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CQ topics

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 How to study guidelines?

1. ESC or ACC?

-ESC is more popular especially in Egypt

So it is the main bulk of studying

-You will need to study the ACC if is the most recent

-If you have enough time, study ESC very well, then have a rapid
look on ACC(recommendations only not full text(

2. Pocket or full text?

-MD level, full text is a must to know the trials

-Master level, study tables and algorithms very well then if

something is unclear, see text

3. -Always start first with tables and algorithms, finish them all first,
study them very well, then go to full text as a last step. When you
do this, you will find the text is easier and will answer the
questions that have been raised by your mind after you have
studied the tables

4. Numbers in tables is very important in MCQ exams especially

those which are not popular in practice

5. When to study Full text, you have to Write the most important
notes in a separate paper by yourself
Final revision before exams, you can revise the tables, algorithms
and your notes about the full text

6. ESC site provide a beautiful summary in form of slide set (power

point presentation), it can help you if you are in hurry

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7. In the ESC guidelines, you will find what's new in these guidelines,
read it rapidly. It is mainly done for those who have read the old
guidelines and they want rapid update. But at exam level, you need
to know mainly the new recommendations

8. You should know the difference between

Class I (it is recommended(
Class III (it is not recommended
Class II-a (should be considered(
Class II-b (may be considered(

As in MCQ, he can give you statement and gives you the above
options

9. You should know very well what is class I and what is class III
recommendations, these are most important, Followed by class II
indications

10.In the beginning of each ESC guidelines, you will find a list with
all trials included in these guidelines
This list is very important, as it will help you you to know the
important trials

11.Do not be surprised when you find a different level of

recommendations for the same statement but in different guidelines
Simply because the writing committee is different
My advice is the study the recommendations in the original topic

12.-Start with the most recent guidelines as these guidelines will not
change before exams

https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines

https://www.acc.org/guidelines

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 Peripartum cardiomyopathy (PPCM(

1. Defined as unexplained cardiomyopathy, EF less than 45% that

occur in the last month of pregnancy or the first 5 months post-
partum
2. Pathophysiology is thought to be related to prolactin degradation
product which has a myocardial toxicity which explain the benefit
of anti-prolactin which is Bromocriptine
3. Other theories include autoimmune, myocarditis, oxidative stress
4. Predictors of poor prognosis include dilated LVEDD more than 60
mm, EF less than 30% and RV involvement
5. According to the ESC guidelines for heart disease with pregnancy,
Bromocriptine is a class II b indication for PPCM
6. There are two regimens:
I-Bromocriptine 2.5 mg once daily for 1 week

II-Bromocriptine 2.5 mg twice daily for 2 weeks then 2.5 mg once

daily for 6 weeks

-The first regimen for uncomplicated cases

-The second regimen is used if the patient is presenting with

cardiogenic shock or EF less than 25%

7. You must give parenteral anticoagulation for patients on

Bromocriptine(either prophylactic or therapeutic(
8. You must continue on ant-failure measures for at least 6 months
after recovery of normal LV function
9. Women who did not recover LV EF above 50% should be
prohibited from further pregnancies
10.Women who have recovered normal LV function still have a
higher risk than those who did have PPCM and risk of recurrence
as well
11.-Levosimendan is the inotrope of the choice due to deleterious
effect of beta agonist on the heart by catecholamines release

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 Takotsubo cardiomyopathy
(Brocken heart syndrome(
1. More common in post-menopausal female
2. Related to severe emotional stress
3. Pathogenesis is related to catecholamine toxicity
4. Moderate Troponin elevation despite extensive ECG change and
Echo findings
5. RWMA in echo involving multiple coronary territories
6. RWMA most commonly involved apex and adjoining apical
segments, less commonly mid myocardial segments, least
commonly involve basal segments
7. Normal coronary angiography or discrepancy between RWMA
findings in echo and coronary angiography findings
8. No late gadolinum enhancement in cardiac MRI
9. Prolonged QT more than 500 msec
10.Usually reversible LV function
11.Most common finding in Left ventriculography is apical ballooning
12.ECG changes include ST elevation or depression

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 Novel oral anticoagulants (NOACs(
1. Other names:

Direct oral anticoagulant (DOACs), non-vitamin KAntagonist oral

anticoagulant (NOACs(

2. Either Direct thrombin inhibitors (dabigatran), anti factorX

(Rivaroxaban, apixaban, edoxaban)
3. Contraindicated in Pregnancy and lactation
4. Contraindicated in Mechanical prosthesis and Mitral stenosis
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(Mitral valve area less than 1.5 cm )
5. Contraindicated in the first three months after mitral valve repair or
tricuspid valve repair
6. Contraindicated in the first 3 months after Implantation of mitral or
tricuspid tissue valve
7. Contraindicated in liver cirrhosis, Child C
8. The approved one in Chronic kidney disease or dialysis is
Apixaban
9. Antidote for dabigatran is Idarucizumab, antidote for Antifactor X
(mainly Rivaroxaban) is andexanet alfa, you can give 4 factors
prothrombin complex concentrate for NOCAs related Bleeding
10.When you switch from Warfarin to NOACs, start NOACs when
INR is 2. 5 or less
11.When switch from NOACs to warfarin, give both till INR reach 2
for two consecutive readings
12.As a general rule, NOACs are stopped 2 days before surgery
(except for dabigatran in patients with CKD, will need longer
interval(
13.As a general rule, you can restore NOACs 3 days after surgery
14.As a general rule, the risk of GIT Bleeding with NOACs is more
than Warfarin except Apixaban 5mg twice or dabigatran 110 mg
twice which have a comparable GIT Bleeding risk similar to
Warfarin
15.INR can be prolonged with rivaroxban , PTT can be prolonged
with dabigatran, and dabigatran is the only one that be cleared
with dialysis in case of toxicity

