KARDIOLOGI 7 FEB 2021

Dr. Dian Paramita, Sp.JP

1.

A 20-year-old man is referred for a cardiology consult due to an episode of non-exertional syncope associated with palpitations (his mother who is a nurse took hisapical pulse and it was>200 bpm and irregular during the event). An electrocardiogramis reported as abnormal but not available. An Echocardiogram was normal. Which of thefollowing examinations suggests a cause for syncope in this patient?

a. Normal S1 and physiologic split S2

b. Normal S1 and persistent split S2

c. Physiologic split S1 and normal S2

d. Normal S1 and fixed split S2

• The patient has Wolf-Parkinson-White (WPW) syndrome with associated rapid AF that led to non-exertional syncope.With a manifest accessory pathway, left- and right-sided WPW may be detected on auscultation due to abnormalities in the splitting of the second heart sound (S2).

• With a left-sided pathway, the A2 component of S2 would occur early since the atrioventricular (AV) node is bypassed and electrical activation of the left heart and therefore completion of ejection would lead to an earlier A2 closure sound. In expiration, A2 and P2 would be separated, and in inspiration, the separation would be increased. This is referred to as persistent splitting of S2.

• When a right-sided pathway is present, the P2 component of S2 occurs early during expiration (P2 before A2) with a single sound during inspiration.Thisis referred to as paradoxical splitting of S2. Physiologic splitting of S,or S2 may be a normal variant and not associated with electrical or structural heart disease. A fixed split S2 may be associated with a hemodynamically significant ASD,though this would not be an expected cause of syncope.

Cardiac Conduction SystemCardiac Conduction System

Type A WPW

Type B WPW

2.

Which of the following structures are not found in the right atrium?

a. Tendon of Todaro

b. Moderator band

c. Koch triangle

d. Pectinate muscle

• Moderator band, located in the right ventricle, is a muscular bridge that connects the distal septum and the right ventricular free wall at the anterior Papillary muscle.

• The tendon of Todaro is a fibrous band located between the valves ofthe inferior vena cava and the coronary sinus in the right atrium.

• Koch triangle is located in the lower medial portion ofthe right atrium, overlying the AV node and the proximal His bundle.

• Pectinate muscles arise from the crista terminalis and course as bands on the right atrial free wall.

3.Which of the following medications will take this patient from point A to point B on the Frank-Starling and force-tension curves shown?

a. Propranololb. Norepinephrinec. Hydralazined. Phenylephrinee. Furosemide

• Hydralazine reduces afterload and increases stroke volume (SV) without changing preload.

• Propranolol acutely reduces contractility and would not be expected to improve SV.

• Norepinephrine and phen ylephrine both increase afterload. Furosemide reduces preload.

4.

Which of the following is not a characteristic of sodium channels?

a. Selective permeation

b. Pump electrolytes exchange mechanism

c. Gating

d. Drug binding

e. Susceptibility to many different neurotoxins

• Sodium channels are characterized by a protein that works as a voltage-gated sodium channel.

• The active portion of this channel is the ⍺-subunit, which consists of a 2,000-amino acid glycoprotein. The other choices are all properties of these channels.

5.Following a cycle of excitation-contraction coupling in cardiac muscle, cytosolic Ca2+ is sequestered in the sarcoplasmic reticulum (SR) primarily by what entity?

a. Na+/Ca2+ exchanger

b. L-Type Ca 2+ channels

c. Phospholamban

d. SERCA2a

e. Ryanodine receptors

• The active sites of the actin filaments are covered in the resting state by two regulatory proteins, tropomyosin and troponin. Intracellular Ca2+ is the most important determinant of myocardial contractility and relaxation. Once contraction ensues, calcium (Ca2+) entry through L-type Ca2+ channels triggers an exponential release of Ca2+ from the SR through ryanodine receptors. Calcium then binds troponin leading to a conformation al alteration of tropomyosin exposing the actin active site, which facilitates a "sliding" interaction between he actin filaments and the myosin heads as well as he hydrolysis of ATP providing energy for contraction. F

• ollowing a cycle ofexcitation-contraction coupling, diastolic relaxation is initiated by cytosolic Ca2+ seques tration in the SR by the SR-Ca2+ ATPase (SERCA2a) pump (-75%) and exportation extracellularlybythe Na+/Ca2+ exchanger (-25%) located on the sarcolemmal mem brane. Phospholamban, a regulatory protein, exerts an inhibitory effect on SERCA2a limiting its ability to remove cytosolic Ca2+ following contraction.

6.

