CARDIOLOGY Flashcards
These can be heard in mitral stenosis, except for:
A) apical holosystolic murmur radiating towards the axilla
B) low-frequency apical diastolic murmur
C) opening snap
D) loud first heart sound
A) Holosystolic heart murmurs that radiate towards the axilla and are best heard at the apex are characteristic of mitral regurgitation, therefore they cannot be heard in mitral stenosis. Severe mitral stenosis might be accompanied by tricuspidal insufficiency that can cause a holosystolic, apical murmur, but it never radiates towards the axilla. The pathomechanism behind the low-frequency, diastolic murmur is the fast, turbulent flow through the stenotic mitral valve. The opening snap (o.s.) is heard as the mitral leaflets buckle in their attempt to open and it cannot be heard when the valve is severely calcified. The loud, tapping first heard sound is especially easy to notice when the heart is in sinus rhythm and when it is introduced by a presystolic murmur.
Part of the therapy of decompensated heart failure, except for:
A) mineralocorticoid-antagonists
B) diuretics
C) digoxin
D) parenteral volume expansion
E) ACE-inhibitors
D) In chronic decompensated heart failure the body is in a state of fluid overload. Treatment with diuretics and mineralocorticoid-antagonists is essential. Digoxin should be given because of its positive inotropic and negative chronotropic effects, while ACE-inhibitors improve long-term survival. Parenteral administration of fluids (infusions) is contraindicated as it increases the preload on the left atrium and the left ventricle and worsens the symptoms. Acute left ventricle failure might be caused by acute myocardial infarction, hypertensive crisis or severe aortic stenosis as well since these all strain the left ventricle while bronchial asthma exerts the right ventricle.
Causes of acute left ventricle failure, except for:
A) asthma bronchiale
B) acute myocardial infarction
C) hypertensive crisis
D) severe aortic stenosis
A) Acute left ventricle failure might be caused by acute myocardial infarction, hypertensive crisis or severe aortic stenosis as well since these all strain the left ventricle while bronchial asthma exerts the right ventricle.
Characteristics of hypertrophic obstructive cardiomyopathy, except for:
A) might be combined with mitral insufficiency
B) digoxin is important in the early stage
C) it often shows a familial distribution
D) diastolic dysfunction is common
E) syncope is a common symptom
B) Hypertrophic cardiomyopathy has a genetic background in most of the cases, so it is usually familial. Characteristic symptoms include syncope and it is often accompanied by mitral insufficiency because the mitral valve is primarily damaged. The valve has functional damage, too: because of the Venturi effect its anterior leaflet moves toward or contacts the interventricular septum (it is called systolic anterior motion: SAM) and the valve doesn’t close completely during systole which can result in severe mitral insufficiency (these changes can be diagnosed with echocardiography). As the hypertrophic myocardium’s ability to relaxe is damaged, the diastolic filling decreases which leads to diastolic dysfunction. Digitalis (Digoxin) is not recommended either in early or in late stages unless the disease reaches its „burn-out”, dilated phase.
Features of atrial myxoma, except for:
A) the most common form of primary cardiac tumors
B) it can be diagnosed with echocardiography
C) it is often metastatic
D) it can mimic mitral stenosis during physical examination
C) Left atrial myxoma is the most common benign, primary neoplasm in the heart. It can be diagnosed with echocardiography because of its pathognomic features. As it is a benign, in situ tumor, metastases are extremely rare. It can mimic the auscultation characteristics of mitral stenosis by protruding into the mitral orifice and causing an obstruction during diastole.
Which one is true about the mechanism of action of digoxin?
A) it inhibits the Na-K-ATPase
B) it lowers intracellular Na+ concentration
C) it increases intracellular ATP levels
D) it enhances cAMP-production
E) it decreases Ca-release from the sarcoplasmic reticulum
A) Digoxin inhibits the Na/K-ATPase. This causes a temporary rise in intracellular sodium levels, which increases intracellular calcium concentration through the sodium-calcium exchanger. Consequently, it is the elevated intracellular calcium level that increases myocardium contractility and has a positive inotropic effect.
All of the following statements about nitroglycerine are true, except for:
A) it increases intracellular cGMP levels
B) it is primarily metabolised in the liver
C) it can induce significant reflex tachycardia
D) it significantly prolongs AV-conduction
E) it can lead to postural hypotension
D) Nitrates don’t alter atrioventricular conduction.
The typical side effect of nitrates is:
A) hypertension
B) headache
C) bradycardia
D) sexual dysfunction
E) anaemia
B) The most common adverse effect of nitrate therapy is headache. In severe cases it could result in the discontinuation of the therapy but most of these headaches resolve in a few days, therefore it is recommended to continue the treatment for a few days.
The typical feature of Prinzmetal angina:
A) ST segment depression during angina
B) negative T waves during angina
C) pathologic Q waves during angina
D) elevated necroenzymes
E) ST segment elevation during angina
E) Prinzmetal angina is a unique type of angina pectoris that is caused by coronary spasm which can affect healthy and stenotic arteries, too. Chest pain is accompanied by ST segment elevation indicating subepicardial or transmural ischemia. ST segment depression during chest pain means subendocardial ischemia, while negative T waves are non-specific features. Pathologic Q waves and elevated necroenzymes are signs of myocardial infarction.
