaise, identifying the malaise as SCA (difficult if not in subjects who have already had a heart attack ) and
arrival of the ambulance is generally greater.
▪ Perform detection of cardiac biomarker values: cTn T or I
▪ In patients with suspicion of infero-basal IMA (circumflex artery) the use of posterior accessory leads may be considered (V7 -V9)
Differential diagnosis of prolonged chest pain

- Acute myocardial infarction - Aortic dissection - Pericarditis (pericardial pain decreases in the genupectoral position , i.e. chest stretched in
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fore and thighs flexed, also called position of (???) also the alteration to the ECG is diffuse, unlike the infarction in which it is regional) - Atypical
anginal pain associated with hypertrophic cardiomyopathy - Esophagodynia, other pain associated with upper gastrointestinal tract or biliary tract -
Pulmonary pathology :
• Pneumothorax
• Pulmonary embolism with or without pulmonary infarction
• Pleural inflammation (infections, malignant conditions, autoimmune diseases)
• Hyperventilation
- Chest wall:
• Skeletal
• Neuropathic
• Psychogen
In chest pain patients who come to the emergency room the prevalence is generally :
• STEMI → 5-10%
• NSTEMI → 15-20%
• Unstable Angina (AI) → 15%
• Other heart conditions → 15%
• Extracardiac conditions → 50%
Particular attention must be paid to differential diagnosis with potentially fatal conditions that must always be taken into consideration:
• Acute dissection of the aorta
• Pulmonary embolism
• Hypertensive pneumothorax
ECG manifestations in myocardial infarction
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It is important to know how to locate a heart attack, also to give prognostic and intervention indications. In white there is the AVR which can only arise
in two situations: either the exchange of electrodes or the obstruction of the common trunk. The lower field is explored by branches DII, DIII, aVF The
lateral field is explored by branches V5, V6, DI, aVL (the last two in particular explore the high lateral field) The front field is explored by branches V3
and V4 The field septal is explored by V1 and V2 Combinations of multiple electrodes will give me intermediate locations. For example:
• an alteration in V1, V2, V3, V4 indicates the antero-septal field;
• in V1, V2, V3, V4, V5, V6 that;
• in DII, DIII, aVF, V5, V6 the infero-lateral one;
• in V1, V2, V3, V4, V5, V6, DI, aVL the anterolateral extended one.
A heart attack is termed large when it is 5-lead. It may be useful to recognize a heart attack as large or small because, depending on the case, I will
take more or less intense therapeutic measures. Furthermore, when a heart attack is large, platelets tend to go to the akinetic part, creating
intracardiac wall thrombi. With new drugs this process is more difficult but not impossible, therefore it is necessary to put the patient on anticoagulants
as long as thrombus and akinesia persist.
ECG STEMI
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Proceeding in order: -DI : PQ normal, based on ST -segment elevation -DII, DIII: normal -avr: normal (the electrodes were placed well) -aVL : ST -
segment elevation -aVF, V1, V2: normal -v3, V4, V5 , V6 : ST sopraslivellati It is a heart attack anterolateral extended .
Common trunk occlusion ECG
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Positive aVR and large IMA complexes Right Ventricle Infarction almost always takes in the left ventricle. In the case of occlusion of the right
coronary artery there can sometimes be involvement of the right ventricle, as well as the infarction of the lower wall of the left ventricle. Many
therapeutic measures used in the event of a left ventricle infarction, on the right ventricle do not work and on the contrary worsen the patient's
condition. For example, an extended anterolateral infarction the left ventricle becomes widely hypokinetic and its ejection fraction becomes extremely
low. In addition to the reopening of the coronary artery, drugs that act on venous return are administered such as nitrates (venodilators), ACE
inhibitors ... which reduce the blood supply to the heart. However, if the right ventricle is also involved, the patient goes into shock: in fact, the right
ventricle, being smaller, does not present areas of regional hypokinesia but an overall paralysis; in itself already pumps less blood to the left ventricle
and the effect is enhanced by pharmacologically induced venodilation. In this way there will be no blood supply to the peripheral tissues. I can
diagnose both echocardiographic and electrocardiographic right ventricle IMA . With ultrasound, I detect global hypokinesia and an extremely
dilated right ventricle (4 cm instead of 2.5 cm). Instead, to make an ECG diagnosis, I place the precordial electrodes on the right side of the chest and
observe an over-leveling. Therapy in the case of a right ventricle IMA consists in the infusion of fluids, an action that in a person with a left ventricle
infarction would induce pulmonary edema. Hence the need for diagnosis by echo or EGC. Through the use of the Swan Ganz catheter I can also
regulate the levels of liquids to be infused, avoiding complications such as pulmonary edema. The Swan Ganz catheter is a very thin catheter with
which I can take any vein and go back to the pulmonary circle. Here the catheter is pushed towards the pulmonary capillaries and in this position it is
able to measure pressure in the left atrium (between 0-6 mmHg). When this becomes dangerously high (in case of heart attack I can keep it at
12mmHg but at P> 30mmHg I have acute pulmonary edema) block
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the infusion of liquids.
Acute Coronary Syndrome: clinic and diagnosis
Continuation of the previous lesson.
Therapy is essential: when waiting for arrival in the emergency room, action is still required. Indeed time is muscle . The intervention intended is not only the
cardiological one, but also pharmacological through the administration of medicines
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The European Society defines some atypical electrocardiographic panels that deserve a prompt management of patients:
• Left bundle branch block: chest pain and high troponin indicate STEMI.
• Ventricular pacemaker: it can be present due to pathologies other than heart attack and is inserted through a vein (eg the femoral) in the right ventricle, where it
is set to 70. In this way when the frequency drops below this value, the pacemaker starts transmitting impulses. The ECG, in the case of a pacemaker that
activates the right ventricle, will have the characteristic appearance of the left bundle branch block, although the patient does not have a left bundle branch block
(but is anticipated to the right).
After making STEMI diagnosis, I will go to implement the specific therapeutic plan.
• Isolated posterior myocardial infarction: in this case I have to see the situation upside down as if it were a mirror, so most of the time I will have an under-leveling
(but I can also have a small level-up). What basically differs is the R: when the front is in V1 and V2 the R is very small, while with the rear the R grows and reflects
a shape of Q, with a sub-leveling of about 3 mm. It is a difficult concept to interpret and it is easy to make mistakes.
Often a patient who shows up at the ps after half an hour from the acute event, which presents chest pain, may not yet show the elevation and the increase in
troponin may not be detectable before 3 hours. What I can see are hyperacute T waves (normally they are low and round), with an evident pointed shape,
which precede the elevation (it is not a rule but it is included in the guidelines as a parameter to be monitored early).
• Common trunk obstruction: associated with aVR elevation.
Acute coronary syndromes without ST elevation (NSTE-ACS)