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16.As a general rule, NOACs are at least as effective as Warfarin and
they are more safe as regard Bleeding risk
17.The risk of Hemorrhagic stroke or cerebral hemorrhage is low with
all NOCAs when compared to Warfarin
18.The only 2 NOCAs that showed superiority over warfarin in stroke
risk reduction are apixaban 5 mg twice and Dabigatran 150mg
twice
19.Other NOACs have a comparable stroke risk reduction VS.
Warfarin
20.Dabigatran is associated with reduction of vascular mortality,
Apixaban is associated with reduction of all-cause mortality,
edoxban is associated with reduction of Cardiovascular mortality
21.Rivaroxaban should be given with meal
22.Highest renal excretion with dabigatran, lowest renal excretion
with apixaban
23.Trials of NOACs with P2 Y12 inhibitors

-Redual PCI(dabigatran(
-Pionner AF(Rivaroxaban(
-Augustus(apixaban(
-Entrust(Edoxaban) (ongoing(
24.Trials of NOACs in A-Fib

-Rely (dabigatran(
-Rocket(Rivaroxaban)
-Aristotle (Apixaban(
-Engage (Edoxaban(
25.Trials of NOACs in venous thromboembolism

-Recover(Dabigatran(
-Einstein(Rivaroxaban(
-Amiplify(Apixaban(
26.No need for concomitant treatment with parenteral anticoagulant
upon starting with apixaban or Rivaroxaban in treatment of venous
thromboembolism. Instead, you can give apixaban 10mg twice for
1 week then 5 mg twice daily thereafter And Rivaroxaban 15mg
twice daily for 3 weeks then 20mg once daily there after.

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 Tips and tricks in management of
Dyslipidemia
1. Atherogenic lipids include LDL and VLDL
2. Apo B is the lipoprotein included in the LDL and VLDL
3. Apo B and Non HDL cholesterol are more representative for
atherogenic risk more than LDL as both of them reflect LDL plus
VLDL
4. Targets in management of dyslipidemia are
LDL
Then non HDL-cholesterol
Then Apo B
5. Lipoprotein(a) is modified form of LDL, level 50 mg or more is
considered risk enhancer, it should be requested in patients with
family history of premature CAD or personal history of
unexplained CAD
6. According to ESC guidelines

-In patients with very high cardiovascular risk, Target LDL

is below 70mg, or if LDL from 70 to 135, Target is 50%
reduction
-In patients with high cardiovascular risk, Target LDL is
below 100, if LDL from 100 to 200, Target is 50%
reduction
-In patients with Moderate cardiovascular risk, Target LDL
is below 115

-Non HDL Target are 30 mg above LDL target

-Apo B Target
Less than 80 mg in very high cardiovascular
Less than 100 in high cardiovascular risk

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7. According to American guidelines, Patients with 10 year risk of
ASCVD 7.5 % and triglycerides level from 175-499 mg are
indicated for Statin
8. Primary prevention include:
Patients with DM
Patients with LDL level 190 mg or more
Patients with high CVD risk

9. High intensity Statin(50% reduction of baseline LDL) include

Atorvastatin 40-80 mg, Rosuvastatin 20-40mg
10.Moderate intensity Statin(30 to less than 50%) reduction of
baseline LDL: Atorvastatin 10-20 mg, Rosuvastatin 5-10 mg

11.Chronic kidney disease not on dialysis, 10 year risk of ASCVD

more than 7.5% are indicated for statin
12.It is class III to initiate Statin for patients on dialysis
13.It is class II-b to continue Statin for patients who Required dialysis
14.The only Statin which did not need dose modifications in CKD is
atorvastatin
15.Fasting lipid profile is recommended if the patient was maintained
on statins, for diagnosis of familial hypercholesterolemia and if
initial triglycerides more than 400 mg.

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 Cardiovascular benefits of
Antidiabetic drugs

Classification of Antidiabetic drugs

A-Insulin dependent

B-Non insulin dependent

A-Insulin dependent:

#Insulin secretagouges:

1. -Sulphonylurea:

Glimepiride (Amaryl(
Glibenclamide (Doanil(
Gliclazide (Diamicron(

2. Incretin based therapy

-Incretin are GIT hormone that stimulate insulin secretion

and inhibit glucagon secretion

-Incretins include:
Gastric inhibitory polypeptide (GIP(
Glucagon like peptide (GLP(

-Incretins are metabolized by Dipeptidyl peptidase 4(DPP4

Inhibitors) enzyme

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-Incretin based therapy include:

*Glucagon like peptide(GLP) agonist

-Semagultide
-Albiglutide
-Liraglutide(Victoza(
-Exenatide

*Dipeptidyl peptidase 4 inhibitors(DPP4 inhibitors (:

-Linagliptin(Trajenta(
-Vildagliptin(Galvus (
-Sitagliptin(Januvia)

3. Meglitinide:

Repaglinide (Novonorm(

#Insulin sensitizer:

*Biguanides:

Metformin (Glucophage or Cidophage)

*Thiazolidindione:

Pioglitazone (Actos) , Rosiglitazone(Avandia)

B-Non insulin dependent

# Glucose absorption inhibitors:

Acrabose (Glucobay (

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#Glucose reabsorption inhibitors:

Sodium glucose co-transporter 2 inhibitors

-Dapagliflozin (Forxiga(
-Empagliflozin (Jardiance)
-Canagliflozin (Invocana (

4. Cardiovascular benefits where shown mainly for

GLP-1agonist

-Semaglutide( Sustain trial(

-Albiglutide (Harmony trial (
- Liraglutide (Leader trial)
- Exenatide (EXSCEL trial)