Types of unstable angina pectoris, except for:
A) angina at rest
B) crescendo angina
C) effort angina
D) new-onset angina
C) Unstable angina pectoris could be defined as a new-onset angina (it presents for the first time), or it might occur with a crescendo pattern (increase in frequency, severity and duration), and it could develop at rest or sometimes during minimal exertion. Contrarily, stable or effort angina pectoris is usually provoked by the same level of exertion in the same circumstances.
The most common pathology of myocardial infarction:
A) coronary embolism
B) rupture of an atherosclerotic plaque
C) dissection of coronary walls
D) growing of an atherosclerotic plaque
E) coronary inflammation
B) The pathomechanism behind acute myocardial infarction is usually the rupture of an atherosclerotic plaque of a coronary artery and the following thrombus formation. The so-called soft plaques are more prone to rupture because their lipid-rich core is only covered by a thin, vulnerable fibrous cap. Coronary endarteritis is a rare cause of acute myocardial infarction.
Normal mean electrical axis in the front plane, except for:
A) +60°
B) +90°
C) –45°
D) 0°
E) +45°
C) The mean electrical axis is considered normal between 0° and +90° in the frontal plane. 0° leftward axis can be physiological, while a +90° axis is common in young people. A -45° axis means distinct left axis deviation, a typical feature in left anterior fascicular block.
If acute myocardial infarction is suspected, the following diagnostic procedures should be carried out, except for:
A) ECG
B) blood tests (to measure CK-MB and troponin)
C) physical examination
D) cardiac stress test
E) echocardiography
D) Cardiac stress test is contraindicated if acute myocardial infarction is suspected. The other choices could be diagnostic steps in NSTEMI.
Ischemic heart disease can present with, except for:
A) acute myocardial infarction
B) stable angina
C) deep vein thrombosis
D) sudden cardiac death
E) ischemic cardiomyopathy
C) Deep vein thrombosis isn’t directly connected to the thrombotic processes in the coronary circulation.
The most important risk factor of atherosclerosis:
A) elevated serum LDL-cholesterol level
B) elevated serum HDL-cholesterol level
C) elevated serum triglyceride level
D) elevated serum cholesterol level
A) Chronic hypercholesterolemia and changes in the LDL/HDL ratio play key roles in the pathomechanism of atherosclerosis. LDL is released into the bloodstream and the toxic metabolites of its oxidation propagate the mechanism that eventualy leads to plaque formation. Elevated LDL concentration is the most significant proatherogenic risk factor. HDL cholesterol has protective qualities. Elevated triglyceride levels are less significant but they are proatherogenic, too.
Risk factors of coronary artery disease, except for:
A) positive family history
B) diabetes mellitus
C) smoking
D) elevated serum HDL-cholesterol level
E) metabolic syndrome X
D) Risk factors are variables that are associated with the later development of atherosclerosis in healthy people. The risk factors of coronary heart disease are (among other things) stress, lack of physical exercise, elevated cholesterol, diabetes, obesity, male sex, age, smoking and family history. Metabolic syndrome X is a cluster term for several of these risk factors (impaired glucose tolerance, dyslipidemia, obesity, hypertension) and it significantly inreases the risk of atherosclerosis. Elevated HDL-cholesterol levels have a protective role against the devlopment of atherosclerosis.
The ideal target value of serum LDL-cholesterol in a diabetic patient after myocardial infarction:
A) < 1,8 mmol/l
B) > 2,6 mmol/l
C) < 3,5 mmol/l
D) > 3,5 mmol/l
A) Total serum cholesterol and HDL/LDL ratio are main factors of atherosclerosis. The target level of LDL in very high-risk patients is below 1.8 mmol/l, lower than in primary prevention.
A 65-year-old patient with a history of smoking presents with sudden pain in his left leg. The limb feels cold, the toes are pale and peripheral pulse can not be palpated. What is the most likely diagnosis?
A) deep vein thrombosis
B) Buerger’s disease
C) embolism in the peripheral arteries
D) Raynaud’s disease
C) These symptoms indicate embolism as they developed quickly. Deep vein thrombosis doesn’t present suddenly, the arterial pulse is palpable and has different symptoms. In Raynaud’s syndrome the tip of the fingers are cold on both sides and it resolves spontaneously. Buerger’s disease has a gradual onset, too.
Paramedics arrive to a 55-year-old patient with chest pain that started 3 hours ago. On the patient’s ECG they notice ST segment elevation in leads I, aVL, V5 and V6. What should they do?
A) transfer the patient to the regional Emergency Department
B) transfer the patient to the regional Coronary Care Unit
C) transfer the patient to the regional Cardiology Department for a troponin test and if it’s positive, transfer to a PCI center
D) transfer the patient directly to the nearest PCI center
D) The patient has an ST Segment Elevation Myocardial Infarction (STEMI). In most of the cases this is caused by a complete coronary occlusion. The opening of the occlusion by percutaneous coronary intervention (PCI) is a life-saving procedure, any unnecessary delay increases the rate of mortality.