They include:
Unstable angina (UA or AI)

• NSTEMI In one case (NSTEMI) we have an increase in troponin and in the other not: high-sensitivity troponin is a very important parameter which
over the years has allowed us to increase the diagnosis of NSTEMI, which previously was often mistaken for unstable angina. Initially the incidence of unstable
angina was 30%, now it has fallen to 10% in favor of NSTEMI. The correct differential diagnosis is fundamental for choosing the most suitable therapy.
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It tells of a patient who was discharged with a diagnosis of stable angina, despite describing a pain that appeared with effort and eased not when he stopped, but
when he kept walking. This is not the description of a stable angina but what is called walking through angina (described for the first time by the British doctor
Heberden as "walking through angina") , not attributable only to a stenosis (it would be a paradox if walking, therefore consuming oxygen and increasing the
discrepancy, the pain diminished in the presence of stenosis) but at least at a coronary vasospasm, so that by "releasing" the vasospasm for unknown reasons, the
patient felt less pain by continuing to walk.
Unstable angina
There are three types of unstable angina, according to the Braunwald classification.
There are three degrees of severity from I to III and from A to C (there would also be a small letter not present in the table).
We have previously described a patient with pain at rest, elevated troponin but without ECG alterations: in an NSTEMI there is no need for underlining, two out of
three symptoms are enough (unlike STEMI, in which it is necessary to observe overlining) .
• I - New onset: people with typical exercise angina (not at rest), in the first month of onset. There is constancy in presenting symptoms for a certain level of effort.
Being of new onset (reports the pain for the first time), it is difficult to determine whether it is a chronic event or not, since we have not had time to evaluate it and
define it as such (it is not excluded that it may be something dynamic, a thrombosis): in the meantime I treat the patient as if it were unstable, giving him drugs,
letting him rest and returning him within a couple of days, in order to monitor the situation without resorting to hospitalization. The other is also known as
crescendo angina or accelerated angina : it is the situation in which one patient has stable angina but on returning to the clinic reports an increase in pain
intensity and onset for less intense activities (initially the pain appears after 800m of walking and after 2-3 months he reports more pain already after 500m): there
is a crescendo and it is no longer stable. All this creates a suspect in the doctor (all medicine is based on the theory of suspicion). I have to play in advance and
understand the extent of the deterioration, since such a situation can for example be linked to the appearance of thrombosis, which in turn can evolve or stabilize:
the situation is managed with frequent visits, intensification of the therapeutic regimen and if the frequency becomes such as to touch the instability at rest, we ask
for the patient to be hospitalized.
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• Angina at rest: it is further subdivided into subacute (II) and acute (III): in the first case it appeared in the last month but not in the 48h preceding the visit and in
the second of recent onset (<48h previous). If a patient has had pain at rest e.g. 10 days ago (subacute), it means that its endogenous fibrinolytic system managed
to avoid the closure of the vessels. If the 48h have not elapsed, I can have a similar situation whereby the organism manages to keep the situation under control or
the vessel can close, but at that moment I cannot know: as a consequence I will have that contrary to level II, the acute event requires immediate hospitalization
and pharmacological intervention. In fact, the doctor cannot be a spectator but must act by administering drugs that can already alleviate the state of thrombosis.
[From the 2017/18 rebounds: What medicines do we give pending 118? Certainly a sublingual nitrate but also an antiplatelet agent, i.e. 300 mg aspirin, therefore a
good dose (today also double antiplatelet agents, aspirin + clopidogrel are given). We also give him 100 mg of Propranolol (which is also a powerful
antiarrhythmic). We tell the patient to lie down, raise his tongue and take the medicine and in the meantime we called 118. So the classification is important
because it gives us instructions on the behavior to be taken on the spot, in real life. ]
A, B and C are three degrees of gravity that indicate the state of the patient in which the AI arises:
• A (Secondary): occurs more frequently in the case of type I AI. It is also defined as extracardiac because I have a crescendo, a worsening of the severity of
angina due to a factor that has become unstable (eg appearance of thrombosis with narrowing of the lumen, which increases and makes the pain earlier). Typically
I have a patient with fever, increased oxygen consumption and mild anemization (12 to 9 g / dL). It is the lowest degree of severity and does not require
hospitalization, but monitoring.
• B (Primary): it is a slightly more serious situation since the event is primary, there is no concomitant cause and is therefore defined as cardiac . The symptoms
are analogous, possibly with a more marked anemia.
• C (Post-infarction): it is the most serious situation and occurs in patients who have already had a heart attack only in the previous 15 days , that is, with the
probability that it is the same artery, even if a stent has been placed - it is gone in acute thrombosis. If the heart attack occurred 3 years ago, we speak of unstable
angina in previous heart attack .
The typical clinical manifestations of angina are shown again.
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To calculate the amount of undercutting at rest of the ST section, I choose a derivation, I find the isoelectric and I measure: 3 squares = 3 mm = 0.3 mV).
There is a sub-leveling in: V1, V2, V3 (V4 is normal): it is an anterior NSTEMI infarction.
What makes the interpretation of the electrocardiographic tracing complex is the doubt between having an elevation in DIII (not accompanied by a DII, to have 2
out of 3: a lower heart attack should have been: DII, DIII and aVF, while here c is only a DIII). Then there is a frank sub-leveling in V2, but in V1 it is not seen. This
patient is treated as an NSTEMI, having only one derivation with leveling so it could be a previous STEMI. Sometimes, if the wall becomes aneurysmal, the leveling
remains. Furthermore, even if we had a negative pattern, the pain and the positive troponin (2 out of 3 elements) suggest an NSTEMI as a diagnosis.
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For a patient who arrives in the clinic with recent retrosternal pain, I must avoid the stress test as the general rule states that 48 hours must pass without painful
manifestations. Therefore you can think of resorting to holter and monitor the patient in 24 hours, in order to highlight any alterations: this examination has still
important clinical validity, albeit now little used since they are few and require a long time for the clinician.
Risk stratification
If in STEMI it is the timing (time is muscle) that matters, in NSTEMI the key word is risk stratification : one wonders if angiography should be done immediately (
early invasive therapy ) on arrival at the clinic. better to wait and before discharge, eventually do an exercise test or other tests, such as an echo ( conservative
therapy ).
The answer seems obvious: if I have an ejection fraction <40% or stress test with 4-5 mm sub-leveling, it is necessary to act urgently by immediately bringing the
patient into angio; otherwise I will do the tests anyway, but with less urgency (in reality, it depends a lot on the waiting lists).
Currently doctors, public opinion, industries are very much in favor of early invasive, without any evidence.
TIMI Risk Score (UA / NSTEMI)