SGLT2 inhibitors

-Dapagliflozin (Declare trial)

-Empagliflozin (Emp-Reg trial)
-Canaglifolizin( Canvas trial)

-These 2 groups of Antidiabetic drugs decreased Cardiovascular

mortality and cardiovascular events (MI, stroke (

-In addition, SGLT2 inhibitors decreased Heart failure

hospitalization

-GLP-1 agonist and SGLT2 inhibitors have Reno-protective effect

and decrease progression of CKD

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-DPP4 inhibitors are neutral as regards Cardiovascular benefits
Except saxagliptin which increase HF hospitalization(Salvos trial)

-Metformin has some cardiovascular benefits(UKPDS trial)

-Sulphonylurea and insulin have neutral CV effect

-Thiazolidindione (especially rosiglitazone) increase HF

hospitalization

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Heart failure with preserved EF (HFpEF(
1. Definition:
*Typical symptoms and signs of HF

*Echo:

-EF 50% or more

-Relevant structural heart disease) LVH, Dilated LA,
Diastolic dysfunction(

*BNP >35 pg/dl

NT-Pro BNP>125 pg/dl

2. Pathophysiology:
Related mainly to failure of relaxation and abnormal
calcium handling during the cardiac cycle

3. Type of patient:

HFpEF is typically a disease of elderly women

-More in elderly
-More in female
-Typically associated with AF, hypertension, LVH,
CAD, Obesity, DM, CKD

4. Diagnosis:

*Echocardiography

*BNP, NT-Pro BNP

)as described above(

*Diastolic stress test

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*Hemodynamic study for assessment of filling pressure,
Confirmation of pulmonary pressure and Fluid challenge to
unmask symptoms in borderline cases

*HFpEF score

5. Management:

A-life style modifications

Salt restriction
Weight reduction

B-Risk factors modifications

-Control of HTN
-Control of DM
-Rhythm control for A-Fib
-Proper Management of CAD(Revascularization may be
Required(

C-Medical

*ACEI/ARBs

-Candesartan may be considered (based on CHARM

Preserved trial(

*ARNI:
-Failed in paramount trial(only improvement in
NYHA class, LA size, NT pro BNP)

-Paragon trial is ongoing

*Beta blockers:

-Nebivilol improved survival (Senior trial(

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 *Spironolactone may be considered (based on American
Side of TOP-CAT(

*Sodium glucose cotransporter 2 inhibitors Canagliflozin,

May be considered (CANVAs trial(

*Ivabradine failed in Edify trial

*Diuretics is the main Stay of therapy to improve

Symptoms of congestion

D-Gene therapy:

-SERCA gene transfer (failed)

-Parvalbumin(calcium buffer)

E-Device therapy:
Interatrial shunt device (based on Reduce-LAP trial)
to create Interatrial communication allow only left to
right shunt to Decrease Left atrial pressure

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 PCSK9 inhibitors

1. PCSK9 Is proprotein convertase subtilisin kexin 9 enzyme

2. In LDL metabolism, LDL bind with LDL receptor followed by
endocytosis
3. Before lysosomal degradation, unbinding of the LDL receptor from
LDL occur
4. PCSK9 prevent unbinding of LDL from its receptor
5. So, there is a destruction of LDL receptor with a subsequent
increase in LDL level (no receptors to bind with)
6. This finding was observed in patients with Familial
hypercholesterolemia, in whom, there is a gain of function
mutation in PCSK9 which explain the main pathological findings
responsible for hypercholesterolemia in these patients (which is
decreased LDL receptors(
7. So, PCSK9 inhibitors (Alirocumab, Evolocumab) are monoclonal
antibodies results in up regulation of LDL receptors with further
increase in LDL uptake and metabolism
8. The main indications of PCSK9 inhibitors are:
Patients with established ASVCD and LDL above 70mg despite
maximally tolerated doses of Statin and Ezetimibe

Or Familial hypercholesterolemia with failure to reach target LDL

despite maximally tolerated dose of Statin and Ezetimibe

9. Trials:

Odyessy trial (Alirocumab), ACS

Fourier trial (Evolocumab), stable ASCVD

10.Trade name

-Repatha(Evolocumab)

-Praluent(Alirocumab(

Given as SC injection every 2 weeks

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 Angiotensin receptor-neprilysin inhibitor
(ARNI(
1. ARNI is considered a breakthrough in management of heart failure
2. ARNI is composed of 2 drugs:

Angiotensin receptor antagonist :Valsartan

Neprilysin inhibitor:Sacubitril

3. Neprilysin is an enzyme responsible for breakdown of natriuretic

peptides as well as bradykinin

4. Mechanism of action:

-Inhibition of neprilysin will result in increase in

natriuretic peptides with a subsequent increase in
diuresis and natriuresis and vasodilation

-Valsartan block angiotensin receptor with a subsequent

blockage of RAAS system>> improve myocardial
remodelling and after load reduction

5. Why sacubitril is combined with ARB not ACEI?

-A previous trial of combining neprilysin inhibitor

with ACEI (Omapatrilat) failed and ended with
angioedema as both ACEI and neprilysin inhibitor
prevent breakdown of bradykinin, so resulted in
angioedema
-For the same reason, when you switch from ACEI to
ARNI, you have to wait for 36 hours, while you can
give ARNI in the time of next dose of ARBs if the
patient is previously maintained on ARB

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6. Evidence of use:

-Paradigm HF trial compared ARNI VS. Enalapril in

Patients with HFrEF, showed 22% reduction in
Composite Endpoint of CV mortality and HF
Hospitalization

-As regard use in HFpEF, paramount trial failed to

Improve outcomes and Paragon trial is ongoing

7. Guidelines:

-ESC recommended ARNI only if patient is still

symptomatic after the standard HF therapy as a
substitute for ACEI or ARBs
-ACC guidelines allowed use of ACEI or ARBs or
ARNI as a first line