Upon the physical examination of a 45-year-old man without any symptoms a soft systolic murmur and ejection click can be heard in 2L2. These have been known since he was a child. What is the most likely diagnosis?
A) patent ductus arteriosus
B) coarctation of the aorta
C) ventricular septal defect
D) Ebstein’s anomaly
E) pulmonary valve stenosis
E) An organic heart disease that has been known since childhood and doesn’t cause any symptoms is most likely a mild pulmonary stenosis. Based on the physical examination and the mild signs and symptoms patent ductus arteriosus (its typical feature is a continuous murmur), coarctation of the aorta (elevated blood pressure on the upper limbs), ventricular septal defect (very loud systolic murmur) or the very rare Ebstein’s anomaly are highly unlikely diagnoses.
Correct statements about aortic stenosis, except for:
A) it causes pulsus parvus et tardus
B) it can cause syncope
C) it can cause anginalike chest pain
D) Austin-Flint murmur can be heard upon auscultation
E) it causes concentric left ventricular hypertrophy
D) The patients’ pulse in aortic stenosis is usually parvus et tardus (slow-rising and anacrotic). A hemodynamically significant aortic stenosis might cause exercise-related syncope. The chest pain that is typically associated with ischemic heart disease might occur in significant aortis stenosis. The increased preload of the heart induces concentric left ventricular hypertrophy. Its severity can be measured with echocardiography. Severe left ventricle might cause strain signs on the ECG. The Austin-Flint murmur can be heard in aortic regurgitation and not in aortic stenosis.
Correct statements about aortic insufficiency, except for:
A) it causes pulsus celer et altus (Corrigan’s pulse).
B) it can be acute and chronic too.
C) it usually doesn’t lead to left ventricle dilation.
D) it can be congenital.
E) it predisposes to infective endocarditis.
C) The patients’ pulse in aortic insufficiency is usually celer et altus (rapidly increasing and suddenly collapsing). It might have a rapid onset (e.g. infective endocarditis, aortic dissection), but its chronic form is the most common. In young adults it is usually predisposed to by congenital bicuspid aortic valve. Aortic regurgitation increases the risk of infective endocarditis because the blood forcefully, turbulently regurgitates from the aorta into the left ventricle. Hemodynamically significant, chronic aortic insufficiency leads to substantial left ventricle dilation through volume overload.
Accessory pathway-mediated reentry tachycardy (AVRT) can be terminated with, except for:
A) propafenone
B) adenosine
C) lidocaine
D) radiofrequency ablation
E) verapamil
C) Drugs that delay the conduction in the AV node or in the bundle are able to terminate an AVRT. Lidocaine doesn’t have this effect. Ablation can be done during tachycardia (e.g. incessant AVRT).
A regular wide QRS complex tachycardia can not be:
A) ventricular tachycardia
B) supraventricular tachycardia with bundle branch block
C) atrial fibrillation with bundle branch block
D) antidromic atrioventricular reentry tachycardia (WPW-syndrome)
E) atrial flutter with bundle branch block
C) Atrial fibrillation might have narrow and wide QRS complexes, too, but it is always an irregular rhythm. Monomorphic ventricular tayhcardia (most common in patients after myocardial infarction) has a regular rhythm with wide QRS complexes. Antidromic atrioventricular tachycardia has a regular rhythm, too. The ventricular activation happens through an accessory pathway which results in pre-excited, wide QRS complexes. Supraventricular tachycardia with (either right or left) bundle branch block always creates wide QRS complexes and has a regular rhythm. Atrial flutter might appear as regular tachycardia if it has a fixed conduction or as an irregular rhythm if the AV-block is variable.
A patient was admitted to the Emergency Department because of a palpitation that started three hours earlier. On his ECG an atrial fibrillation with rapid (150 bpm) ventricular response was seen. His blood pressure was 130/90 Hgmm. In the patient’s history there wasn’t anything that indicated structural heart disease. What is the best first step in this situation?
A) pharmacological cardioversion
B) immediate electrical cardioversion
C) coronarography
D) immediate anticoagulation to prevent thromboembolism
E) cardiac stress test
A) The patient is hemodynamically stable, doesn’t require immediate electrical cardioversion and long-term anticoagulation is not needed in atrial fibrillation that is only a few hours old. Exercise testing and coronarography are later diagnostic steps if ischemic heart disease is suspected. Pharmacological cardioversion is the logical first step.
Which one is the most common permanent arrhythmia?
A) ventricular extrasystoles
B) atrial fibrillation
C) ventricular tachycardia
D) supraventricular tachycardia
E) junctional escape rhythm
B) The prevalence of atrial fibrillation is 0.4-14% depending on the age, which means that it the most common permanent (longer than 30 seconds) arrhythmia. Everyone has ventricular extrasystoles but they are not permanent. The other arrhythmias aren’t nearly as common as atrial fibrillation.
