Cardiology Intensive Board Review, 3 ed.

Congestive Heart Failure

Miriam S. Jacob • Gary S. Francis • Leslie Cho

ANSWERS

1.c. Use of rapamycin as part of the immunosuppressive regimen. Transplant vasculopathy is a possible complication after transplant that is best to be avoided. The recommended intervention is to control cardiovascular risk factors and start every patient on a statin. Once there is vasculopathy, proliferation signal inhibitors (PSIs) such as sirolimus and everolimus can be used (substituted for mycophenolate mofetil or azathioprine).

2.b. EF of 20% and dyspnea while doing chores at home (New York Heart Association [NYHA] class II symptoms). Based on the results of Emphasis-HF trial, patients with NYHA class II symptoms and EF <30% are eligible for adding eplerenone to their regimen if they were hospitalized in the last 6 months or had an elevated brain natriuretic peptide. This extended the patients who could be placed on an aldosterone blocker. Previous studies studied the benefit of spironolactone in patients with NYHA class IV symptoms in the last 6 months and EF ≤35% and eplerenone in patients 2 weeks post-MI with EF ≤40% and signs of heart failure. Aldosterone antagonists should not be used in patients with creatinine clearance <30 mL/min/1.73 m2. EF or QRS alone are not enough to determine patients who would benefit. Functional class assessment is important.

3.b. No viability found on dobutamine echo with EF of 15%. The use of surgical revascularization of coronary disease and systolic heart failure is reasonable in patients with acute coronary syndrome and symptomatic angina. Although in the STITCH (Surgical Treatment for Ischemic Heart Failure) trial, a study of medical therapy versus CABG in patients with EF ≤35%, there was no difference in all-cause mortality, there was a suggestion of a trend toward patients with CABG having fewer hospitalizations for heart failure or death from cardiovascular causes. The choice of CABG in a patient with no viability and very low EF is unlikely to be successful in improving morbidity or mortality from heart failure.

4.c. Normal tissue Doppler measurement of the left ventricular (LV) lateral and septal walls. Patients with amyloid heart disease usually show restrictive pattern of diastology with low tissue Doppler of the LV myocardium.

5.b. Downregulation primarily of β1-receptors with little change in β2-receptors. In the cardiac myocyte, there are 3 adrenergic receptors (α1, β1, and β2). In a normal heart the predominant β receptor is β1. In a failing heart there is selective down-regulation of β1 receptors not β2 receptors.

6.b. Hydralazine plus nitrates. In the V-HeFT II trial, although ACE inhibitors improved survival, it was hydralazine in combination with nitrates that had greater improvement in LV function and exercise tolerance.

7.c. All of them except losartan. There is no trial evidence that angiotensin II receptor blocker improved mortality in post-MI patients. The Studies of Left Ventricular Dysfunction (SOLVD) prevention used ACE inhibitors in patients with an EF less than 35%.

8.b. Digoxin reduces hospitalization. In the large Digitalis Investigation Group study, digitalis only improved hospitalization. It had no effect on survival.

9.e. No known treatment. Allograft vasculopathy is the leading cause of long-term morbidity and mortality for cardiac transplant patients. Routine cardiac catheterization has been advocated for these patients but has not shown survival benefit with revascularization. Statin therapy appears to improve long-term survival in these patients and should be used for all heart transplant patients. However, its effect on allograft vasculopathy is unknown.

10.d. She should have a positron emission tomography (PET) scan to assess the area of viability before proceeding with CABG or PCI. This patient is at high risk for any type of intervention because of her low EF. However, if there are areas of viability on the PET scan, her EF might improve with complete revascularization. Studies have consistently shown that patients with low EF do better with CABG than with PCI.

11.b. Start dopamine. This patient is in cardiogenic shock. She needs BP support before all else. In these patients, dopamine is the first line of choice, followed by norepinephrine. If there is no change with dopamine and norepinephrine, then dobutamine may be added while the patient is being prepared for IABP placement.

12.c. Consider LV assist device. This is a relatively young patient with no contraindication to cardiac transplant. However, in the current state, she is not eligible for transplantation. LV assist device as a bridge to transplant has been performed with success.

13.c. Acute right ventricular (RV) failure. His hemodynamic pressures are characteristic of acute RV failure. He needs aggressive fluid resuscitation.

