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Fisiopatologia 3) CARDIOPATIE ISCHEMICHE Antonio Nenna

CARDIOPATIE ISCHEMICHE

Presentazioni cliniche:
- angina pectoris
- infarto miocardico
- scompenso cardiaco congestizio
- morte improvvisa

Una ischemica cardiaca causa una diminuzione del batmotropismo e facilita la fibrillazione atriale (FA).

La cardiopatia ischemica ha sette fattori di rischio (FdR) che si dividono in:


NON MODIFICABILI: età (> 55 a), sesso (M), familiarità
MODIFICABILI: sigarette, ipertensione arteriosa, iperlipoproteinemia, diabete mellito

Target di riferimento terapeutici del colesterolo LDL


norme terapia
numero FdR target LDL
comportamentali farmacologica
0–2 < 160 > 160 > 190
>2 < 130 > 130 > 160
rischio < 80 > 80 > 130
no prolemi dieta, attività dieta, attività, farmaci

Le iperlipoproteinemie che interessano le cardiopatie ischemiche si classificano secondo Frederickson in:


- tipo 2a: ipercolesterolemia, LDL elevate, trigliceridi normali, HDL normale (aterosclerosi) (plasma chiaro)
- tipo 2b: ipercolesterolemia, LDL elevate, trigliceridi alti, HDL normale
- tipo 3: ipercolesterolemia, LDL elevate, trigliceridi alti, VLDL elevati, HDL normale (xantomi)

Cause di cardiopatie ischemiche:


- aterosclerosi coronarica (90%) (dovuta ai fattori di rischio modificabili!)
- vasculiti (lupus), trombofilia, estroprogestinici (aumento del rischio di 35 volte), stupefacenti

Quadri clinici:
- angina stabile [dopo uno sforzo prolungato, scompare a riposo]
- sindrome coronarica acuta (angina instabile, infarto miocardico Q, infarto miocardico non-Q)
- angina variante di Prinzmetal [per vasospasmo di arterie con placche aterosclerotiche]
- sindrome X [ECG da angina ma coronarie indenni => problema intramiocardico, difficilmente corretto]
L’ischemia miocardica acuta (ST sopralivellato) può procedere in infarto Q (onda Q) o angina di Prinzmetal
(ST normale => ST sopralivellato => fibrillazione atriale => fibrillazione ventricolare => morte).

L’onda Q in alcune derivazioni è fisiologica ma in altre è patologica e indica un infarto Q.


Una onda Q è patologica quando ha ampiezza maggiore di ⅓ del complesso QRS o durata > 0,04 s.
Un infarto può essere transmurale (infarto Q) o subendocardico (infarto non-Q).
L’infarto transmurale impegna tutto lo spessore della camera ventricolare, come se fosse un buco nella ser-
ratura; l’infarto subendocardico, invece, occupa solo una parte dell’endocardio e non tutto lo spessore.
Il segno di cicatrizzazione (visualizzabile anche all’ECG) è visibile per l’infarto transmurale, ma non per quel-
lo endocardico.

Infarto inferiore: II, III, aVF


Infarto laterale: I, aVL
Infarto anteriore: derivazioni toraciche
Fisiopatologia 3) CARDIOPATIE ISCHEMICHE Antonio Nenna

ANGINA
Angina stabile: placca che limita il flusso sanguigno sotto sforzo
Angina instabile: distruzione della placca con sovrapposizione di trombo, vasospasmo e erosione. Cause:
stenosi critica prossimale dell’aorta discendente anteriore; malattie del tronco comune o dei “tre vasi”.
L’angina instabile è un nuovo esordio di angina grave o una angina in crescendo o una angina “nuova”.

La diagnosi di angina instabile si basa sull’ECG. In corso di dolore l’ECG è normale, ma dopo 12 ore si hanno:
- T bifasico
- elevazione minima degli enzimi
- modificazione dell’ECG durante il dolore
- ST sopralivellato in aVR e V1
- ST sottolivellato in almeno 8 derivazioni

INFARTO DEL MIOCARDIO


Per fare diagnosi di infarto devo avere almeno due dei tre elementi caratteristici:
1. DOLORE
2. E.C.G.
3. ENZIMI CARDIACI

Dolore nell’infarto:
- dolore retrosternale (anteriore) aggravativo
- torpore o irradiazione dolorifica all’arto superiore sinistro
- dolore interscapolare (posteriore)
- dolore epigastrico nell’infarto inferiore
- dispnea, sudorazione, nausea, vomito
I diabetici possono non presentare sintomi a causa della neuropatia degenerativa diabetica.