The TIMI Risk Score is a risk assessment score which is used to help the doctor in choosing the therapy based on the urgency with which the patient is to be
treated. It is important to act promptly by calling 118 and starting drug therapy before arriving at the hospital (about 2 hours before):
• Aspirin (300 mg)
• Clopidogrel (75 mg in acute but 600 mg in the room), an antiplatelet. These drugs are associated in what is called Dual Antiplatelet Therapy , i.e. therapy based
on two antiplatelet agents .
• I can possibly administer beta-blockers (eg propanolol, metaprolol) with anti-arrhythmic function: this is important both for the decrease in the consumption of O 2
in acute, but also because in the first 72h from the event I have the highest frequency of lethal arrhythmias . In history, these therapies and the invention of the
Coronary Unit (in the 1950s) have lowered mortality from 25% to 17-18%.
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When we first approached thrombolysis, in 1992 there was a trial ( ISIS-2 ) in which various subjects were analyzed:
• One group was not treated pharmacologically

• Some treated with thrombolytics (streptokinase)
• Some treated with aspirin
• Some treated with streptokinase + aspirin
It was seen that in patients treated only with aspirin or only with streptokinase, it had the same beneficial effect, while put together, a superior result was obtained.
This means that aspirin is a very powerful antiplatelet and therefore early administration is the minimum required. It is therefore very important to know these drugs,
in order to intervene promptly.
I can also decide to administer anticoagulants (e.g. heparin) but it all depends on the severity and the clinic helps me to define the level:
• 6-7 points → high risk score
• 3-4 (5) points → medium risk score
• 1-2 points → low risk score
CAD = Coronary artery disease

ASA = AcetylSalicylic Acid
It is made up of 7 points and the important aspect is that not only high ECG and troponins are present, but other important clinical variables are also added . So
you can also assign 5 points with the clinic alone, despite having ECG and troponin negatives.
So if a patient has only elevated biomarkers and elevation, he has only 2 points and is low risk. Therefore, importance is given to the clinic: only by questioning the
patient can the score rise by 5 points, passing to a high risk.
The professor hints at current controversies about the use of drugs because of their side effects. There is controversy over the use of aspirin as primary prevention
(75mg), although the side effects are gastritis,
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gastric bleeding, cerebral hemorrhage. With the arrival of statins, the administration of aspirin is suggested infrequently , that is, not often. However, it is good to
remember that statins have a protective role against atherosclerosis, but do not reduce aggregation. In fact, if the plaque breaks, it is aspirin that avoids
thrombosis, not statins.
GRACE Risk Score

The Grace Risk Score is more recent (about 10 years ago) and more popular than the TIMI Risk Score and is based on several components:
1. Age 2. CF 3. Systolic arterial pressure 4. Killip class * 5. Use of diuretic (in the absence of information on the Killip class) 6. Serum
creatinine 7. Renal failure (in the absence of information on creatininemia) 8. Deviation of the ST segment 9. Cardiac arrest at the entrance
10. Elevated troponin
* Killip Class is the extent of heart failure at the time of the clinical presentation. The classes are:
• KILLIP I: the patient has no signs or symptoms of heart failure
• KILLIP II: there is an initial decompensation because there are rales in the lower half of the lung (in the upper half we speak of acute pulmonary edema)
• KILLIP III: the decompensation is severe, there is acute pulmonary edema with widespread rales
• KILLIP IV: cardiogenic shock or heart failure, with a huge prognostic value. In fact, the probability of death - in Killip III and IV - increases by 7-8 times.
Criticism the influence given by age and decompensation. In fact, in the event of a failure, an increase in frequency is observed with a drop in blood pressure: the
heart does not pump, the systolic range is lowered and the pressure drops and, to compensate for this drop, the frequency increases.
ECG acute pericarditis
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There is a widespread ST elevation and its concave morphology is significant : this is the typical pattern of an acute pericarditis.
Acute Coronary Syndrome: therapy