A patient who has been taking amiodarone for a long time was prescribed a fluoroquinolone antibiotic because of a respiratory infection. She had recurring short-term syncopes that had never occurred before. Which one is the most likely cause of the syncopes?
A) hypotension induced by the medications
B) torsade de pointes ventricular tachycardia induced by the medications
C) sinus bradycardia induced by the medications
D) her symptoms are not induced by her medications, it is just a coincidence
E) AV block induced by the medications
B) Both Class III antiarrhythmic agent amiodarone and fluoroquinolone antibiotics can prolong the QT interval (long QT syndrome). Their concomitant administration increases the chance of polymorphic ventricular tachycardia (torsade de pointes), syncope because of ventricular arrhythmia and sudden cardiac death. At the onset of these symptoms the therapy or therapies should be immediately discontinued.
These could be the first ECG findings in the acute phase of myocardial infarction, except for:
A) pathologic Q waves
B) inverted T waves
C) ventricular fibrillation
D) ST segment elevation
E) ST segment depression
A) ST segment elevation with lasting chest pain are characteristic of ST Segment Elevation Myocardial Infarction. However, in Non-ST-Segment Myocardial Infarction the ECG findings range from ST segment depression to T wave inversion. Sometimes the first ECG recording of a severe myocardial infarction already shows ventricular fibrillation. The manifestation of pathologic Q waves takes hours, sometimes days.
Pathologic Q wave in leads II, III and aVF with isoelectric ST segment and positive T waves indicate:
A) acute ischemia
B) acute phase of a progressing myocardial infarction
C) previous myocardial infarction
D) aneurysm after myocardial infarction
E) subendocardial ischemia
C) The typical ECG findings of acute myocardial ischemia are ST segment elevations and depressions. ST segment depression and T wave abnormalities (changes in amplitude, inversion) indicate subendocardial ischemia. During the progression of a myocardial infarction these changes are accompanied by a decrease in R wave amplitude, the appearing of pathologic Q waves and T wave inversion. In the recovery phase of the myocardial infarction the ST segment becomes isoelectric and in most cases the T wave normalizes, too. The pathologic Q wave is permanent. If the ST segment stays elevated for more than 2-3 weeks after the onset of the symptoms, a left ventricle aneurysm is likely.
In the diagnostic workup of a 60-year-old patient with a history of smoking who has chest pain at exertion, the first step should be:
A) stress echocardiography
B) exercise test
C) stress perfusion scintigraphy
D) Holter ECG monitoring
E) stress MRI
B) The patient’s symptoms are most likely to be caused by significant coronary artery disease. Unless stress testing is contraindicated, an exercise test should be the next step. If significant ST segment changes appear during the test, then an invasive diagnostic procedure is necessary. If the results of the stress test are questionably or the symptoms are atypical, diagnostic imaging tests (echocardiography, coronary CT angiography) or stress tests with imaging (stress echocardiography, stress MRI) should be considered. Holter ECG is not suitable to detect significant coronary artery disease, this test is only recommended if we need additional information (e.g. the duration of ischemic burden, possibility of Prinzmetal angina).
The best first-choice drug for bradycardia during myocardial infarction is:
A) isoproterenol
B) theophyllin
C) atropine
D) dobutamine
C) Myocardial infarction, especially posterior wall infarction often induces bradycardia. These usually respond well to atropine since they are partially caused by an increase in vagal tone. Sympathomimetic drugs should be avoided because they raise the myocardial oxygen demand which is unfavorable in ischaemia. Although diaphyllin elevates the heart rate but it should be avoided in myocardial infarction because of its proarrhythmogenic effect.
The most common side effect of ACE inhibitors is:
A) diarrhea
B) cough
C) vomiting
D) erythema
E) anasarca
B) The most common side effect of ACE inhibitor therapy is cough (5-10%). It is a consequence of the elevated bradykinin concnentration (its metabolism is inhibited). All of the other side effects are rare or non-existent.
Which disease(s) cause(s) systolic hypertension?
1) aortic insufficiency
2) thyreotoxicosis
3) beriberi
4) atherosclerosis
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Patients with aortic insufficiency have increased cardiac output because of the regurgitated volume. In thyreotoxicosis the thyroid hormone accelerates the circulation which also leads to a higher cardiac output. Beriberi (vitamin B1 deficiency) can induce a special form of dilated cardiomyopathy with extremely high cardiac output, so all of these conditions can lead to systolic hypertension. Arteriosclerosis causes systolic hypertension through the increased vascular resistance.
Aortic aneurysm can be caused by:
1) arteriosclerosis
2) Marfan’s syndrome
3) vascular syphilis
4) giant-cell arteritis
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) Arteriosclerosis, Marfan’s snydrome and vascular syphilis can all cause aortic aneurysm. All of these diseases damage the arterial wall’s tunica media that leads to its weakening, the loss of its elastic elements and the consequent dilation (aneurysm). Aneurysm formation is unusual in giant-cell arteritis, its characteristic feature is the throbbing pain of the temporal arteries.
