Heart Failure

1. Heart Failure Bill Wolf Edited from Vicki Shanmugam, Bob Rabbani and Navreet Sandhu

2. Definintion: “Defined as a pathophysiological state in which an abnormality of cardiac function is the cause of the heart to pump blood at a rate that is not able to keep up with the needs of the body.”

3. Heart Failure • 5 million Americans with heart failure today • 6-10% of people older than 65 yo have it • 500,000 are diagnosed with HF each year • Reason of at least 20% of all hospitalizations (6.5 million hospital days each year) • Over past decade, rate of hospitalization has increased by 159% (550,000 to nearly 900,000 per year) • Symptomatic heart failure has a worse prognosis than most cancers, with a one-year mortality of almost 45% • Thus, we have a strong incentive to identify, predict, and treat the factors contributing to hospitalizations

4. Heart Failure • Heart failure is a clinical syndrome arising from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. Because not all patients have volume overload, “heart failure” is generally preferred to “congestive heart failure”

5. Two types of heart failure • Systolic • EF<40%, dilated LV, Congestion and cardiomegaly on CXR, S3 • Assoc with previous MI, HTN, DM, sleep apnea • Diastolic • EF>40%, LV hypertrophy, Congestion without cardiomegaly on CXR, S4. • Assoc with HTN, DM, Obesity, COPD, dialysis

6. Diastolic Heart Failure • Associated conditions include: • Restrictive (infiltrative) cardiomyopathy: • Amyloidosis • Sarcoidosis • hemochromatosis • Obstructive and nonobstructive hypertrophic cardiomyopathy • Pericardial constriction • LVH from HTN

7. Characteristics of Patients with Diastolic Heart Failure and Patients with Systolic Heart Failure Jessup, M. et al. N Engl J Med 2003;348:2007-2018

8. Diastolic Failure • Diagnosis often made by clinician who recognizes the typical signs and symptoms • Relatively little evidence to guide care of patients with this condition • Patients are treated with risk factor modification, controlling blood pressure, heart rate, ischemia, and volume

9. Systolic Heart Failure • Coronary artery disease is the cause in 2/3 of patients • Other causes include: • HTN • Thyroid disease • Valvular disease • Alcohol • Myocarditis • No identifiable cause (i.e. idiopathic dilated cardiomyopathy)

10. CAUSES

11. Heart Failure as Progressive Disorder • Ventricular dysfunction begins with injury or stress to the myocardium, and progresses • The heart chamber generally dilates, hypertrophies, and becomes spherical (remodeling) • This increases the hemodynamic stress on the walls of the heart

12. Remodeling • Left ventricular remodeling involves mechanical, neurohormonal, and genetic factors that alter the ventricular size and function • Patients with HF have elevated levels of norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines • Remodeling occurs in several conditions, including myocardial infarction, cardiomyopathy, hypertension, valvular heart disease • One sees hypertrophy, myocyte death, and increased interstitial fibrosis

13. Ventricular Remodeling after Infarction (Panel A) and in Diastolic and Systolic Heart Failure (Panel B) Jessup, M. et al. N Engl J Med 2003;348:2007-2018

14. Consequences of Remodeling • Mitral Regurgitation • Arrhythmias and Bundle Branch Block

15. Mitral Regurgitation • As the left ventricle dilates and the heart becomes globular, the papillary muscles and mitral leaflets change orientation, leading to distortion of the papillary apparatus • Mitral regurgitation results in volume overload on an overburdened ventricle, further causing progression of disease

16. Arrhythmia • Another consequence of ischemia, inflammation, fibrosis, and aging is arrhythmia • SVT, especially a. fib., often marks the onset of systolic or diastolic heart failure • In patients with HTN or abnormal myocardial function, elevation in ventricular end-diastolic volume leads to atrial stretch, which in turn causes electrical instability

17. Arrhythmia • Abnormal myocardial conduction can also lead to left bundle branch block, which is a predictor of sudden death • LBBB causes abnormal ventricular activation and contraction, ventricular dyssynchrony, delayed opening and closure of the aortic and mitral valves, and abnormal diastolic function • LBBB can result in reduced ejection fraction, cardiac output, and arterial pressure, and paradoxical septal motion, increased LV volume, and mitral regurgitation