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FMC
The FMC can be performed in the hospital or before and it is always very important for the concept that time is muscle , so if I can intervene even before the arrival
of the ambulance, I recover precious time.
There are differences between the American and European systems: for example, if for the first ones a primary angioplasty (PCI) should be done within 2 hours at
most from the onset of symptoms, for Europeans the 2 hours are calculated starting from the FMC (Americans add a one hour time margin to surgery - since
symptoms started, for up to 3 hours). In addition, from the moment in which the first manifestation of the symptoms occurs to the moment in which they are called
aid, precious time elapses: about 50 minutes for women, 40 for men. In fact, not everyone thinks they have a heart attack and there is a part of us who rebels
against the idea of having one in place.
This is important on the choice of surgery: primary angioplasty, fibrinolysis or both.
Primary PCI strategy

It is an emergency coronary angiography with possible PCI (angioplasty), if indicated, on the infarcted coronary artery.
fibrinolysis
Fibrinolytic therapy is performed immediately, for example when there is no possibility to immediately bring the patient to the hemodynamic room, avoiding the
occurrence of major heart failure. The vessel reopens, the pain decreases but at some point it can also recur. Another fibrinolysis can be done but it carries a great
risk, because I have to take into account that a cerebral hemorrhage may occur
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because of the two consecutive fibrinolytic therapies. At this point I must necessarily make a rescue (even if 3 hours have passed).
Rescue PCI
It is an emergency PCI, performed after fibrinolytic treatment failure.
There are fixed European rules: after a maximum of 2h from the FMC (3h in the USA from the beginning of the symptoms) → immediate fibrinolysis, afterwards the PCI is
performed. It's called a drug-invasive strategy , whose effectiveness * has been demonstrated through studies carried out by the Canadian Armstrong. Difference
between efficacy * and efficiency : efficacy is tested with a trial. Ex: Thrombolysis has been determined to be lower than angioplasty through studies with specific
recruitment criteria:
- Arrive within 2h - Age between 45 and 75 However the study is subject to bias, because it only applies to patients who participate.
Instead, efficiency is measured in the field with the clinic.
A primary hemodynamic center must always be available to carry out the PCI in a timely manner, with a doctor and three nurses ready to intervene at any time (in
the Emilia-Romagna region there is not, but only one of availability for which the doctor presents himself on call).
Target time intervals (maximum expected times)
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The professor recalls the importance of the ability to read an ECG in first aid and underlines that the only areas for which specialization is required by law are
forensic medicine and anesthesia. He adds that for a long time the therapeutic delays due to the non-readiness of the operating rooms have been frequent,
problems now partially solved.
Initial management of the patient with STEMI
The first intervention in case of diagnosis of STEMI is pharmacological (aspirin, clopidogrel and possibly beta-blockers). After:
- If the SaO 2 is <90% or PaO 2 <60mmHg I must administer oxygen but only for such marked decreases, while it is usually not administered: in fact - according to a
trial from last year - O 2 has an important vasoconstriction effect and therefore the coronary situation worsens. Oxygen deficiency, for which administration is
required, is more frequent for pulmonary embolism. - Regarding the use of opioids, the professor disagrees because, for example, if we are carrying out fibrinolytic
therapy (with the PCI and the contrast medium we see that the vessel is no longer occluded) and the pz does not feel pain due to the effect of analgesics, it is not
possible to understand if the therapy is having an effect and reperfusion has taken place, therefore the ECG must be forced. The maneuver is not very painful,
therefore the patient can endure even with the administration of tranquilizers. Recently the guidelines have shown that opioids also reduce the effects of
antiplatelet agents.
Leave the following slides as "notes".
Page 70 of 97
Ischemic therapy
Stem Reperfusion:
By reperfusion therapy is meant the restoration of coronary flow and the reperfusion of myocardial tissue through two ways:
• mechanical reperfusion therapy, ie primary angioplasty (primary PCI) where I go inside the vessel with the balloon and go to dilate the coronary artery. Primary
PCI means an angioplasty and / or stent implantation without prior or concomitant fibrinolytic therapy.
P. 71 of 97
• drug therapy, through an infusion of thrombolytics, or substances that dissolve the thrombus, are potently anticoagulants, the first is Streptokinase then there are
others such as the bolus of t-PA (? 2:21) that is used more . Unfortunately, before realizing that you are having a heart attack, in woman in particular, they are able
to spend hours and hours of time, but the 12 h limit is considered as insurmountable. But why 12 h? How many times do you spend so much time? In 30% of the
population 12 hours pass before the intervention and this delay occurs especially in women and the elderly and in any case it is not possible to reperfuse all, the
proportion of non-reperfused has fallen to 25% but it is not zero also because we must consider the Eastern countries such as Romania where there are transport
difficulties. In addition, there was also a mental malformation of the doctor, the so-called defensive medicine, or that of sending immediately after the detection of
the symptom or the first medical contact (FMC) the transfer to the central medical center to make a PCI, sometimes even before the therapeutic administration
(aspirin). Why 12 h? everything was born from fibrinolysis, after its discovery in the 90s, hospital mortality was substantially reduced (11%), these drugs were given
to everyone at any time by the cardiovascular event, also thanks to the economic benefits that the industries derived from being these expensive drugs, the
hypothesis of "open coronary" (better always an open than closed coronary) was created, in reality then this caused many bleeding accidents such as cerebral
hemorrhages and heart ruptures, in fact the ischemic tissue if made hemorrhagic tends to break more easily. More than 12 hours later, the advantage of fibrinolysis
is lost (max efficacy in the following 2-3 hours), afterwards it is more evil than good. Why has the advantage of 12 h fibrinolysis been extended to PCI? Indeed, the
risks of the benefits were seen to be greater.
But in the case of unstable STEMI, angioplasty must also be done over 12 hours without time limit, in particular in the presence of:
• clinical evidence: I still do the surgery because we have persistence of pain and ischemia (continuous changes in the ECG) despite drug therapy.
• Hemodynamic instability (in cardiogenic shock or acute pulmonary edema with risk of shock): reperfusion is essential (despite the drugs, because after 5-6 h
dopamine loses its effectiveness and the doses must be tripled for tolerance phenomena).
• Electrical instability after ventricular fibrillation (potentially fatal arrhythmias).
Furthermore, in stable STEMI, PCI can be performed after 12 h but within 48 h, as was established by the new European guideline, which however is based on
data from small, unimportant clinical trials, i.e. not based on scientific evidence. such as mortality and heart attack, but on other surrogate markers of lesser value
such as size of the infarcted area (which does not necessarily correspond to mortality by scintigraphy / pet), this guideline (not based on certain evidence but on a
"consensus" among experts) in Europe he therefore extended the intervention to 48 h.
Coronary stents in STEMI:

-Bare Metal Stent (BMS): metal stents
-Drug Elutin Stent (DES): BMS preferred medicated stents for primary PCI in STEMI.
For those of the first generation it must be remembered that they caused acute and immediate thrombosis by 48 h late if coinciding with the suspension of
Clopidogrel.
Primary PCI and concomitant antithrombin and antipoatrinic therapy

The main drugs used are:
o Aspirin os o ev o ADP inhibitors and receptors: Clopidogrel, Prasugrel, Ticagrelor.
With BMS, Clopidogrel therapy should be maintained for 1 month while with DES it continues for 1 year if there is acute coronary syndrome while if chronic for 6
months. Hence the strong contraindication for these drugs
Page 72 of 97
(double aspirin therapy) are the surgeries in the 12 months following the stent implantation (risk of bleeding).
Phosphodiesterase inhibitor drugs equal to Clopidogrel were created, which had become generic and was no longer profitable for industries, such as Prasugrel and
Ticagrelor. The classic attack Clopidogrel dose was 300 mg then for one year or 6 months 75 mg per day.
The Oasis7 study was published in the 2007 New England Journal which showed that there was a significant difference between a double dose of initial clopidogrel
(600 mg load, 150 mg for the next 7 days and 75mg thereafter) and the standard regimen ( 300 mg of load and subsequently 75 mg / day). Adopting the double
dose has seen a 20% improvement in mortality with more frequent but not fatal (non-cerebral) bleeding with great success of the double dose. In the two new
drugs there was a comparison error as the 300 mg dose for Clopidogrel was used, obtaining marginal successes only in Ticagrelor, the guidelines therefore
consider them equal to discretionary use by the doctor. However, the best is always the Clopidogrel.
o GPIIb / IIIa inhibitors: powerful antiplatelet drugs but at great risk of bleeding, today
they are no longer used except in the no-reflow phenomena where the blood does not flow and all possible means are used to reopen the patient, also breaking the
plaque creates microthrombi in the microcirculation that I try to dissolve with inhibitors. o Anticoagulant therapy together with platelet therapy: unfractionated
heparin in the vein (older) in the
late patient after 12 o'clock whom nothing is done, enoxaparin subcutaneously used only if coupled with fibrinolysis which already alone has a clear scalding effect
(PCI). If I am "firing" a thrombolysis it is better to use a less powerful anticoagulant subcutaneous and not in the vein. Drugs to be given in the emergency on the
street: Aspirin 100 mg, Clopidogrel 300 mg (in the hemodynamic room it starts from 600 mg), Beta-blocker 100 mg (1 pill) and Enoxaparin subcutaneous bolus
from 5000 (we are on the street we will think later if it was better to give more!).
If I see bruising, I stop the Tivagrelor and give the Clopidogrel.
When do I decide to carry out fibrinolysis or to send to the Major for invasive surgery? Drug-invasive therapy is performed: first the drug and then the invasive
action is considered if the arrival in the hospital is expected beyond 2 to 3 h from the symptoms, otherwise an primary PCI invasive intervention is immediately
performed.
FIBRINOLYTIC AGENTS
Fibrinolytic agents are:
• non-fibrin specific: Streptokinase (SK)
• fibrino specific: Alteplase (t-PA), Reteplase (r-PA) and Tenecteplase.
Contraindications to fibrinolytic therapy
• Refractory hypertension (hypertension already treated with antihypertensive drugs) at PAS 180 and / or PAD 110 mmhg, a condition in which it is easier to have a
cerebral hemorrhage, if you take a sublingual Nifedipine pill (it lowers PA by 30 mmhg) or with intravenous nitroglycerin and fibrinolysis I destroy the heart.
• Active peptic ulcer: but it is related to the severity of the bleeding because in certain cases thrombolysis is still necessary.
• Ischemic stroke in the previous 6 months or recent brain trauma (risk of cerebral hemorrhage)
• Known coagulation disorders: VWF, rare hemophilic diseases
• Aortic dissection (I was wrong to diagnose because together dissection and myocardial infarction are practically impossible)
P. 73 of 97
• Non-compressible punctures (lumbar puncture in the previous 24 h), which presumes the clinical suspicion of a hemorrhagic stroke, today with the CT it is
immediately clear whether the stroke is hemorrhagic or ischemic without the need to do lumbar puncture.
Contraindications to fibrinolytic therapy
Absolute contraindications
• Hemorrhagic stroke or stroke of unknown etiology at any time
• Ischemic stroke in the previous 6 months
• Pathology or neoplasm of the central nervous system
• Recent adjunct trauma / surgery / head injury (in the previous 3 weeks)
• Gastrointestinal bleeding in the past month
• Known coagulation disorders
• Aortic dissection
• Non-compressible stings (eg liver biopsy, lumbar puncture) in the previous 24 hours
Interventions after fibrinolysis
Relative contraindications
• Transient ischemic attack in the previous 6 months
• Oral anticoagulant therapy
• Pregnancy or childbirth in the last week
• Refractory hypertension (PAS> 180 mmHg and / or PAD> 110 mmHg)
• Advanced liver disease
• Infectious endocarditis
• Active peptic ulcer
• Refractory resuscitation
• PCI of rescue (rescue): evidence of failed fibrinolysis (ST segment resolution 50% lower than 60 minutes after the administration of the lytic agent) or in patients
with extensive heart attack, if performed within 12 h from the onset of symptoms, the pain symptom makes it clear if the patient is unclogged (avoid opioids).
• Emergency PCI: recurrent ischemia, re-inclusion after effective fibrinolysis or in patients with heart failure / shock.
• Angiography: with the intent to revascularize after effective initial fibrinolysis. Optimal timing of angiography: in stable patients with evidence of effective
fibrinolysis, the examination is done after 3-24 h (better 24 h because the effect of fibrinolysis has passed) from the beginning of fibrinolytic therapy.
Concomitant therapy with antithrombin and antiplatelet drugs in combination with fibrinolytic therapy
▪ Concomitant therapy with platelet aggregation inhibitors: If the patient and is not already being treated with ASA
• ASA os (soluble or chewable / unprotected) or IV in addition to:
• Clopidogrel os loading dose if age → ▪75 years
• maintenance dose if age> 75 years
▪ Concomitant antithrombin therapy
▪ with t-PA, r-PA, TNK-tPA:
• Enoxaparin bolus ev. followed by a first sc administration (if age → ▪75 years)
• Age> 75 years begin with reduced dose SC administration
• Unfractionated heparin (UFH) IV administration adjusted for body weight with first control of aPTT after 3h)
▪ With strepkokinase: Fondaparinux
Page 74 of 97
At the beginning, everyone was always given a fibrinolysis before ending up in the hemodynamic room (facilitated, before drug-invasive therapy) regardless of
whether the hospital could be reached on time or not, with load therapy. In case the patient gets sick again after fibrinolytic therapy, we move on to the "rescue
PCI" case and immediately send the patient to the hemodynamic room without worrying about the time that must pass from the administration of the same.
Questions and clarifications:

But do I have to make a prescription for the pharmacist while I am there? Of course not, you give the card and get the drug immediately, under penalty of
denunciation.
Speech of 3-24 h: the ideal time to do PCI after fibrinolysis would be 24 h, but it is also legitimate 3 h because the effect of fibrinolysis should disappear. If the
patient does not reperfuse with fibrinolysis, he passes to the rescue plan, everything is done to save it, such as intramyocardial adrenaline injections.
PCI and fibrinolysis it is preferable to do them within 12h (strictly 12 fibrinolysis) at most 24h.
PCI is done in any case, even if fibrinolysis has worked, I have to carry out a cleaning, but not after 48 h, after which nothing is done.
Flow classifications (at the end of the course it will show it applied to angiography)
A successful angioplasty is defined not only anatomically (with the stent, less than 20% of residual stenosis), but also with the TIMI flow (i.e. the flow that can be
seen angiographically) which must be 3.
TIMI 0: nothing passes

TIMI 1: there is an advancement up to half of the contrast medium vessel, it does not reach the distal bed
TIMI 2: descends very slowly so there is still something that obstructs, arrives at the distal bed with delayed speed
TIMI 3: descends instantly, there is a normal flow
Women die more than men because after an anatomically successful operation, TIMI flow is more than 2 times more than 3, probably the woman is more
vasoconstricted (greater coronary reactivity, one of the causes).
G radii of flow in the vessel related to the heart attack according to the classification of the TIMI group
Quantitative evaluation by heart-related artery blood flow angiography The goal of re-effusion therapy is a TIMI grade 3 flow
TIMI 0 ▪ Complete occlusion of the artery that caused the heart attack.
Absence of antegrade flow beyond the TIMI 1 occlusion point ▪ The contrast medium passes through the obstruction area, but
without perfusion of the coronary bed distal to the TIMI 2▪ obstruction perfusion of the entire infarcted artery towards the coronary bed
distal but with delayed flow (velocity) compared to that of a normal TIMI 3 artery ▪ complete reperfusion of the infarcted artery with normal flow
Pag. 75 of 97
In patients without reperfusion therapy, Aspirin, Clopidogrel and Unfractionated Heparin (stronger parenteral anticoagulant that avoids relapses and new crises) are
administered as soon as possible.
Right ventricular infarction treatment
-Maintain adequate right ventricular preload

-Inotropic support: Dobutamine, works for a few hours, but little action in shock
-PCI, as soon as possible
Often in therapy, the aim is to reduce the load failure of the left ventricle as ACE inhibitors which, however, cause a reduced venous return to the heart with
consequent shock due to failure to fill the right ventricle.
So avoid Nitrates and ACE inhibitors and prefer to give a load of fluid (2 L), by monitoring the pressure of the left atrium which must be below 20 mmhg (limit, you
are in the abnormal, but the ventricle pushes little, if you load a little more is not a big problem).
NSTE-ACS therapy
Routine invasive approach or selective invasive approach?