The possible cause(s) of pericarditis:
1) uremia
2) transmural myocardial infarction
3) tuberculosis
4) metastatic cancer
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) The most common causes of pericarditis are tuberculosis, uremia, metastatic cancer and (less frequently) transmural myocardial infarction.
Secondary cardiomyopathy can be caused by:
1) hyperthyroidism
2) beriberi
3) amyloidosis
4) glycogenosis
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Secondary or specific cardiomyopathies can be caused by endocrine disorders, e.g. hyperthyroidism (dilated cardiomyopathy); deficiency diseases, e.g. beriberi (vitamin B1 deficiency) might induce dilated cardiomyopathy while amyloidosis can precipitate restrictive infiltrative cardiomyopathy; and metabolic (storage) diseases, like glycogenosis can lead to hypertrophic-restrictive secondary cardiomyopathy.
ACE inhibitors:
1) decrease blood pressure
2) decrease aldosterone levels
3) increase bradykinin levels
4) stop the deterioration of the left ventricle ejection fraction
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Due to the inhibition of the ACE the serum level of angiotensin II decreases in parallel with an increase in the production of bradykinin and a reduction in blood pressure. In heart failure the increased pre- and afterload lead to the gradual dilation and remodeling of the left ventricle and its ejection fraction progressively deteriorates. Treatment with ACE-inhibitors decelerates this process.
Which one(s) is/are correct?
1) Aspirin has no effect on the prostacyclin production of the endothelial cells.
2) According to multicenter trials aspirin reduces the chance of a second myocardial infarction.
3) It takes 24 hours for heparin to build up its anticoagulant effect.
4) Heparin and alteplase are treatment options in pulmonary embolism.
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
C) Aspirin works by inhibiting the cyclooxigenase enzyme and by blocking the synthesis of prostacyclin. Several multicenter trials proved that low-dose aspirin reduces cardiovascular mortality. Heparin enhances the activity of antithrombin-III and thus has an anticoagulant effect by inhibiting the fibrinogen-thrombin reaction. Both intravenous and subcutaneous heparin have a rapid onset of action. Fibrinolytics (e.g. alteplase) are used to dissolve fibrin-bound thrombin.
Which diuretic side effect combination(s) is/are correct?
1) furosemide - hyperuricemia
2) chlortalidone – ototoxicity
3) spironolactone – gynecomasty
4) etacrynic acid - hyperuricemia
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
B) Furosemide and chlortalidone can occasionally provoke gout by reducing uric acid excretion. Spironolactone can cause gynecomasty through its antialdosterone effect. Etacrynic acid (and furosemide) therapy can lead to temporary, and in some cases permanent hearing loss.
Risk factors of ischemic heart disease:
1) smoking
2) hypercholesterolemia
3) hypertension
4) family history
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) The risk factors of ischemic heart disease are variables that have a positive correlation with the development and progression of atherosclerosis. These are: smoking, lack of physical exercise, obesity, hyperlipidemia (hypercholesterolemia, hypertriglyceridemia), diabetes mellitus, hypertension, age, male sex, family history (a history of coronary heart disease or its risk factors in the family).
Treatments that reduce morbidity and mortality after myocardial infarction (secondary prevention):
1) beta-blockers
2) antiplatelet drugs
3) HMG-CoA reductase inhibitors
4) ACE inhibitors
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Heart-rate-lowering beta-blockers reduce both mortality and (through their antiarrhythmic effect) the risk of sudden cardiac death in patients after acute myocardial infarction. They also reduce the oxygen demand of the myocardium, decrease myocardial ischaemia and are especially recommendatory in cases of hypertension and ventricular arrhythmias. It has also been proven that inhibition of platelet aggregation has a favorable effect on survival, microcirculation, vasoconstriction and atherogenesis. Inhibition of HMG-CoA reductase: by lowering serum cholesterol statins mitigate and even reverse atherogenesis. Several clinical trials proved that reducing serum total cholesterol, LDL and triglycerides (all major risk factors of ischaemic heart disease) improve the survival and quality of life of patients suffering from coronary artery disease. 4S (Scandinavian Simvastatin Survival Study) was the first large-scale (n=4444) clinical trial to prove their favorable effect on survival: mortality decreased by 30%, coronary-mortality by 42% and myocardial infarction by 37% during the 8-year follow-up. ACE inhibitors: their most important effect is to stop the postinfarction remodeling, therefore (unless contraindicated) all patients who have suffered a myocardial infarction should be given ACE inhibitors as soon as possible.
Diagnostic options to determine myocardial viability:
1) low-dose dobutamine stress test
2) positron-emission tomography
3) stress perfusion scintigraphy with Tl-201 reinjection
4) Doppler ultrasound
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) Methods to measure the metabolism of the myocardium in vivo: positron-emission tomography (PT) and thallium-201 myocardial perfusion scintigraphy. Low-dose dobutamine stress helps the motion of the viable myocardium walls through its positive inotropic effect. PET is highly sensitive and specific in detecting perfusion-metabolism mismatches. Myocardial perfusion scintigraphy using Tl-201 reinjection is highly sensitive but it is less specific while dobutamin stress testing is very specific but has a slightly lower sensitivity. Conventional Doppler ultrasound isn’t suitable for determining myocardial viability, but the newer tissue Doppler ultrasound seems to be promising.