Ms. G. is a 28-year-old woman who immigrated from South Asia approximately 4 years ago. She has been told in the past that she has a heart murmur and recently noted the onset of exertional dyspnea. Her electrocardiogram (ECG) is notable for atrial fibrillation, and examination reveals a diastolic murmur best heard at the apex. Her chest radiograph is displayed below. Her atrial fibrillation is most likely secondary to:

a. Atrial myxoma

b. Increased transmitral gradient

c. Idiopathic "primary" pulmonary hypertension

d. "Lone" atrial fibrillation

e. Advanced left ventricular dysfunction

• sing the organized approach to radio graph interpretation, the pulmonary vascular pattern shows evidence of vascular redistribution suggestive of pulmonary venous hypertension.

• The left atrium is enlarged and the left ventricle is normal in size, suggesting possible mitral valve pathology. No chamber calcification is present to assist in the diagnosis.

• The case vignette describes a classical presentation for mitral stenosis.Though persistent inflammation may contribute to atrial fibrillation in this disorder, the primary mechanism in mitral stenosis is still felt to be elevated atrial pressure resulting in stretching of the atrial myocardium.

7.All of the following statements regarding the Doppler equation are true except:

a. In order to obtain the true velocity of blood flow at a certain point, the beam needs to be parallel to the direction of blood flow.

b. The measured velocity of blood is over estimated when the beam is at a greater angle to the direction of blood flow.

c. There is no Doppler shift when the beam is perpendicular to the direction of blood flow.

d. The true velocity of blood flow is equal to the measured velocity divided by the cosine of the angle the beam makes with the direction of blood flow.

• The true velocity of blood flow is equal to the measured velocity divided by the cosine of the angle the beam makes with the direction of blood flow.The Doppler equation enables us to measure the velocity based on knowing the frequency shift, the transmitted frequency, and the speed of sound in blood. When the beam is parallel to the direction of blood flow, the angle is 0 degrees and cos 0 = 1 ; therefore, the true velocity is equal to the measured velocity. However, when the beam is perpendicular to the direction of blood flow, the angle is 90 degrees; cos 90 = 0, so there is no Doppler shift.

• The greater the angle between the beam and the direction of blood flow, the greater is the error in measuring the velocity of blood flow. In actuality, the measured blood flow will be underestimated

• in this scenario, and the true velocity will actually be higher than what is reported.Therefore, it is essential to keep the beam parallel to the direction of blood flow in order to minimize velocity errors because it is important to assess the velocity of blood flow in cases such as valvular stenosis.

• Angles that are <20 degrees may be acceptable because there is less velocity error.

8.

Which of the following statements about heart failure is true?

a. It is a clinical syndrome.

b. It can be caused by any form of heart disease.

c. It is diagnosed primarily by history and physical exam.

d. All of the statements are true.

• Heart failure, like renal failure or anemia, is a clinical syndrome with a constellation of signs and symptoms. It has many possible etiologies, since virtually any form of heart disease can lead to heart failure. Pa tients must have signs and symptoms (i.e., a low EF does not equal heart failure) that usually consist of dyspnea and fatigue at rest or with exertion.There must be under lying cardiac structural and/or functional abnormalities. There is no laboratory test for heart failure (i.e., a history and physical exam are necessary),though a plasma BNP level may help facilitate the diagnosis in certain settings.

9.

Which of the following lifestyle modifications has been demonstrated to decrease mortality in heart failure (HF) patients?

a. Sodium restriction to < 2 g/day from all sources

b. Regular aerobic exercise 30 minute/day, 5 to 7 days/week

c. Fluid restriction to < 1 .5 L/day

d. Daily weights and blood pressure monitoring

e. None of these modifications

Although some studies have suggested a reduction in hard endpoints with aerobic exercise in HF,the large HF-ACTION trial did not show any effect on mortality. Other lifestyle measures in HF have not been studied in large clinical trials.

10.A 45-year-old female came to see you because of intermittent chest pain and progressive shortness of breath for the last 3 days. She was seen last week by her primary physician because of sinusitis and was placed on azithromycin for 5 days without relief. Exam: BP 110/80 mmH g, pulse 110 bpm regular, JVP 10 cmH2O, bibasilar rales, S3 gallop, 1 to 2+ pedal edema. ECG: sinus tachycardia, nonspecific T wave changes. Echocardiography: left ventricular ejection = 25% 1 to 2+ mitra l regurgitation. Which of the following is not an appropriate next course of action?

a. Cardiac catheterization

b. Endomyocardial biopsy to rule out acute lymphocytic myocarditis

c. Start diuretics and angiotensin-converting enzyme (ACE) inhibitors

d. Blood testing for thyroid function tests

• New-onset HF in a relatively young patient who had a recent bout of upper respiratory tract infection can be a potential clinical presentation of acute myocarditis.