8. Contraindications of ARNI:

-History of angioedema
-Liver cirrhosis Child C
-Pregnancy
-Hyperkalemia

9. Dose modifications:

Start with half standard dose (start with 50 mg twice

Daily( in any of the followings:

-CKD, GFR less than 30ml

-Liver cirrhosis Child B
-Patients previously not maintained on ACEI or ARBs
Or maintained but on low doses (not equivalent to
enalapril 10 mg twice)

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10.Standard dose is 100 mg twice daily, Can be increased after 2-4
weeks interval to 200 mg twice daily

11.Recently, Transition trial, and Pioneer HF trial showed safety of in-

hospital initiation of ARNI for patients admitted with acute
decompensated HF after stabilization of their condition and before
hospital discharge

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 Cardiac amyloidosis
1. Types:

-Primary (AL) amyloidosis due to deposition of Amyloid light

chain most commonly due to multiple myeloma
-Secondary (AA) amyloidosis due to deposition of Amyloid A
protein, in Chronic Inflammatory state Such as rheumatoid arthritis
-Familial Amyloidosis (ATTR) due to deposition of mutated Type
of transthyretin
-Senile systemic amyloidosis (SSA) due to deposition of wild type
of transthyretin

2. One of the most common causes of Restrictive cardiomyopathy

3. ECG:
Low voltage despite increased wall thickness in Echocardiography,
pathological Q waves in absence of ischemia

4. Echo:

-Ground glass appearance of the myocardium with 2 small

ventricles, 2 large atria
-Grade III diastolic dysfunction
-Thickened AV valves
- Thickened interatrial septum
- Marked LA dysfunction that can be manifested as very small A
wave in PW Doppler(called atrial arrest)
-MR, TR, PH
-Pericardial effusion

5. -Diagnosis:

-Abdominal fat aspirate, congo red stain

-Free light chain assay, protein electrophoresis, immune-fixation,
bone marrow aspirate (to diagnose primary amyloidosis(
-Genetic study to diagnose Familial type
-Cardiac-MRI for tissue characterization

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 -Technitium scintigraphy can be used for diagnosis of TTR related
amyloidosis

6. Associated Features:

-Carpal tunnel syndrome

-Postural hypotension (due to peripheral neuropathy secondary to
transthyretin
-Hepatomegaly disproportional to degree of congestion

7. Treatment:
I- Tafamidis is now approved for treatment of Familial type with
autonomic neuropathy based on ATTR-ACT trial, Decrease all-
cause mortality and HF hospitalization.
-There are 2 preparations: Vnydaqel and Vyndamax
Both are contraindicated in Pregnancy

II- Anti-failure measures

-ACEI used cautiously as it can result in profound hypotension
-Beta blocker used cautiously as there is fixed stroke volume and
COP depend mainly on HR
-Better to avoid digitalis due to high incidence of digitalis toxicity

III- Anticoagulation:
For AF regardless CHADS-VASc score due to high incidence of
LAA thrombus due to marked reduction of LA function

IV-Liver transplantation can be considered in Familial type

V-Chemo therapy and steroid for primary type

VI-Immunosuppression and anti-inflammatory in secondary

type

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 10 points to remember about role of
prophylactic revascularization before
elective non cardiac surgery

1- Control of myocardial ischaemia before surgery is recommended

whenever non-cardiac surgery can be safely delayed.

2-There is, however, no indication for routinely searching for the

presence of myocardial (silent) ischaemia before non-cardiac surgery.

3-The main reason for pre-operative myocardial revascularization is the

potential prevention of perioperative myocardial ischaemia that leads to
necrosis or electric/haemodynamic instability at the time of surgery.

4-Coronary pathology underlying fatal perioperative myocardial

infarctions revealed that two-thirds of the patients had significant left-
main or three-vessel disease.

5- Most of the patients did not exhibit plaque fissuring and only one-third
had an intracoronary thrombus.

6-These findings suggest that a substantial proportion of fatal

perioperative myocardial infarctions may have resulted from low-flow,
high-demand ischaemia, owing to the stress of the operation in the
presence of fixed coronary artery stenosis and therefore amenable to
revascularization.

7-In patients who underwent coronary angiography before vascular

surgery, a number of non-fatal perioperative myocardial infarctions
occurred as a consequence of plaque rupture in arteries without high-
grade stenosis.
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8-These results are not surprising, considering the extreme and complex
stress situations associated with surgery—such as trauma, inflammation,
anaesthesia, intubation, pain, hypothermia, bleeding, anaemia, fasting,
and hypercoagulability—which may induce multiple and complex
pathophysiological responses.

9&10 see the attached tables

Reference: ESC guidelines 2014 on non-cardiac surgery

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CQ pearls

25
 Cardiology pearls (part I)

1. RHD : almost always involve mitral valve with or without

other Valves
2. HF with impaired LV function: Keep serum Potassium
above 4.5meq to avoid precipitation of ventricular
arrhythmia
3. Atrial flutter carries the Same thrombo-embolic risk as AF
and should managed as AF as regards indication of
anticoagulation
4. Always ask for CXR in patient with chest pain and normal
ECG
5. Always check for lead AVR in ECG before interpretation
(you may activate primary PCI cath team based on wrong
ECG(
6. ECG leads V1-V2 in the fourth intercostal space (not the
second space(
7. In left sided infective endocarditis , ask for multislice CT
cerebral angiography to exclude mycotic aneurysm
8. In reading CXR , always look for lung apex it is frequently
missed
9. In infective endocarditis,a always ask for serology for
aspergillus, Bartonella, Brucella, Coxiella, legionella
10.Hypotension after Coronary angiography either due to:

A-Hypovolemic shock:
Bleeding from sheath or retroperitoneal hematoma

B-Cardiogenic shock:
Acute instent thrombosis

C-Anaphylactic Shock:
From contrast

D: Vasovagal: pain during sheath removal

26
 Cardiology pearls (Part II)
1. Any hospitalized patient who develop new onset AF during
hospital stay, you should suspect Pulmonary embolism
2. Enoxaprin is contraindicated if GFR is less than 15 m and if
GFR is from 15-30 we give 1mg/Kg every 24 hours as a
therapeutic dose
3. Any wide complex tachycardia in patient with ischemic
heart disease should be managed as VT until proved other
wise
4. Causes of very high ESR(more than 100 In first hour)
includes:
-TB
-Connective tissue disorders
-Malignancy
5. D-Dimer is a good negative test in pulmonary embolism but
not specific
6. Uro-sepsis is the most common cause of delirium in elderly
7. Anemia in old age carries the possibility of malignancy and
ideally upper and lower GIT endoscopy should be done
8. It is recommended to do lipid profile within 48 hours of
onset of ACS as after that there is a possibility of false low
cholesterol levels due to enhanced sympathetic activity and
lipolysis
9. You can calculate the LDL level from this equation
(LDL=Total cholesterol -(HDL + Triglycerides/5(
10.You can calculate the creatinine clearance from this equation
(140-ageX weight(/72X serum creatinine ,and multiply by
0.85 if female

27
 Cardiology pearls (Part III(
1. Metolazone is the only thiazide that can be used in Renal
impairment
2. It better to avoid imipenem(Tienam) and
levofloxacin(Tavanic) in elderly as the former can causes
convulsions and the latter can precipitate encephalopathy
3. The most common congenital heart disease is bicuspid aortic
valve
4. Bicuspid aortic valve can be associated with
-Aortopathy and aortic aneurysm
-Aortic coarctation
-Aneurysm in circle of Willis
5. Never wait for cardiac enzymes in patient with STEMI
6. Congenital complete heart block carries the best prognosis
among the all causes of CHB and sometimes can be
managed conservatively for years
7. Always check for BP equality on both sides in patient with
acute Coronary syndromes to exclude dissection
8. Always ask about history of sildenafil use before using
nitrates
9. Never use sublingual Nifedipine
10.Do not diagnose Rheumatic fever based on arthralgia that is
associated with elevated ESR , You should use modified
Jones criteria

28
 Cardiology pearls (Part IV(

1. Diagnosis of DM:
-FBS more or equal to 126 mg/dl in two separate occasions
Or
-Postprandial blood glucose more or equal to 200mg /dl on
two separate occasions
Or
-HbA1c is more or equal to 6.5%
Or
-Random blood glucose more or equal to 200 mg/dl in
Presence of symptoms (Polyurea, polyphagia and loss of
weight(
2. Targets in DM control

-HbA1c less than 7%

-FBS: 80-130mg
-2Hours post prandial less than 180mg

3. Light's criteria for diagnosis of etiology of pleural effusion

-Pleural fluid protein/serum protein more than 0.5

-Pleural Fluid LDH/Serum LDH more than 0.6

-Pleural fluid LDH more than 2/3 of the upper normal value

for the serum LDH

One criteria is sufficient to diagnose exudate, and all the three

criteria must be negative to say that it is transudate

4. The most common cause of convulsions in elderly is stroke

5. Unilateral Horner syndrome with ipsilateral neck pain is
suggestive of Carotid dissection until proved other wise
6. Mitral valve prolapse should diagnosed only in Parasternal
long axis view not apical 4chamber view

29
7. Drop out of the interatrial septum in Apical 4 chamber is not
suggestive of ASD except after confirmation with color flow
across and further assessment in subcostal view
8. Dynamic LVOT obstruction with significant LVOT gradient
could be seen in elderly dehydrated tachycardiac patients
(especially if hypertensive with LVH and small LV cavity( .
After rehydration and control of HR, The gradient across the
LVOT disappear
9. Verapamil increase the digitalis toxicity and it is better to
combine Diltiazem rather than verapamil with digitalis
10. Digoxin toxicity can occur despite of normal digoxin level
and can be diagnosed only based on clinical basis and ECG

30
 Cardiology pearls (Part V(

1. ACE inhibitors can be considered for all patients with CAD if no

contraindications
2. In patients with CHF and there is contraindication for ACE
inhibitors, you can give instead: Hydralazine (Arteriolar dilator)
with isosorbide dinitrate (venodilator(
3. Spironolactone should be given for patients with resistant
hypertension as it act as aldosterone antagonist
4. Spironolactone should be given for patients with right sided HF
(congestive hepatomegaly and Ascites ) as one of the mechanisms
of fluid retention in these patients is failure of the liver to
metabolize the aldosterone , so we give anti aldosterone
5. Enoxaparin should not be given for pregnant women with
prosthesis without monitoring of antifactor X level
6. Lidocaine and phenytoin are the antiarrhythmic drugs of choice in
patients with ventricular arrhythmia secondary to digitalis toxicity
7. Causes of Bidirectional VT are CPVT and digitalis toxicity
8. Spodick's sign in ECG:

Downsloping TP segment in lead II can help to differentiate

pericarditis from other causes of ST elevation

9. Dewinter Sign in ECG: is hyperacute T waves with upsloping ST

depression in anterior precordial leads ; indicative of acute
proximal LAD occlusion and considered as STEMI equivalent

10.The Safest drugs that can be given for patients with pericarditis and
ACS are Ibuprofen (as it increases Coronary blood flow) or high
dose acetyl salicylic acid