Contraindications of cardiac exercise tests:
1) acute myocardial infarction
2) chronic heart failure
3) unstable angina
4) beta-blocker therapy
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
B) The 1. and 3. answers are absolute contraindications of exercise stress tests. In chronic heart failure symptom-limited exercise testing is a safe and optimal way to measure the patient’s current condition. Beta-blocker treatment (an essential medication of ischemic heart disease) doesn’t contraindicate exercise stress testing but it limits the maximum achievable heart rate and might prevent the appearance of repolarization abnormalities and arrhythmias.
Diagnostic tests with the ability to detect asymptomatic angina pectoris (silent ischemia):
1) dobutamine stress echocardiogram
2) Holter ECG monitoring
3) exercise test
4) ABPM
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) The first-line diagnostic test of ischemic heart disease is exercise testing. If the results are questionable or if the test is contraindicated then the next step is stress echocardiography using dobutamine. Ischemic signs (ST segment depression or wall motion abnormalities) without any symptoms indicate silent ischemia. Holter ECG monitor can be used to detect episodes of angina to determine a silent/symptomatic ratio. Ambulatory Blood Pressure Monitoring, a 24-hour measurement of blood pressure is obviously unable to detect silent ischemia.
Early and late complications of acute myocardial infarction:
1) ventricular fibrillation
2) left ventricular aneurysm formation
3) cardiogenic shock
4) pericardial effusion
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Cardiogenic shock can be an early complication of acute myocardial infarction. Ventricular fibrillation can be an early ischemic complication and because of the ischemic scarring it can present in the later stages, too. Left ventricular aneurysm is considered a late complication. Pericardial effusion typically develops 4 to 6 weeks after the infarction and it is a consequence of pericarditis (Dressler’s syndrome).
Treatment option(s) of heart failure:
1) pharmacotherapy
2) heart transplant
3) mechanical circulatory support devices
4) cardiac resynchronization therapy
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Early stages of heart failure are treated conservatively with medication. However, in severe heart failure non-pharmacologic treatment options (in addition to pharmacotherapy) have recently been given a more important role. Examples are cardiac resynchronization therapy, mechanical circulatory support devices and as a final option, heart transplant.
Risk factors of atherosclerosis:
1) stress
2) AV-nodal reentry-tachycardia
3) smoking
4) hypotension
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
B) Stress and smoking are well-known risk factors of atherosclerosis. AV-nodal reentry tachycardia doesn’t have a role in the development of atherosclerosis, but if it presents frequently and for longer durations, it might cause tachycardia-induced cardiomyopathy. Hypotension, unlike hypertension, is not an atherosclerotic risk factor.
Drugs that lower serum cholesterol level:
1) rosuvastatin
2) ezetimibe
3) atorvastatin
4) ivabradine
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) Statins can reduce serum cholesterol levels. They work by inhibiting the HMG-COA reductase and the intracellular cholesterol production. Currently the most effective statins are rosuvastatin and atorvastatin. Ezetimibe lowers serum cholesterol levels by blocking the absorption of cholesterol in the small intestine. They are mostly used in combination with statins. Ivabradine acts by blocking the If (funny) Na-K channel, it is used to decrease resting sinus heart rate in ischemic heart disease.
Drugs that lower serum triglyceride levels:
1) special diet
2) niacin
3) fibrates
4) alcohol
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) Elevated serum triglyceride levels were considered to be the risk factors solely of pancreatitis but recently it has been recognized as a risk factor of coronary heart disease. It can be lowered by diet, fibrates and niacin. Statins (with a few exceptions) only have a modest effect on triglyceride levels. Moderate to heavy alcohol intake raises triglyceride levels.
Characteristic features of Prinzmetal angina:
1) it usually occurs at dawn during rest
2) ST segment elevation can be seen during angina
3) it is caused by coronary spasm
4) it should be treated with calcium-channel blockers
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Prinzmetal angina is caused by coronary vasospasm that can affect healthy and stenotic arteries, too. The symptoms usually present in the early morning at rest and temporary ST segment elevation can be seen on the ECG.
Possible complication(s) of deep vein thrombosis:
1) pulmonary infarction
2) crural ulcer
3) pulmonary embolism
4) Raynaud’s syndrome
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) Blood clots that break off from deep vein thrombi can cause pulmonary embolism and infarction. Crural ulcers are local complications. Raynaud’s syndrome consists of vasospastic attacks, it is not a thromboembolic disease.
Possible complication(s) of atherosclerosis:
1) dry gangraena of the feet
2) aortic aneurysm
3) myocardial infarction
4) stroke
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Atherosclerosis can cause a wide range of symptoms depending on which vessels are affected.