• That being said, the usual course of action should involve cardiac catheterization to rule out coronary ischemia, blood testing to rule out reversible causes of HF such as hypo- or hyperthyroidism, and start therapy with diuretics, ACE inhibitors, and beta-adrenergic blockers. Routine endomyocardial biopsy, even though it may elucidate the definitive diagnosis, does not change the management at this point, and should be reserved only when patients require further evaluation due to decompensation.

11.

A 45-year-old woman with a history of hypertension presented with dyspnea upon exertion. You obtained an echocardiogram showing normal left ventricular systolic and diastolic function, normal right ventricular (RV) size and function, normal valvular function, but an estimated right ventricular systolic pressure (RVSP) of 56 mmHg with 1 to 2+ tricuspid regurgitation. Your next step should be:

a. To perform a pulmonary angiogram

b. To perform to right heart catheterization (RHC)

c. To start oral bosentan therapy and follow-up in 6 weeks

d. To repeat an echocardiogram in 6 months

• Echocardiographic estimations of RVSPs may potentially overestimate the true PAPs, and should be confirmed by RHC in the setting ofaclinical suspicion for PH.

12.

A 63-year-old male engineer undergoes echocardiography 2 months following a large posterolateral myocardial infarction due to acute stent thrombosis in his proximal left circumflex coronary artery.

Which of the following is associated with a better prognosis?

a. Ejection fraction (EF) of 29%

b. E/e' of 23

c. Presence of mode rate-to-severe mitral regurgitation (MR) with ERO = 0.3 cm2

d. Lateral wall e' of 6 cm/s

e. Deceleration time of 133 milliseconds

• Regional ischemic injury will decrease the longitudinal systolic and diastolic excursion of the affected wall. Therefore, a lower value of e' in the lateral wall of this patient is not an entirely unexpected finding (lateral e' should normally be ::2'.1 0 cm/s). It is now recommended to acquire and measure tissue Doppler signals at least at the septaIand lateral sides of the mitral annulus and calculate their average to measure E/e’. The other possible answers each have been shown to carry important prognostic information in patients with a history (recent or not) of myocardial infarction.

13.

All of the following increase the gradient in hypertrophic cardiomyopathy (HCM) except:

a. Valsalva maneuver

b. Squatting

c. Amyl nitrite

d. lsoproterenol

• The Valsalva maneuver decreases venous return and thus decreases ventricular volume, thus accentuating the systolic anterior motion (SAM) and thus increasing the gradient.

• Amyl nitrite causes peripheral vasodilation and tachycardia. Both of these factors cause the LV to decrease in size and thus increase the gradient.

• lsoproterenol increases the contractility and thus decreases ventricular volume, which increases the gradient.

• Standing decreases venous return and decreases ventricular volume.

• Squatting increases the vascular resistance and venous return,thus increasing ventricular volume and reducing the SAM, which reduces the gradient.

14.You are seeing a 27-year-old female postal employee in outpatient clinic. She has a history of asthma treated with inhalers, though her pulmonary function tests and methacholine challenge were recently normal . She has noted progressive fatigue over the past months and finds that getting uplarge hills on her mailroute gets her out of breath. On examination, she has a fixed split second heart sound and soft systolic ejection murmur over the left upper sternal border. Her lungs are clear and all her extremity pulses are equal and of normal intensity. All the following would be expected to be present on her diagnostic studies except:

a. Unexplained right heart enlargement on echocardiography

b. An RSR' (incomplete bundle branch block) pattern on electrocardiogram (ECG)

c. Unexplained mild pulmonary hypertension

d. Right-to-left shunt by bubble study on echocardiography

e. Decreased pulmonary vascularity on chest x-ray

• The lung x-ray in this case would be expected to demonstrate increased lung vascularity. The patient describe in this case has an ASD.\

• The telltale physical examination findings are the pulmonic outflow murmur resulting from increased pulmonary blood flow due to left-to-right shunting and the fixed split second heartsound.ASDs,if sufficiently large,lead to right heart enlargement and an incomplete right bundle branch block pattern on electrocardiography.

• Pulmonary hypertension can result from increased blood flow and up to 1 0% may develop Eisenmenger physiology

• if uncorrected. As with any atrial flow communication a bubble study on echocardiography would be expected to be positive providing the right atrial pressure can be made to exceed the left atrial pressure (such as follow ing a Valsalva maneuver).