31
 Cardiology pearls (part VI(

1. As regard second degree heart block, there is a distinct subtype

called 2:1AV block , Can be either Mobitz type I or type II

-If it improves with atropine and narrow complex,

Most probably it is type I

-If it worsens with atropine or wide complex,

Most probably it is type II

2. Reciprocal ST depression in I and AVL may precedes frank ST

elevation in Inferior MI
3. To diagnose MI in paced rhythm with LBBB morphology, we
apply sgarbossa criteria
4. Anteroseptal STEMI and isolated RV infarction both can causing
ST elevation from V1-V3, But the difference is
- If the ST elevation is maximum in V1 and decreases gradually to
V3, then it is RV infarction
-If the ST elevation is gradually increasing towards V3, then it is
anteroseptal MI
5. -To differentiate Course AF from Atrial flutter with variable block,
You should notice that the flutter waves are identically the same
morphology, so if the atrial activity waves are different, then it is
course AF
6. -In Echocardiography, we assess pericardial effusion in diastole (as
regards measurement(
7. In patient with Interatrial septal aneurysm, you should exclude
PFO
8. Central venous pressure is a poor indicator of volume status and we
should IVC collapsibility index better
9. In assessment of Aortic prosthesis, Dimensionless velocity index is
a useful tool , (LVOT VTI/Aortic VTI) if this ratio is Lee than 0.25
it denote significant stenosis
10.In assessment of mitral prosthesis , MV VTI/LVOT VTI

If this ratio more than 2.5, it denote significant stenosis

32
 CQ
Questions

33
Q: ACE inhibitor is a good option for management of
hypertension in patients with aortic coarctation?
Answer:

Q: What is the best mode for delivery for pregnant

lady who stopped her oral anticoagulant 10 days before
delivery?
Answer: CS
Women on OAC within the previous 2 weeks should underdo CS
delivery due to risk of neonatal intracerebral hemorrhage with
normal vaginal delivery

Reference: ESC guidelines for management of heart disease with

pregnancy 2018

True or false:
Risk of Intracerebral hemorrhage is more with
streptokinase when compared to alteplase
Answer: false

The risk of intracerebral hemorrhage is more with alteplase (0.7%)

vs. 0.5% with streptokinase

34
True or false:

As per most recent guidelines, No role at all for aspirin

in primary prevention?
Answer: No

It is class II-b in some cases

ACC guidelines for primary prevention 2019
ADA guidelines 2019
Most patients above 50 and up to 70 years
With DM and other cardiovascular risk factor
And low risk of bleeding

It is class II-b to give aspirin for primary prevention 75-100 mg per

day

ACC guidelines for primary prevention 2019

35
Q: Causes of type 2 MI?
Answer: According to ESC guidelines for fourth universal
definition of MI 2018

36
Q: Triad for cholesterol embolism? (Trash foot(
Answer:

Lower limb pain

Palpable pulse
Livedo retricularis

Q: Myocardial injury vs. Myocardial

infarction?
-The term myocardial injury should be used when there is evidence of
elevated cardiac troponin values (cTn) with at least one value above the
99th percentile upper reference limit , The myocardial injury is
considered acute if there is a rise and/or fall of cTn values.

-The term acute myocardial infarction should be used when there is acute
myocardial injury with clinical evidence of acute myocardial ischaemia
and with detection of a rise and/or fall of cTn values with at least one
value above the 99th percentile and at least one of the following:

- Symptoms of myocardial ischaemia

- New ischaemic ECG changes
- Development of pathological Q waves
- Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality in a pattern consistent with an
ischaemic aetiology
- Identification of a coronary thrombus by angiography or autopsy

Reference: ESC guidelines for fourth universal definition of MI

2018

37
 Case scenario to explain myocardial injury vs.
myocardial infarction
You have been consulted to review a 35 year old male patient, chronic
kidney disease on regular dialysis, hypertension, and blood pressure
160/100.
The resident in charge consulted you as he found that his troponin is
positive. ECG was normal apart from LVH with non- specific ST-T wave
changes. Cardiac wise, the patient is asymptomatic.
How will you proceed?
My approach (according to the ESC guidelines for fourth universal
definition of MI, 2018)
Few steps
1-Positive cardiac biomarker is considered cardiac injury VS. Myocardial
infarction
2-If cardiac biomarker is only positive with no evidence of ischemia by
symptoms; ECG changes; Echo, then it will be considered myocardial
injury
3-Myocardial injury is 2 types: Acute or chronic
4-To differentiate between both, you should ask for second set
If there is at least 20% change, then it is acute injury
If no change or change less than 20%
Then It is Chronic injury
Back to our case
The only available data are symptoms, ECG and one set of enzymes
The best approach is
1-Serial ECG
2-Second set troponin
3-Echo
The investigations were done and showed
1-No significant change of cardiac troponin after 6 hours
2-Echo: hypertensive heart diseases
3-No dynamic ECG changes
Final diagnosis:
Chronic myocardial injury secondary to uremic toxins and hypertension
Management:
BP control, proper management of the renal condition

38
Q: Tamponade after cardiac surgery and Pericardial Fluid
analysis was rich in triglycerides?
Answer: Iatrogenic thoracic duct injury with chylopericardium

Q: Indications of anticoagulation for patients with Mitral

stenosis and sinus rhythm?
Answer: In patients in sinus rhythm, oral anticoagulation is indicated
when there has been a history of systemic embolism or a thrombus is
present in the LA (class I, level of evidence C) and should also be
considered when TOE shows dense spontaneous echo contrast or an
enlarged LA (M-mode diameter >50 mm or LA volume >60 mL/m2
(recommendation class IIa, level of evidence C).ESC gudielines , valvular
heart disease, 2017.