Might mimic the ECG findings of myocardial infarction:
1) pericarditis
2) pancreatitis
3) myocarditis
4) pulmonary embolism
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) ST segment elevation in the precordial leads is not exclusive for myocardial infarction. Pericarditis and myocarditis can cause ST elevation (sometimes in every lead), too. Acute pancreatitis might present with aspecific ST segment and T wave abnormalities. Pulmonary embolism can mimic the ECG findings of a posterior wall myocardial infarction.
Enzyme(s) that is/are elevated in myocardial infarction:
1) creatine kinase (CK-MB)
2) lactate dehydrogenase
3) troponin
4) alkaline phosphatase
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) CK-MB, troponin and LDH serum levels can be used in the diagnostic workup of myocardial damage. Elevated alkaline phosphatase levels indicate gastrointestinal, bone or hematologic diseases.
A 55-year-old patient with a history of hypertension has been rushed to the emergency room because of severe chest pain and ST segment elevation. Possible diagnosis/diagnoses:
1) peptic ulcer
2) acute myocardial infarction
3) mitral valve prolapse
4) aortic dissection
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
C) Chest pain with ST elevation might be the sign of myocardial infarction and aortic dissection, too. Peptic ulcers and mitral valve prolapse can both cause chest pain but they don’t cause ST segment elevation.
A 70-year-old patient had an anterior wall myocardial infarction three weeks ago. He suddenly develops a fever and complains of chest pain. On his ECG there are no new Q waves and his CK-MB level is normal. What is/are the most likely diagnose(s)?
1) myocardial reinfarction
2) pulmonary embolism
3) lobar pneumonia
4) Dressler’s syndrome
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
D) The onset of Dressler’s syndrome is typically three weeks after myocardial infarction and it presents with recurring chest pain and fever but cardiac marker levels are usually normal. In reinfarctions and pulmonary embolism cardiac enzymes are often elevated. Although lobar pneumonia can not be ruled out, in the combination of the above-mentioned findings you should always think of Dressler’s syndrome at first instead of other, less likely diagnoses.
Correct statements about mitral insufficiency:
1) it leads to the dilation of all heart chambers
2) it might be the complication of infective endocarditis
3) left atrial pressure can be elevated even when the ejection fraction is preserved
4) its severe form requires surgical treatment
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Significant mitral regurgitation can lead to the dilation of every heart chamber because of the substantial volume overload. A number of acute mitral regurgitations are caused by infective endocarditis through the destruction of the valve. In hemodynamically significant mitral regurgation the left atrial pressure can be notably elevated. The left ventricle ejection fraction might be preserved for a long time because during the ventricular systole the left ventricle empties itself quite easily into the left atrium. Symptomatic cases with significant left ventricle dilation might require surgical solutions.
Correct statements about mitral stenosis:
1) it doesn’t increase the risk of atrial fibrillation
2) it predisposes to left atrial thrombus formation
3) during auscultation a muffled first heart sound and a mesosystolic click can be heard
4) it might be a late complication of rheumatic fever
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
C) Mitral stenosis increases the risk of thrombus formation in the left atrium. It can be a late complication of rheumatic fever. The narrowing of the mitral valve predisposes to atrial fibrillation. Muffled first heart sound and mesosystolic click are not characteristic auscultation findings of mitral stenosis. A loud first heart sound and an opening snap can be heard in patients with mitral valve stenosis.
Echocardiographic findings of aortic stenosis:
1) the end-diastolic diameter of the left ventricle is not significantly enlarged
2) concentric left ventricle hypertrophy can often be seen
3) the left atrial diameter can be abnormally large
4) a pathologic transvalvular gradient can be measured at the level of the aortic valve with Doppler ultrasound
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) During the echocardiographic assessment of isolated aortic stenosis the left ventricle has a normal size, but concentric left ventricle hypertrophy can be visualised. The parasternal diameter of the left atrium is often abnormally large. The pathologic transvalvular gradient can be measured in four chamber view at the level of the aortic valve.
Echocardiographic findings of isolated mitral stenosis:
1) large left atrial diameter
2) the unidirectional movement of the anterior and posterior leaflets in M-mode
3) an abnormal transvalvular gradient can be measured in diastole at the level of the mitral valve with continuous wave Doppler ultrasound
4) the calcification of the whole mitral valve can be visualised with 2D-echocardiography
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) During the echocardiographic assessment of isolated mitral stenosis the following signs are characteristic: increased left atrium end-systolic diameter and the unidirectional movement of the anterior and posterior leaflets in M-mode. A pathologic transvalvular gradient can be measured at the level of the mitral valve during diastole. In 2D-echo the mitral calcification can be visualised.
Characteristic(s) of mitral valve prolapse:
1) it can cause ventricular extrasystoles
2) it can present with chest pain
3) it is common in Marfan’s syndrome
4) an opening snap can be heard during auscultation of the heart
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) Mitral valve prolapse syndrome is quite common in Marfan’s syndrome and it can cause chest pain and ventricular extrasystoles. The opening snap cannot be heard, as it can be evidence of mitral and tricuspidal stenosis, too.