While there is occlusion in STEMI, there is subocclusion here so there is no evidence that invasive therapy within 12 h is necessary. The intervention, however, is
done more frequently than a conservative approach (first the stress test or an ultrasound that if denotes an FE less than 40% then requires an invasive approach,
but only in these exceptional cases). But often this type of intervention does not reflect the right timing (less than 12 h) because the services are jammed.
NSTE-ACS therapy : invasive or medical (more conservative). They fought for twenty years, in the end with the fact that there is no precise argument, everyone
decides to do which he prefers. The two therapies are not mutually exclusive, but the difference lies in the timing.
Page 76 of 97
There is early basic therapy : in 24 hours I have already done angio and PCI. The other one is called conservative : I don't do it because it seems to me that you
are fine, but if you feel bad, if the ultrasound tells me that the fraction is less than 40%, if you get an attack of pain, if the stress test is markedly positive then I'll do
it: it doesn't exclude it, but I won't do it right away.
Here the key word is not "time is muscle" but risk stratification or risk stratification, the risk profile is important for the choice of the strategy to be carried out, as
there are more risk categories assessed with the TIMI score, with the GRACE score , but also with the clinic, when I see an elderly or diabetic patient, for whom
invasive therapy is preferred. In the guidelines, a GRACE score above 140, a depressed left ventricular obstruction (FEVS = left ventricular ejection fraction <40%),
new crises in progress, elevation or decrease of hs-cTn (fundamental parameter! If it varies, first use this parameter because troponin is a very sensitive index I am
not interested in the GRACE score which instead is important in the therapy of unstable angina where troponin does not vary). The population on which risk
stratification is eventually done is greatly reduced because it is the one that has never had elevated troponin (as for unstable angina), these patients are very few,
about 10%.
Timing invasive strategy regardless of whether STEMI or NSTEMI, or even for stable angina:
immediate in hemodynamic instability, arrhythmic instability, in ventricular fibrillation.
Invasive routine approach
Coronary angiography (early invasive strategy)
Class I - Level of Evidence A
• Hemodynamic instability or cardiogenic shock
• Active or recurrent angina / ischemia refractory to maximal medical therapy
• Ventricular tachycardia or sustained cardiac arrest
• Acute heart failure with refractory angina / ischemia and ST-segment deviation
• Left ventricular function depressed (FEVS <40%) or congestive heart failure
• Sub-leveling of the new or presumably new ST-section
• Elevations or decreases in hs-cTn concentrations
• Results of non-invasive tests suggestive of high risk
• GRACE score> 140
• Recent PCI (last 6 months)
• Previous CABG
Page 77 of 97
Timing of the invasive strategy
Immediate invasive strategy (<2h): in the presence of any of the following very high risk criteria
• Hemodynamic instability or cardiogenic shock
• Recurrent or refractory chest pain in medical therapy
• Life-threatening arrhythmias or cardiac arrest mechanical complications of MI
• Acute heart failure with refractory angina or ST segment deviation
• Recurrent dynamic modifications of the ST section or T wave, especially in the event of intermittent elevation of the ST section
Early invasive strategy (<24h) in the presence of any of the following high risk criteria
• Elevation or decrease of troponin concentrations suggestive of IM
• Dynamic modifications of the ST segment or T wave (symptomatic or silent)
• GRACE score> 140
Invasive strategy (<72h) in the presence of: any of the following intermediate risk criteria :
• Diabetes mellitus
2
• Kidney failure (eGFR <60ml / min / 1.73m )
• LVEF <40% or congestive heart failure
• Early post-infarct angina
• Recent PCI
• Previous CABG
In patients without any of the aforementioned risk criteria
• GRACE score between> 109 and <140 and without relapsing symptoms ▪
• Relapsing symptoms or evidence of non-invasive detection of ischemia (preferably
of ischemia on non-invasive tests
with imaging tests) before opting for invasive evaluation
Disputes between invasive and non-invasive therapy: the 1998 Vanqwish trial proves that invasive therapy gives more deaths or heart attacks than conservative,
while the 2000 Frisk is clearly in favor of the invasive. Complications on a hot plate (early invasive therapy) are easier, microembolizations that give non-reflow, if
hot, are more easily created.
A group of American researchers said that the stent can create more thrombi of the balloon, in a trial they then went to open with the balloon only, leaving the
catheter in place and after 16 h go to put the stent with TIMI flow results clearly better, the guidelines leave the choice between the two therapies (go immediately
or later), apart for the high risk categories, but the trend is still to open more than the conservative approach.
Page 78 of 97
Acute phase therapy in NSTE-ACS (the same already treated)
Beta blockers
Nitrates
-Asa (initial load 150-300 mg followed by a maintenance of 75-100 mg / day)
-Clopidogrel (initial load 300-600 mg followed by 75 mg / day)
-Ticagrelor (initial load 180 mg followed by 90 mg)
-Prasugrel (initial load 60 mg followed by 10 mg / day)
- GPIIb / IIIa inhibitors only in case of thrombotic complications.
Anticoagulant therapy in acute phase in NSTE-ACS:
-Enoxaparina
-Unfractionated heparin (since there is no associated thrombolysis, it is preferred in this case)
Oasis-7 trial: Clopidogrel standard (300 mg) vs Clopidogrel double (600 mg).
15% reduction in heart attack using double the standard dose.
Tritoton trial (single study): Prasugrel vs Clopidogrel (BUT COMPARE WITH 300 mg!)
Obviously Prasugrel should have won the game, but in reality the mortality did not improve, the reinfarction improved a little at 6 months, and then if I analyze the
analysis of the subgroup there is a non significant (= non trend, odd ratio a intercepts the line) in females, in patients over 65 years, in patients with renal
insufficiency (creatinine clearance). Why then is it used instead of clopidogrel if I have to exclude a category of people?
Ticagrel is also compared with clopidogrel 300 mg (single study), but here we see at least a reduction in mortality (from 4.3 to 3.4%). If the 600 mg load is used
(Swedish trial), however, ticagrel is no longer significant. Nonetheless, European society continues to regard all 3 as equal.
Pag. 79 of 97
ARRHYTHMIAE
Definition: irregular origin, frequency, rhythm, conduction speed and activation sequence of the cardiac conduction system.
Causes: (many)
-Myocardial ischemia: most arrhythmias are induced by myocardial ischemia
Congestive heart failure: death from pulmonary edema if acute, if chronic instead from arrhythmia because in dilated pathologies the disarray is formed (the fibers
are no longer exactly lined up) with ventricular fibrillations and tachycardias.
-Acute hypotension: if you collapse for hypotension you go to tachycardia to maintain the output (= systolic range x heart rate), if the systolic range falls by nature
the frequency increases
Acid-base and electrolyte balance imbalances: with cardioplegia surgeons during the surgery stop the heart thanks to excess potassium (potassium-sparing drugs
+
such as aldosterone antagonists cause a K even at 9, severe renal failure with creatininemia at 1, no, insufficiency with creatininemia at 1 is impossible, you are
chronically taking aldosterone inhibitors)
-Caffeine: causes tachycardia but there is addiction in consumption
Ethanol (after a hangover collapse and tachycardia)
Mechanisms (slide)
-Irregular beat formation: ectopic beat or triggered activity (post-potential)