18. Arrhythmia • Rate of sudden cardiac death in patients with heart failure is 6-9 times that in the general population

19. History • Typically will present with symptoms of: • Dyspnea on exertion • Orthopnea • PND • Ankle swelling • Weight gain • Sometimes abdominal distension • Tiredness and weakness

20. Special Questions to ask • Chest pain or exertional angina – strongly suggests IHD as cause • Recent flu like illness – consider viral myocarditis • History of longstanding alcohol or HTN – consider alcoholic or hypertensive cardiomyopathy • History of proteinuria or chronic inflammatory condition, consider amyloid • Recent blood transfusion or Sx consider volume overload • FHx, along with diabetic “bronzed” pt – consider hereditary hemochromatosis. • Things that worsen underlying heart failure: • NSAIDS • Antiarrhythmics – disopyramide and flecanide • Ca channel blockers – esp. Verapamil • B Blockers

21. Physical exam – look specifically for evidence of how bad their HF is and clues to the underlying cause • Sympathetic overdrive (to compensate for low CO) – evidenced by sinus tachycardia, diaphoresis, and peripheral vasoconstriction • Pulsus alternans – alternating strong and weak peripheral pulses, exact pathophysiology not known. • Manifestations of volume overload • JVP • Pleural effusions, alveolar edema – crackles • Peripheral edema • Ascites, hepatomegaly, splenomegaly • Ventricular enlargement – displaced PMI • S3 or S4 • Pulmonary hypertension – complaints of chest pain, palpable pulmonic tap, pulmonary insufficiency.

22. Labs • CBC – R/o anemia as ppt. • Chem 7 – assess BUN/Creat/K • LFT – may rise with hepatic congestion • Fasting glucose – screen for DM • TFT – r/o thyrotoxicosis or hypothyroidism • Fe/TIBC – if hemochromatosis is a risk • BNP -- >100 is 90% sensitive for HF, equally as predictive as finding cardiomegaly on CXR, or rales on clinical exam. Cost only $20

23. CXR • Cardiomegaly • Prominent upper lobe vessels • Kerley B lines • Pleural effusions • Bats wing pulmonary edema

26. EKG and Echo • EKG • Look for arrhythmias e.g. A fib, V Tach • Conduction abnormalities – esp. seen in pts with dilated cardiomyopathy • Echo • EF – helps distinguish systolic and diastolic HF • Regional wall motion abnormalities suggesting ischemia • Valvular disease • Pulmonary artery pressures.

27. Framingham Criteria • 2 major • 1major and 2 minor

28. NYHA (functional classes)

29. ACC/AHA Stages of heart failure • “Staging” introduced to get people to realize that there is an element of preventability in HF and that pts need screening while asymptomatic in order to prevent progression (just like cancer screening)

30. Stages of Heart Failure • Examples of patients in each stage: • Stage A: patients with HTN, CAD, DM, history of cardiotoxic drug therapy or alcohol abuse, h/o rheumatic fever, FHx of cardiomyopathy • Stage B: LVH or fibrosis, LV dilatation or hypocontractility, asymptomatic valvular heart disease, previous MI • Stage C: dyspnea or fatigue due to LV systolic dysfunction, asymptomatic pts undergoing tx for prior sx of HF • Stage D: pts frequently hospitalized for HF and can not be safely d/c ed from hospital, pts in hospital awaiting transplant, pts at home receiving IV inotropes or LVAD, pts in hospice

31. How do you manage this patient? • ASA • B-Blocker • ACE • Spirnolactone • Lasix • Nitrates • Hydralazine

32. Heart Failure • Large trials have looked at the effects of ACE inhibitors, angiotensin receptor antagonists, beta-blockers, spironolactone, biventricular pacing, CABG, and the use of multidisciplinary teams. All have been shown to reduce rates of hospitalization and improve functional status.

33. Treatments

34. Stage A Heart Failure • Treat risk factors! • Treatment of hypertension decreases incidence of left ventricular hypertrophy and cardiovascular mortality and reduces incidence of heart failure by 30-50% • Use of ACE inhibitors in asymptomatic high-risk patients with DM or vascular disease reduces rate of death, MI, and stroke • Use of ARBs (losartan) has delayed the first hospitalization for heart failure in patients with DM and nephropathy • Goal of treatment is to prevent remodeling!