Q: In presence of Pericardial effusion more than 10mm in

setting of myocardial infarction you must exclude?
Answer: subacute rupture

Q: How to differentiate between HOCM and AS clinically?

Answer

I-Maximum intensity of the murmur

1-AS: First aortic area

2-HOCM: Second aortic area (site of LVOT)

II-Carotid

1-AS: Bruit and thrill propagating to carotid

2-HOCM: No propagation to carotid

III- Dynamic auscultation, standing:

1-AS: Decrease

2-HOCM: increase

39
Q: Patient presented to non-PCI capable facility with acute
chest pain, diagnosed as STEMI. Onset of chest pain since 2
hours, transfer to primary PCI will take 90 minutes. How
would you treat?
Answer:

Fibrinolysis then transfer to the nearest primary PCI capable facility

The accepted delay for primary PCI in early presenters within the first 3
hours from the chest pain onset is only 60 minutes, not the standard 120
minutes. Reference: ESC STEMI guidelines 2017

Q: True or false?
Statin and antiplatelet therapy are indicated in all patients
with lower extremity arterial disease (LEAD) or carotid
disease (symptomatic or asymptomatic)
Answer: False

Statin is indicated in all patients with lower extremity arterial disease

(LEAD) or carotid disease (symptomatic or asymptomatic), While
antiplatelet therapy is indicated in all patients with carotid disease (50%
stenosis or more) and only symptomatic patients with Peripheral arterial
disease (ESC guidelines for management of peripheral arterial disease,
2017(

40
Q: How to use high dose aspirin for treatment of post
MI pericarditis without losing its antiplatelet action?

Answer:
Dose of Aspirin up to 1500 mg/day is effective as antiplatelet and
anti -inflammatory (ESC guideline 2015 in treatment of
pericarditis)

Q: What is the difference between peripheral arterial

disease and Peripheral artery disease?
Answer: According to ESC guidelines for management of
peripheral arterial disease, 2017

41
Q: What is the safest Fibrinolytic therapy during pregnancy
and why?
Answer: Alteplase as it does not cross the placenta

Q: What is the preferred antiplatelet in patients with LEAD

and patients with carotid disease?
Answer: Clopidogrel is the preferred antiplatelet in Lower extremity
disease (LEAD) , While aspirin is the preferred one in patients with
carotid disease

Q: What are the Features of fetal heart failure by US and

fetal echo?
Answer:
Scalp edema

Pericardial effusion

Ascites

Decreased fetal movement

Mention the expected Survival in patients with aortic

stenosis when they develop?
1. Angina
2. Syncope
3. Heart Failure

Answer: 5 Years, 3 years, 2 years respectively

42
Q: Enumerate Uses of thrombolytic therapy in Cardiology?
1. STEMI
2. Pulmonary embolism
3. DVT catheter based
4. Peripheral arterial thrombosis (catheter based)
5. Prosthetic valve thrombosis
6. Acute ischemic stroke

Q: How to differentiate between intranodal or infranodal

block?

Answer:
-2:1 AV block is either intranodal (in the AV node) or infra nodal

-Features of Intra-nodal disease (in the AV node(

1. Narrow complex
2. Improve with exercise and atropine
3. Worsened with carotid sinus massage

-Features of infra-nodal disease (in the his-Purkinje system)

1. Wide complex
2. Worsened with atropine and exercise and atropine
3. Improve with carotid sinus massage

43
Q: What is the first choice of Antidiabetic drugs in cardiac
patients?
Answer: Metformin

Q: Why Statin can decrease triglycerides only when it is

below 500 while it is in-effective when TG exceeds 500?
Answer:

1. If the triglycerides level below 500:

The main lipoprotein carrier for triglycerides is VLDL

Statin can reduces VLDL and it is preferred due to pleotropic

effects and mortality benefits of Statin

2. -While if triglycerides are above 500, The main lipoprotein

carrier is chylomicron, Statin cannot reduce chylomicron
So you have to give fibrates and omega 3

Q: Can we see occasional P waves in patients with

atrial fibrillation?
Answer:
"Presence of some P waves, does not exclude AF".AF is defined as
absence of consistent P waves. Some fibrillatory waves may mimic
sinus P waves.

44
Q: Patient was maintained on Ticagrelor, can we shift
to maintenance clopidogrel therapy?

Answer: Yes, this is called De-Escalation of P2Y12 inhibitor;

If you have started a strong P2Y12 inhibitors like Ticagrelor or
prasugel, Then during the maintenance period, the patient
developed a significant Bleeding or cannot afford the price
You can de-escalate or downgrade the P2Y12 inhibitors to
clopidogrel guided by platelet function

Evidence: Tropical trial

Q: What are the main Indications for ICD

implantation?

Answer: Keep in mind these numbers

First 2 days
40days
90 days

1. Secondary prevention of ventricular arrhythmias in the first

48 hours post MI is revascularization and guideline directed
medical therapy (not ICD(
2. ICD is indicated for Primary Prevention of sudden cardiac
death and ventricular arrhythmias for patients post MI, EF
less than 40%, 40 days after MI, or 90 days post
revascularization
3. ICD is indicated for Primary prevention of sudden cardiac
death and ventricular arrhythmias for patients with Dilated
cardiomyopathy, EF less than 35%, 90 days(3 months) after
optimal medical therapy, NYHA class II or III), expected
survival at least one year

45
Q: Triad for fat embolism?
Answer: Skin rash, disturbed conscious level, respiratory distress

Q: Cabrera vs. Chapman sign?

Answer:

-Carbrera sign used for diagnosis of acute MI in setting of LBBB

Characterized by notching at 40 ms in up sloping of S wave in lead
V3, V4

-Chapman sign characterized by notching in up sloping of R wave

in lead I, AVL, V6

-Both have low sensitivity for detection of acute MI in preexisting

LBBB should be used together with sgarbossa criteria

Q: What is the hallmark of type I MI?