14.b. Suggest nitroprusside. This patient is in heart failure and needs to have her BP and SVR lowered. BP is adequate and does not need vasopressor or IABP support. Although nesiritide has been approved for use in acute heart failure, it only mildly lowers the BP.

15.a. Place an implantable defibrillator. She fits the criteria of the initial Multicenter Automatic Defibrillator Trial (MADIT). Therefore, based on randomized clinical trial data, she would benefit from an implantable defibrillator. Also, secondary prevention trials such as the Antiarrhythmics Versus Implantable Defibrillators Trial, the Canadian Implantable Defibrillator Study, and the Cardiac Arrest Study Hamburg trial also support an implantable defibrillator in this patient.

16.d. β-Blockers should be started in stable CHF patients. They should not be started when the patient is congested. Although nonselective agents with vasodilating effects may be preferred, this is not clear at this time.

17.e. Amlodipine proved to be of small benefit in a NYHA class III or IV patient with an EF <30%. This benefit was seen more in dilated cardiomyopathy patients. In the Prospective Randomized Amlodipine Survival Evaluation Trial, in which NYHA class III or IV patients with an EF less than 30% were enrolled, there was a statistically insignificant reduction in the combined mortality and morbidity in the amlodipine group. However, the benefit appeared to be greater in patients with nonischemic cardiomyopathy.

18.b. Begin ACE inhibitor and β-blockers. She has well-compensated cardiomyopathy. Only medication that prolongs her life needs to be started. She does not need medication for symptom relief; therefore, ACE inhibitor and β-blockers should be started.

19.b. Stop diuretics. This patient has prerenal azotemia caused by aggressive diuresis. His renal function should recover.

20.c. Bears little relation to the severity of LV dysfunction. Short-term administration of positive inotropic agents and vasodilators does not improve maximal exercise capacity in patients with CHF. Moreover, ACE inhibitors have failed to show consistent improvement in exercise tolerance. Numerous studies have not shown a correlation between LV function and exercise tolerance.

21.e. Enrolling her in an exercise training program. As stated, there is no medication that has consistently shown improvement in exercise tolerance; exercise training is the only method that has shown consistent improvement in these patients.

22.b. E/O2 slope during exercise. This is the best correlate of prognosis. There is a higher ventilation for any given CO2 production (E/O2 slope), which reflects the severity of heart failure and prognosis.

23.a. Glucagon and milrinone. Milrinone is a second-generation phosphodiesterase inhibitor. It has no β-effect; therefore, it is an ideal vasopressor in the setting of β-blocker overdose. Although a pacer is a good idea and should be placed, giving medication is faster and should be instituted first.

24.b. Atenolol. Atenolol is most affected by reduced renal function. Depending on how severe his creatinine clearance is, he should have his medication dose or frequency adjusted.

25.c. PCWP is 26 mmHg. Restrictive mitral inflow pattern in the presence of a short E-wave deceleration time has been shown to correlate with high pulmonary capillary pressure, impaired functional class, and bad prognosis in postinfarction patients.

26.d. High filling pressure and reduced LV compliance. These conditions are indicated by a restrictive mitral inflow pattern with short E-wave deceleration time.

27.c. Abnormal HR recovery predicts mortality in all patients; however, there is no treatment. A delayed decrease in HR after exercise or an abnormal HR recovery predicts all-cause mortality in healthy adults and in patients referred for exercise testing—independent of ischemia. However, at this time, there is no treatment to improve abnormal HR recovery.

28.c. CABG. This patient has left main trunk equivalent with low EF. He is a candidate for CABG with left internal mammary artery to the LAD. CABG will prolong his long-term survival compared with PTCA/stent.

29.d. She should undergo exercise testing for better assessment. Recurrent peripartum cardiomyopathy occurs in 20% of patients with normal resting LV function but abnormal stress ventricular response. Recurrent peripartum cardiomyopathy with decompensation occurred in 41% of patients with abnormal resting LV function.

30.d. Although this has been seen in retrospective trials, it has not been validated in a randomized trial; therefore, continue the current regimen. In a substudy done by the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico, aspirin did not decrease the mortality benefit of lisinopril after MI or increase the risk of adverse clinical events. There have been some retrospective studies to assess this question that have had conflicting results; therefore, it is best to stay with the current regimen.

31.b. Refer the patient for biventricular pacing based on QRS duration. Patients with QRS duration greater than 150 to 160 milliseconds derived the greatest benefit from biventricular pacing.