ECG nell’infarto:

normale normale depol e ripol

ischemia
ritardata ripol ST sottolivellato
(zona periferica)

lesione
ritardata depol e ripol ST sopralivellato
(zona intermedia)

infarto
assenza di depol e ripol onda Q
(zona centrale)

Enzimi cardiaci nell’infarto:


enzima evidenza picco normalizzazione
CK 6h 24-30 h 3-4 gg
CK-MB 4-6 h 18-24 h 2 gg
troponina 6h 12 h 7 gg
mioglobina 2h 12 h 7 gg
AST 8-12 h 36-48 h 3-5 gg
LDH 12-24 h 48-96 h 7-10 gg
Fisiopatologia 3) CARDIOPATIE ISCHEMICHE Antonio Nenna

Algoritmo diagnostico della sindrome coronarica acuta:

Approccio iniziale al paziente con IMA:


- accertare il tempo di inizio del dolore
- registrare ECG in 12 derivazioni (sede dell’IMA, ST sopralivellato, onda Q, disturbi di conduzione)
- identificare il trattamento
- registrare V4destra nell’infarto inferiore (a destra e non a sinistra come solito) per escludere l’infarto di VD

La registrazione di V4destra nell’infarto inferiore è importante perchè permette di:


- identificare l’arteria occlusa
o ST sopralivellato con T positiva => occlusione prossimale della coronaria dx (infarto DX)
o ST normale con T positiva => occlusione distale della coronaria dx (infarto DX)
o ST normale con T negativa => occlusione della coronaria sn circonflessa (infarto SN inferiore)
- identificare l’IMA del VD
- valutare il rischio di blocco atrioventricolare (1°, 2°, 3° grado)
- identificare il beneficio della tromboembolisi

Soffi sistolici associati a infarto:


- soffio sistolico all’apice (insufficienza mitralica transitoria dovuta a ischemia della base del m. papillare)
- soffio olosistolico all’apice, può essere irreversibile in caso di rottura del m. papillare (infarto)
- soffio olosistolico margino-sternale inferiore sn, per rottura del setto interventricolare
Fisiopatologia 3) CARDIOPATIE ISCHEMICHE Antonio Nenna

ISCHEMIC HEART DISEASE1 2 3


ISCHEMIC HEART DISEASE
Ischemic Heart Disease (IHD) is a condition in which there is an inadequate supply of blood and oxygen to a
portion of the myocardium. This occurs when there is an imbalance between oxygen supply and demand.
The most common cause of myocardial ischemia is atherosclerotic disease of an epicardial coronary artery.
A high-fat and energy-rich diet, smoking and a sedentary life-style are associated with IHD. Other risk fac-
tors include obesity, insulin resistance, type-2 diabetes mellitus.

Under normal conditions, for any given level of demand for oxygen, the myocardium will be supplied with
oxygen-rich blood to prevent underperfusion of myocites and subsequent ischemia and infartion. The de-
terminants of myovardial oxygen demand are heart rate, myocardial contractility and wall tension. An ade-
quate supply of oxygen to the myocardium requires oxygen-carrying capacity of the blood (level of oxygen
inspired, pulmonary function, hemoglobin concentration) and adequate coronary blood flow. Coronary vas-
cular bed can only vary its resistance (and so the blood flow), because the myocardium already extracts a
high and fixed percentage of oxygen from blood.
By reducing the lumen of the coronary arteries, atherosclerosis limits increases in perfusion when the de-
mand for flow is augmented (exertion, excitement). Coronary blood flow can also be limited by spasm
(Prinzmetal’s Variant Angina), arterial thrombi, coronary emboli, aortitis. Myocardial ischemia can also oc-
cur if myocardial oxygen demands are markedly increased and when coronary blood flow is limited, as in LV
hypertrophy due to aortic stenosis. Anemia rarely causes myocardial ischemia by itself, but may lower the
threshold for ischemia in patients with coronary obstruction.
Frequently, more causes coexist, such as an increase in oxygen demand due to LV hypertrophy secondary
to hypertension and a reduction in oxygen supply secondary to atherosclerosis.