15.

A cleft mitral valve (MV) is associated with which of the following conditions?

a. Secundum atrial septaI defect (ASD)

b. Primum ASD

c. Coarctation of the aorta

d. Sinus venosus (SV) ASD

e. Tetralogy of Fallot

• A cleft MV is part of an atrioventricular (AV) canal defect,which is due to failure of the embryonic endocardial cushions to meet and partition the heart normally. A complete endocardial cushion defect has four components: primum ASD, cleft MV, inlet VSD, and a widened anteroseptal tricuspid commissure.

• A partial AV canal defect does not have the VSD.

16.Clinical features associated with increased risk for sudden cardiac death (SCD) among patients with hypertrophic cardiomyopathy (HCM) include all of the following except:

a. Septal thickness > 3 cm

b. Syncope or hypotension associated with exercise

c. Dynamic left ventricular outflow-tract (LVOT) gradient > 100 mmHg by Doppler echocardiography

d. Non sustained ventricular tachycardia (N SVT)

• Clinical features associated with SCD among patients with HCM include NSVT, hypotension associated with exercise, unexplained syncope, septaI thickness >3 cm, and a family history of sudden death in a first-degree relative younger than 50 years old.

• Dynamic LVOT gradients by Doppler echocardiography, even when elevated, are not a commonly applied as a guidelines-based risk stratification tool for SCD.

17.

Which of the following antiarrhythmic medications are appropriate for use in patients with significant left ventricular (LV) hypertrophy due to hypertension?

a. Flecainide

b. Sotalol

c. Propafenone

d. Amiodarone

e. Quinididine

• amiodarone is the only acceptable pharmacologico p t i o n fo r t h e t r e a t m e n t o f a t r i a l fi b r i l l a t i o n i n p a t i e n t s with hypertension and significant left ventricular hypertrophy

18.

A 44-year-old patient with no previous cardiovascular history, who presents with a wide-QRS, irregular, and fast tachycardia (on ECG) is best treated with:

a. Lidocaine

b. Procainamide

c. Metoprolol

d. Diltiazem

• This patient has atrial fibrillationwith pre-excited QRS and should be treated with procainamide.

• AV node-blocking agents are absolutely contradicted because they will favor conduction over the accessory pathway with increased risk of degenera tion into ventricular fibrillation.

19.An 83-year-old man comes to see you in your office complaining of three episodes of abrupt loss of consciousness (LOC) in the last year. His PMH is negative. His internist recently performed a stress echo test and Holter monitoring that were normal. His electrocardiography (ECG) revea l s "trifascicular block." What is the next step?

a. Perform electrophysiologic studies (EPS), and if negative, implant a Reveal device.

b. Perform EPS, and if negative, implant an implantable cardioverter-defibrillator (ICD).

c. Consider EPS for ventricular tachycardia (VT), and if negative, recommend a pacemaker.

d. Schedule a tilt test.

• The presence of trifascicular or bifascicular block on the ECG suggests that the underlying etiology of syncope may be intermittent heart block, Mobitz type II, third-degree heart block, the so-called Stokes–Adams block.

• Given a normal stress echo test and normal LV function, electrophysiologic testing will likely be negative for ventricular tachycardia.

• Based on current American College of Cardiology/American Heart Association (ACC/AHA) guidelines, when no other cause for syncope is found, pacemaker implantation is indicated for syncope that has not been demonstrated to be due to AV block.

20.A 42-year-old man with hypertension , but no prior cardiac history, presents with increasingdyspnea on exertion. Physical exam reveals a heart rate of 75 beats/min (bpm) and blood pressureof 175/67 . The jugular venous pattern (JVP) is unremarkable. S1 is soft, S2 is normal, and there isan early systolic sound . There is a soft II/VI systolic ejection murmur (SEM) at right upper sternalborder (RUSB) radiating to the neck, and a 111/VI decrescendo, holodiasto lic murmur near LLSB.The reisal so a low-pitched diastolic rumble heard at the apex. The PMI is laterally displaced.Carotid pulsations are brisk and have a rapid upstroke, immediately followed by a second systolicpulsation. Femoral pulses are normal, and are slightly delayed compared to the radial pulse. Whichof the following findings would you not expect to see on transthoracic echocardiography?

a. Fluttering of the anterior mitral leaflet on M-mode echocardiography

b. Mitral stenosis

c. Bicuspid aortic valve

d. Dilated left ventricle (LV) cavity

e. Coarctation of the aorta

• This patient is fairly young and has hypertension with a wide pulse pressure.The cardiac exam suggests a diagnosis of bicuspid aortic valve (younger patient with Al and an ejection click) with significant Al. The holodiastolic murmur is characteristic of chronic Al, and the displaced PMI suggests long-stand ing disease that has dilated the LV. Likewise, bounding carotids and a bisferiens pulse are classic findings of Al.