-Irregular conduction of the beat: re-entry or conduction block
Classification
Bradycardia (hypokinetic arrhythmias)

-Tachycardia: subdivision in case by case, supraventricular or ventricular, sustained or not, synchronized or de synchronized, paroxysmal, persistent, permanent
and iterative
60 to 100 is the normal frequency
Hyperkinetic arrhythmias: supraventricular tachycardias
Sinus tachycardia:
Page 80 of 97

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3/13/2020 https://translate.googleusercontent.

Medicine and Surgery - Channel A - 3rd year

Introduction to the course

Other "classic" risk factors are:

Heart attack symptoms

Reverse Robin Hood phenomenon [Sbobine 2017/2018]

CAUSES OF MYOCARDIC ISCHEMIA :

Example of plaque occluding 30% of the vessel.

Glagov's Coronary Remodeling Hypothesis

Determinants of plaque rupture:

Bidra med en bättre översättning

OCT by ophthalmologists can be used easily to perform operations on the retina.

Vulnerability of the patient

A vulnerable plaque is often associated with patient vulnerability factors:

ECG, Stress Test and SPECT

It is the wave of atrial depolarization. A non-normal P can only be of 2 types:

We will see the axial deviations on the field.

Normal basal ECG

There are 2 of them:

Arrhythmias necessarily have negative prognoses. Modifications of the t wave

Duke Treadmill Score

Stable coronary artery disease (SCAD)

The professor did not mention it.

DIFFERENTIAL DIAGNOSIS FOR THORACIC PAIN FROM ISCHEMIA:

The pharmacological MANAGEMENT STRATEGY is based on 2 cornerstones:

ACUTE CORONARY SYNDROMES

Fourth definition of myocardial infarction

Type 4 is in turn divided into

Indeterminate or multifactorial group

Differential diagnosis of prolonged chest pain

ECG manifestations in myocardial infarction

Common trunk occlusion ECG

Acute Coronary Syndrome: clinic and diagnosis

Continuation of the previous lesson.

• Common trunk obstruction: associated with aVR elevation.

Acute coronary syndromes without ST elevation (NSTE-ACS)

Unstable angina (UA or AI)

The typical clinical manifestations of angina are shown again.

TIMI Risk Score (UA / NSTEMI)

• One group was not treated pharmacologically

CAD = Coronary artery disease

GRACE Risk Score

ECG acute pericarditis

Acute Coronary Syndrome: therapy

This is important on the choice of surgery: primary angioplasty, fibrinolysis or both.

Primary PCI strategy

Target time intervals (maximum expected times)

Initial management of the patient with STEMI

Leave the following slides as "notes".

Coronary stents in STEMI:

Primary PCI and concomitant antithrombin and antipoatrinic therapy

Contraindications to fibrinolytic therapy

Contraindications to fibrinolytic therapy

Questions and clarifications:

TIMI 0: nothing passes

Right ventricular infarction treatment

-Maintain adequate right ventricular preload

Routine invasive approach or selective invasive approach?

Acute phase therapy in NSTE-ACS (the same already treated)

Anticoagulant therapy in acute phase in NSTE-ACS:

-Irregular beat formation: ectopic beat or triggered activity (post-potential)

Bradycardia (hypokinetic arrhythmias)

60 to 100 is the normal frequency