Answer: Presence of Intracoronary thrombus

Q: What are the conditions in which Clopidogrel is

preferred over other P2Y12 inhibitors?

1. PCI for patients with Stable CAD

2. First 48 hours post Fibrinolysis in STEMI
3. Patients with lower extremity disease(LEAD)
4. Patients on triple anti thrombotic therapy
5. ACS with contraindications for Ticagrelor and prasugrel:
-History of Intracerebral hemorrhage
-High risk of Bleeding
-CKD, GRR less than 15ml
46
 *If Ticagrelor is not available, Clopidogrel is preferred over
prasugrel if there is contraindication for Prasugrel which include:

-Age above 70
-Weight less than 60 kg
-History of TIA or stroke
-Medically managed ACS patients

Q: What is the baseline from which we calculate the ST

elevation?
Answer: QRS onset

Reference: ESC guidelines, fourth universal MI definition, 2017

Q: When to start antihypertensive medication for elderly 80

years or above?
Answer:

-For people >80 years who have not yet received treatment for their
BP, treatment is recommended when their office SBP is >160
mmHg, provided that the treatment is well tolerated (Class I C)
*ESC guidelines for hypertension, 2018.

Q: What are the Functions of cholesterol in the human

body?

Answer:

Cell membrane synthesis

Steroid and sex hormones synthesis
Bile synthesis

47
Q: What is the possible explanation for this finding?

X ray in left lateral position, heart shift to Left, then

X ray in right lateral position, heart shift to the right

Answer: Congenital pericardial absence

Q: What are the Causes of dynamic LVOT obstruction?

Answer: APCD

1. Acute coronary syndrome

2. Postoperative(AVR(
3. Concentric LVH
4. Cardiomyopathy(Hypertrophic(
5. Cardiac tamponade
6. Dehydration(hypovolemic shock(

Q: When to use FFR cut off value 0.8 and when to use cut
off value 0.75?
Answer: To improve prognosis, in patients with stable CAD, It is
justified to do revascularization if Left main or proximal LAD 50%
stenosis with FFR is 0.8 or less
Or any other vessel with FFR with less than 0.75

Q: What is meant by Vascular in CHADS-VASc score?

Answer:

Aortic plaque

PAD

Previous MI

48
Q: What is meant by "S" in CHADS-VASc score?
Answer:

Stroke, TIA or thromboembolism

Q: What is meant by Brockenbrough Phenomenon?

Answer: Pressure tracings Post extra systole

1. HOCM

Pressure gradient increase and pulse pressure Decrease

2. AS

Pressure gradient slightly increases and Pulse pressure increases

Q: Calcium chloride vs. Calcium gluconate?

Answer: Calcium chloride contains three times the concentration of
elemental calcium compared with calcium gluconate

Q: What are causes of apical thrombus on normally

contracting apex?
Answer:

Loffler endocarditis (hyperoesinophilic syndrome) or endomyocardial

fibrosis or hypercoagulable state

49
Q: True or false?
Verapamil is a good option for patients with positive vaso-reactivity test
and pulmonary arterial hypertension?

Answer:

No role for verapamil with PAH

The approved CCB are amlodipine, nifedipine and diltiazem

Q: How to differentiate between ischemic and non-ischemic

causes of pathological Q waves?
Answer: Presence of ST segment deviation plus or minus T wave change
raise the possibility of ischemic origin of pathological Q waves, while
normal ST segment with normal T waves raise the possibility of non-
ischemic etiology like HOCM, amyloidosis, WPW

Q: When to consider ablation for PVC induced

cardiomyopathy?
Answer: When the PVC burden is more than 15% of the total beats

Reference: American guidelines for management of ventricular

arrhythmias and prevention of sudden cardiac death 2017

50
Q: What are the Features of non- bacterial thrombotic
endocarditis (Libman sacks endocarditis)?

1. Presenting with thromboembolism rather than fever

2. Not responding to antibiotics
3. Negative blood culture
4. Could be bilateral(Mitral and tricuspid for example(
5. Mass attached to the base of the leaflet
6. Small in size(usually did not exceed 10mm(
7. Attached to the leaflet with broad base attachment
8. Sessile mass(no pedicle(
9. The mass did not show Independent motion
10.Not associated with leaflet destruction

Q: What to suspect in patient presenting with acute chest

pain and stroke?
Answer:

-Aortic dissection or MI complicated by LV thrombus

-Whenever you encounter a Dilated Ascending aorta in patient with acute

chest pain you have to exclude dissection

Q: True or false?
Nebivilol and Carvedilol are a good choice for patient with
HOCM?
Answer:

False. The recommended beta blocker in patients with HOCM are non-
vasodilatory beta blockers (eg ; bisoprolol or metoprolol)

51
Q: Mention the conditions in which you should give
anticoagulation in AF regardless of CHADS-VASc score
1. HCM
2. Fontan
3. Systemic RV
4. Intra-cardiac repair in congenital heart disease
5. Cyanotic heart disease
6. After ablation for 8 weeks
7. After cardioversion for 4 weeks
8. Mechanical prosthesis
9. Moderate or severe MS
10. Anticoagulation for other indications(DVT, PE, LV thrombus, etc(
11.Thyrotoxicosis(in some papers)
12. Amyloidosis

Q: What are indications of vascular dose of Rivaroxaban?

Answer: Rivaroxaban 2.5 mg twice daily .Patients with which was

studied in ATLAS trial (post ACS) and Compass trial (in patient with

stable vascular disease)

Compass Conclusion:

52
Q: What are the Eligibility criteria for NOACS?
Answer: according to EHRA

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