32.a. 20%. There is no role for routine EP study in the asymptomatic hypertrophic cardiomyopathy patient.

33.c. Dofetilide was used in patients with an EF less than 35%. The study compared dofetilide with amiodarone. Dofetilide did not increase mortality. It has not been studied against β-blockers or calcium channel blockers in patients with normal EF.

34.b. Losartan showed neither mortality benefit nor reduced hospitalization. In the large Evaluation of Losartan in the Elderly II study, losartan did not show mortality benefit or reduced hospitalization. Losartan was better tolerated than captopril. Because the patient has no side effects with enalapril, her prescription should not be changed.

35.c. Spironolactone in addition to standard therapy decreases mortality and rehospitalization. In the Randomized Aldactone Evaluation Study, patients with NYHA class III or IV with an EF less than 35% had improvement in mortality, reduction in hospitalization, and improvement in functional class when spironolactone was taken in addition to standard therapy (ACE inhibitor and diuretic).

36.e. Cardioversion. This patient has post-MI AFib. He has LV dysfunction and renal insufficiency. Procainamide should be used in patients with normal LV and renal clearance. Amiodarone would take too long to work, and he is already in distress. Lidocaine is not used in AFib. Metoprolol tartrate would exacerbate his heart failure; therefore, cardioversion is the only choice.

37.An LV pressure–volume loop.

a.= 1. Mitral valve opening

b.= 2. End diastole

c.= 3. Aortic valve opening

d.= 4. End systole

38.c. Up. The response of the LV to increased afterload is to shift the loop up. Increased preload would shift the loop to the right.

39.a. Normal. The initial peak of the carotid puse waveform reflects the ejection of the blood from the LV into the aorta before it goes into the periphery. After the pressure peaks, it begins a decline as ejection slows and blood continues to flow to the periphery. There is a reversal of blood flow from the compliant central arteries back toward the ventricle. With this reversal of flow, the aortic valves close. A notch on the descending limb of the aortic pressure curve is associated with this transient reversal of blood flow. The smaller secondary positive wave is attributed to the elastic recoil of the aorta and aortic valve.

40.b. Aortic stenosis. Pulsus parvus et tardus which is characteristic of aortic stenosis. Small and delayed carotid pulse.

41.c. Aortic regurgitation. Pulsus bisferiens or bifid arterial pulse.

42.d. Hypertrophic cardiomyopathy. This can also be characterized by a bisferiens carotid pulse with rapid fall in first wave with rapid rise of the second.

43.e. Severe CHF decompensation. Demonstrates the dicrotic pulse which can occur in diastole in patients with low stroke volume being ejected. This can occur in severe heart failure, cardiac tamponade, and hypovolemic shock.

44.a. Constrictive pericarditis. The high initial venous wave (a wave) is characteristic of atrial contraction. The rapid y descent is suggestive of rapid ventricular filling.

45.c. Tricuspid regurgitation. The v wave is a reflection of ventricular contraction and the pressure that is transmitted back to the atrium from a tricuspid valve that pushes back into the atrium. In the tricuspid regurgitation, there is increased pressure during ventricular systole.

46.e. Tamponade. There is constant pressure from the pericardium that does not allow for atrial relaxation so the y descent is blunted.

SUGGESTED READINGS

Greenberg B, Kahn AM. Chapter 26: Clinical assessment of heart failure. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine, 9th ed. Elsevier Saunders.

Chatterjee, K. Chapter 16: Physcial examniation. In: Topol EJ, Califf RM, eds. Textbook of Cardiovascular Medicine, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.

Costanzo MR, Dipchand A, Starlin R, et al. The International Society of Heart and Lung Transplantation guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2010;29(8):914–956.

Francis G. Pathophysiology of the heart failure clinical syndrome. In: Topol EJ, ed. Textbook of Cardiovascular Medicine, 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2002.

Iyengar S, Haas GJ, Young JB. Chapter 86: Acute heart failure management. In: Topol EJ, Califf RM, eds. Textbook of Cardiovascular Medicine, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.

Mann D. Chapter 28: Management of heart failure with reduced ejection fraction. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine, 9th ed. Elsevier Saunders.

Tang WHW, Young JB. Chapter 87: Chronic heart failure management. In: Topol EJ, Califf RM, eds. Textbook of Cardiovascular Medicine, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.