35. Stages B, C, and D Heart Failure • Goals of those with low ejection fraction are to slow progression of disease and alleviate symptoms • Lifestyle modification remains a mainstay, for example: • Moderate sodium restriction • Weight monitoring • Medication regimen compliance • Moderation of alcohol • Exercise program for selected patients

36. Stages B, C, and D Heart Failure • ACE inhibitors limit the physiologic consequences of angiotensin II levels, and decrease degradation of bradykinin (which promotes vasodilation and natriuresis in the kidney) • ACE inhibitors after an MI improve survival, rates of hospitalization, symptoms, cardiac output and promote reverse remodeling • Optimal target dose of ACE inhibitors is not clear, with trials showing low and high doses as having similar effects on mortality • Not certain whether any difference among the many different ACE inhibitors out there today

37. Stages B, C, and D Heart Failure • Beta-blockers counteract the effects of the sympathetic nervous system during heart failure • Beta-blockers improve survival, morbidity, ejection fraction, remodeling, quality of life, rates of hospitalization, and incidence of sudden death • Should be used in select patients who are not decompensated • In those with asthma, DM with frequent hypoglycemia, and bradycardia +/- heart blocks should use caution

38. Stages B, C, and D Heart Failure • With beta-blockers one sees improvement in systolic function even after 3 mos, with reversal of remodeling after 4 mos • Carvedilol (nonspecific beta-blocker with alpha effects) and metoprolol (beta-1 selective with no alpha effects) are approved for the treatment of heart failure, but the most prescribed med is atenolol

39. Stages B, C, and D Heart Failure • ARBs should be used for those who can not tolerate ACE inhibitors, with trials showing that ARBs have similar efficacy in heart failure to ACE inhibitors

40. Stage C and D Heart Failure • Spironolactone, which blocks deleterious effects of increased aldosterone (salt retention, hypertrophy, etc), has been shown to be helpful in patients with NYHA class III or IV symptoms

41. Stage C and D Heart Failure • Diuretics are used to control congestion • Thiazide or loop diuretics often prescribed, and combination therapy may be helpful in advanced cases • Digoxin has no improvement in mortality, but reduces rates of hospitalization and worsening heart failure

42. Stage C and D Heart Failure • Biventricular pacemakers (where one lead is in the right ventricle and the other is passed through the right atrium, through the coronary sinus, and into a cardiac vein on the lateral wall of the left ventricle) improves ventricular synchrony • The pacemaker can be used to treat patients with heart failure and a wide QRS • Effects include reverse remodeling (leading to decreased heart size, improved EF, and decreased mitral regurgitation) • Exercise tolerance improves, as does quality of life, and rate of hospitalization • Has not been shown to enhance survival

43. Stage C and D Heart Failure • Revascularization (either PCI or CABG): • Improves symptoms • Improves cardiac performance • Reduces risk of sudden death • Mechanical devices (e.g. LVADs) are continuing to evolve for patients awaiting heart transplantation or as destination therapy

44. AHA/ACC Recommendations • The following classification system has been used by the AHA/ACC: • Class I: conditions for which there is evidence and/or general agreement that a given procedure/therapy is useful and effective • Class II: conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of performing the procedure/therapy • Class III: conditions for which there is evidence and/or general agreement that a procedure/therapy is not useful/effective and in some cases may be harmful

45. Specifically… ACE Inhibitors • Class I AHA/ACC recommendations: • Stage A patients with a history of atherosclerotic vascular disease, DM, or HTN and associated CV risk factors • Stage B patients with recent or remote history of MI regardless of EF • Stage B patients with reduced EF, whether or not they have experienced an MI • In all Stage C and D patients unless contraindicated

46. ACE inhibitors

47. Specifically… Beta-Blockers • Class I AHA/ACC recommendations: • Stage B patients with recent MI regardless of EF • Stage B patients with reduced EF, whether or not they have experienced an MI • Stable Stage C and D patients. They should have no or minimal evidence of fluid retention and have not recently required positive inotropic agent

48. Beta-Blockers

49. Relative contraindications for B-blocker use • HR<60 • Systolic<100 • Signs of peripheral hypoperfusion • PR interval>0.24 • Second or third degree heart block • Severe COPD • Asthma history • PVD

50. Specifically… Spironolactone • Low doses of spironolactone given with an ACE inhibitor in patients with class IV symptoms reduced the risk of death and hospitalization • Class IIa recommendations: • Spironolactone in Stage C patients with recent or current Class IV symptoms, preserved renal function and a normal potassium concentration