CORONARY ATHEROSCLEROSIS
The major risk factors for atherosclerosis (high LDL, low HDL, smoking, hypertension, diabetes mellitus) dis-
turb the normal function of the endothelium, and result in subintimal collections of fat, fibroblasts and in-
tercellular matrix, with develop in different segments of the epicardial coronary tree and lead eventually to
reductions in cross-sectional area.
Segmental atherosclerosis is caused most commonly by the formation of a plaque, which is subject to rup-
ture or erosion of the cap separating the plaque from the bloodstream. So, platelets are activated and ag-
gregate, the coagulation cascade is activated leading to deposition of fibrin strands. A thrombus composed
of platelet aggregates and fibrin traps red blood cells and reduces coronary flow, leading to ischemia.
The location of the obstruction influences the quantity of ischemic myocardium and determines the severi-
ty of the clinical manifestations.
With progressive worsening of a stenosis, the distal resistance vessels dilate to reduce vascular resistance
and maintain coronary blood flow. A pressure gradient develops across the prossimal stenosis, and post-
stenotic pressure falls. When the resistance vessels are maximally dilated, myocardial blood flow becomes
dependent on the pressure in the coronary artery distal to the obstruction. Ischemia can be precipitated by
increases in myocardial oxygen demand caused by physical activity, emotional stress, tachycardia.
Regional disturbances of ventricular contractility cause segmental akinesia or diskinesia, which can greatly
reduce myocardial pump function. The relatively poor perfusion of the subendocardium causes more in-
tense ischemia of this portion of the wall, compared with the subepicardial region.
Ischemia of a large portion of the ventricle can cause transient LV failure, and if the papillary muscle is in-
volved, mitral regurgitation is present. When ischemia is transient, it may be associated with angina; when
it is prolonged, it can lead to myocardial necrosis (acute MI).
The normal myocardium metabolizes fatty acids and glucose. With severe oxygen deprivation, fatty acids
cannot be oxidised and glucose is degraded to lactate, thus reducing intracellular pH. The stores of high-

1
Ischemic Heart Disease, Harrison, cap. 237
2
Unstable Angina and Non-STsegment-elevation Myocardial Infarction, Harrison, cap. 238
3
Stsegment-elevation Myocardial Infarction, Harrison, cap. 239
Fisiopatologia 3) CARDIOPATIE ISCHEMICHE Antonio Nenna

energy phosphates (ATP, creatine-P) are reduced. Impaired cell membrane function leads to the leakage of
K+ and the uptake of Na+, with an increase in cytosolic Ca++. This causes characteristic changes in the ECG.

STABLE ANGINA PECTORIS


This episodic syndrome is due to a transient myocardial ischemia. In these patients, coronary stenosis and
myocardial oxygen supply are fixed, and ischemia is precipitated by an increase in oxygen demand.
Patients complains of chest discomfort (described as heaviness, pressure, squeezing, smothering, only rare-
ly as frank pain). The sensation is localised over the sternum, with a squeezing, central, substernal discom-
fort (Levine’s sign). Angina is usuallt crescendo-decrescendo, lasts 2-5 min, and can radiate to shoulders
and arms (especially the ulnar surfaces) (also to the back, interscapular region, root of the neck, jaw). This
discomfort does not radiate to trapezius muscles (this pattern is typical of pericarditis).
Anginal-equivalents are symptoms of myocardial ischemia other than angina. These include dyspnea, nau-
sea, fatigue and faintness.
Coronary atherosclerosis is ofter accompained by a similar lesion in other arteries; so, the patient should be
asked and examined for peripheral arterial disease (claudicatio intermittens, transient ischemic attack).
Episodes of angina are typically caused by exertion (exercise, hurrying, sex) or emotions (stress, anger) and
are relieved by rest. They also can occurr at rest or while the patient is recumbent (angina decubitus). Noc-
turnal angina may be due to episodic tachycardia, diminished oxygenation as the respiratory pattern
changes during sleep or expansion of the intratoracic blood volume that occurs with recumbency, which
causes an increase in LVEDV, which in turns increases the oxygen demand.