• BAV usually results from fusion of the right and left coronary cusp leaflets, which then causes a posteriorly directed Al jet.This jet frequently hits the anterior leaflet ofthe mitral valve,which is manifested on M-mode echocardiography as fluttering of the anterior mitral leaflet and on exam as an Austin-Flint murmur.

• A history of hypertension in a young patient with Al should prompt an evaluation for aortic coarctation, because up to 20% of patients with BAV also have coarctation. On physical exam, the slightly weaker and delayed femoral pulsations suggest that coarctation might be present.

21.

MitraI valve regurgitation is not associated with which of the following?

a. Heart failure

b. Atrial fibrillation (AF)

c. Stroke

d. Pulmonary hypertension

e. Increased pulse pressure

• AR is associated with increased pulse pressure due to the excess run-off of flow back into the LV in diastole. Prior to end-stage MR with secondary abnormalities, the cardiac output and forward stroke volume are normal. Arterial pressure is usually normal, and pulse pressure is normal.

• All the other choices are in some circumstances associated with MR, including the development of left atrial thrombi, often from concomi tant AF, leading to systemic embolization.

22.All of the following are true statements except:

a. By definition, "early" prosthetic valve endocarditis refers to the development of infection within 60 days of surgery.

b. Aztreonam is not an acceptable alternative for the treatment of HACEK endocarditis.

c. Gram-negative bacilli are important pathogens causing hospital-acquired endocarditis.

d. Endocarditis with Streptococcus bovis should prompt a search for a colonic neoplasm.

e. Surgery is often necessary in infective endocarditis (IE) with Brucella organisms.

• Early-onset prosthetic valve endocarditis is usually attributed to pathogens from perioperative contamination (health care-associated), and therefore within 60 days from implant of the valve. Aztreonam (gram-negative organism only) will not be active against HACEK organisms.

• Staphylococcus aureus is the most common health care-associated cause of IE (not gram-negative organisms). Brucella IE almost always requires surgery for cure.

23.Assuming no other thromboembolic risk factors, what is the recommended anticoagulation therapy for a St. Jude mitral valve?

a. International normalizing ratio (INR) of 2 to 3 for life of valve

b. INR of 2.5 to 3.5 for life of valve

c. Anticoagulation therapy with INR of 2.S to 3.5 for first 3 months, then aspirin therapy thereafter

d. INR of 3.S to 4.5 for life of valve

e. INR of 3 to 4 for life of valve

• Embolic event rates are higher for mitral valves than for aortic valves and therefore generally require higher anticoagulation therapy. Caged ball and single tilting valves also carry greater embolic risk than double tilting mechanical valves. Bioprosthetic valves generallycarrythe lowest riskofembolization,yet according to AMA guidelines, anticoagulation is still rec ommend in the first 3 months after placement, although this varies according to institution.

24.

A 23-year-old peripartum female presents with substernal chest pain. Electrocardiogram (ECG) demonstrates ST elevations in II, Ill, and aVF. The next appropriate step is:

a. Administer aspirin 325 mg, clopidogrel 600 mg, oxygen, nitrates, and heparin weight-adjusted bolus.

b. Administer aspirin 650 mg, clopidogrel 300 mg, oxygen, nitrates, and heparin weight-adjusted bolus.

c. Administer aspirin 650 mg, clopidogrel 600 mg, oxygen, nitrates, and heparin weight-adjusted bolus.

d. Administer oxygen, beta-blocker, and order gated computed tomography (CT) of the chest.

e. Administer oxygen, beta-blocker, and order nongated CT of the chest.

• 1 . Answer D: The patient is most likely presenting with dissection. Most appropriate test for a patient who is at a higher likelihood of presenting with an acute dissection rather than ACS is a gated CT of chest or cardiac CT.

25.

All of the following are recommended mechanisms to decrease bleeding complications in the management of unstable coronary syndromes, except:

a. Decreasing the maintenance dose of aspirin from 325 to 81 mg daily

b. Stopping clopidogrel a minimum of 5 days prior to a major surgical procedure

c. Stopping the routine use of heparin after percutaneous coronary intervention

d. Withholding the loading dose of clopidogrel

e. Reducing the dose of heparin for patients who are also on aspirin and a glycoprotein lib/Illa

inhibitor