Hypertrophic cardiomyopathy:
1) is caused by genetic mutations.
2) can cause dynamic left ventricle outflow obstruction.
3) can cause sudden cardiac death.
4) should not be treated with beta-blockers.
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) Point mutations of the genes that code different parts of the sarcomer (beta-myosin heavy chain, troponin T, tropomyosin, myosin-binding protein C) can be detected in most cases of hypertrophic cardiomyopathy. Septal hypertrophy can cause left ventricle outflow obstruction and a systolic gradient. The sudden cardiac deaths of hypertrophic cardiomyopathy patients are most likely caused by ventricular arrhythmias. Beta-blockers are the recommended first-line therapy because with the right dosage they decrease ventricular contractility and they can reduce the outflow obstruction. In addition to this they have antiarrhythmic potential, too.
The treatment of ventricular extrasystoles:
1) All cases must be treated with antiarrhythmic agents.
2) Frequent, symptomatic extrasystoles require antiarrhythmic pharmacological therapy.
3) Class Ic agents have been proven to be the best choice.
4) In most cases antiarrhythmic treatment is not required.
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
C) Basically everyone has ventricular extrasystoles. They are considered important only if they accompany organic heart diseases, especially after myocardial infarction. So far no medication has been proven to improve survival by decreasing the number of ventricular extrasystoles and a few of them (Class Ic agents) worsened mortality. Ventricular extrasystoles that present without any symptoms and/or without organic heart disease don’t require any treatment, but in cases of frequent, symptomatic, monomorphic extrasystoles ablation therapy should be considered to prevent tachycardia-incuded cardiomyopathy and to improve quality of life.
In the differential diagnosis of wide QRS complex tachycardia helps:
1) Knowing the organic status of the heart
2) Frequency of tachycardia
3) Physical or ECG signs of atrioventricular dissociation
4) Hemodynamic instability of the tachycardia
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
B) Ventricular tachycardia occurs as wide QRS-complex tachycardia or supraventricular tachycardia in case of bundle branch block or accessorius pathway conduction. The more common mechanism is ventricular tachycardia, this is especially true in organic heart disease, primarily in post-infarction state, this helps in the differential diagnosis based on probability. The sure sign of ventricular tachycardia is atrioventricular dissociation. Dissociated p-waves and QRS-complexes, fusion and capture beats can be observed on the ECG, the Cannon-wave on the jugular pulse can be seen during physical examination and the I. sound (cannon sound) with varying intensity can be heard during auscultation which indicate the atrioventricular asynchrony. The frequency of the tachycardia and the hemodynamic status of the patient doesn’t help to differentiate.
Principles of the treatment of wide QRS complex tachycardia:
1) If we are not sure in the mechanism, we should treat it as ventricular tachycardia.
2) Carotid sinus massage should be tried first before the medical treatment.
3) Immediate synchronized cardioversion is required in case of hemodynamic instability.
4) Always start the treatment with group 1/C agent.
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
A) If we have doubts about the mechanism of the wide QRS tachycardia, we make less of a mistake if we treat as ventricle tachycardia, because the medicines (amiodarone, procainamide, lidocaine) used in the treatment of ventricle tachycardia is effective as well in some cases of supraventricular tachycardia, but at least do not worsen the patient’s state. Contrary to this, the intravenous Verapamil which is most commonly used as the treatment of supraventricular tachycardia may cause immediate circulatory collapse in case of ventricle tachycardia. Carotid-sinus massage can terminate the supraventricular tachycardia which involve the AV-node, in case of ventricle tachycardia it doesn’t help, but doesn’t worsen the patient’s state. In case of hemodynamic instability any kind of tachycardia (regular or irregular, narrow or wide QRS-complex) require cardioversion with synchronized DC-shock. Echocardiography is a basic test method for evaluation of the organic heart status in any kind of arrhythmia, but not during acute treatment, but rather after it.
Etiologic factors of atrial fibrillation:
1) Hyperthyroidism
2) Mitral valve disease
3) Cardiomyopathy
4) Ischemic heart disease
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) Atrial fibrillation could be associated with all the listed disease. The most common etiologic factor is the ischemic heart disease and hypertension which is not listed here.
It’s true about the proarrhythmic effect of antiarrhythmic drugs:
1) Organic heart disease does not have influence on the proarrhythmic risk
2) Dangerous proarrhythmia is most commonly caused by beta blockers
3) Chinidin has the least proarrhythmic potential
4) Antiarrhythmic drugs in some cases cause different type, often worse arrhythmia than the arrhythmia which made the use of these types of drugs reasonable. This effect is called proarrhythmia.
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
D) The 4th point contains the correct definition of pro-arrhythmia. The risk of pro-arrhythmia partly depends on the patient and partly depends on the medication used. Bad left ventricular function, active ischemia increases the risk of pro-arrhythmia. Among the medicines chinidin has the largest, beta blockers have the smallest pro-arrhythmic potential.