PHYSICAL EXAMINATION
This is often normal in patients with stable angina when they are asymptomatic, but it may reveal evidence
of atherosclerotic disease at other sites (abdominal aortic aneurysm, diminished arterial pulse in legs).
There may also be signs of anemia, thyroid disease, nicotine stains on fingertips from cigarette smoking.
If acute ischemia or previous infarction ah impaired papillary muscle function, is present an apical systolic
murmur due to mitral regurgitation.
Examination during an anginal attack is useful, since ischemia can cause transient LV failure with the ap-
pearance of S3 and S4, a diskinetic cardiac apex, mitral regurgitation and pulmonary edema.

ECG
ECG recorded at rest may be normal (obviously, there will be signs of an old myocardial infarction). Repola-
rization abnormalities, LV hypertrophy and conduction disturbances are suggestive for IHD but non-specific
(since they can occur in pericardial, myocardial or valvular heart disease).
ECG recorded during exercise (treadmill) is far more useful. With angina, after 3-4 min of exercise appears
ST-segment depression of about 3 mm, especially on V4, indicating a positive test for ischemia.

MANAGEMENT OF THE PATIENT


Aortic valve disease and hypertrophic cardiomyopathy may cause or contribute to angina. Obesity, hyper-
tension and hyperthyroidism should be treated aggressively in order to reduce the frequency and severity
of anginal episodes. Patient must give up smoking.
Obesity impairs the treatment of other risk factors and increases the risk of adverse coronary events. Also,
obesity is accompained by three other risk factors: diabetes mellitus, hypertension, hyperlipidemia.
Cigarette smoking accelerates coronary atherosclerosis in both sexes and increases the risk of thrombosis.
By increasing myocardial oxygen needs and reducing oxygen supply, it aggravates angina.

DRUG THERAPY
NITRATES. Sublingual nitroglicerine rapidly relieves angina. This action is not due to vasodilation of coro-
nary artery, but is due to systemic venodilation with reduction of LVEDV, thereby reducing myocardial wall
tension and oxygen requirements. The organic nitrates when metabolised release nitric oxide (NO) which
binds to guanylyl cyclase in vascular smooth-muscle cells, leading to an increase in GMPc, which causes re-
laxation of vascular smooth muscle. They also have anti-thrombotic effects, impairing calcium flux. The ab-
sorption of these agents is most rapid and complete through the mucous membranes (sublingual tablets).
Fisiopatologia 3) CARDIOPATIE ISCHEMICHE Antonio Nenna

β-ADRENERGIC BLOCKERS. They reduce myocardial oxygen demand by inhibiting the increases in heart
rate, arterial pressure and myocardial contractility caused by adrenergic activation (exercise). Contraindica-
tions include asthma and airway obstruction in patients with chronic lung disease, atrioventricular conduc-
tion disturbances, Raynaud’s phenomenon, mental depression.
CALCIUM CHANNEL BLOCKERS. They are coronary vasodilators that produce reductions in myocardial oxy-
gen demand, contractility and arterial pressure. They are indicated when beta-blockers are contraindicated
or ineffective. Verapamil may produce disturbances in cardiac conduction and bradyarrhythmias. They also
exerts negative inotropic effects and are likely to aggravate LV failure. Prinzmetal’s variant angina responds
particularly well to calcium channel blockers (class DHP), supplemented by nitrates.
ANTIPLATELETS. Aspirin is an irreversible inhibitors of platelet cyclo-oxygenase activity and interferes with
platelet activation. Also, it reduced coronary events in asymptomatic and MI-survivors.
MISCELLANEA. Use of non-steroidal anti-inflammatory drugs (NSAIDs) in patients with IHD may be asso-
ciated with a small increased risk of MI (they are generally avoided in these patients). Transient LV failure
with angina may be controlled by nitrates. Treatment of congestive HF with ACEi, diuretics and digoxin re-
duced heart size, wall tension, and oxygen demand, which helps to control angina and ischemia.

UNSTABLE ANGINA AND NON-ST-ELEVATION MYOCARDIAL INFARCTION


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