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Heart Failure Bill Wolf Edited from Vicki Shanmugam, Bob Rabbani and Navreet Sandhu 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.” 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 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” 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 Diastolic Heart Failure Associated conditions include: – Restrictive (infiltrative) cardiomyopathy: Amyloidosis Sarcoidosis hemochromatosis – Obstructive and nonobstructive hypertrophic cardiomyopathy – Pericardial constriction – LVH from HTN 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 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 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) CAUSES 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 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 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 Consequences of Remodeling Mitral Regurgitation Arrhythmias and Bundle Branch Block 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 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 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 Arrhythmia Rate of sudden cardiac death in patients with heart failure is 6-9 times that in the general population History Typically will present with symptoms of: – Dyspnea on exertion – Orthopnea – PND – Ankle swelling – Weight gain – Sometimes abdominal distension – Tiredness and weakness 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 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. 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 CXR Cardiomegaly Prominent upper lobe vessels Kerley B lines Pleural effusions Bats wing pulmonary edema 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. Framingham Criteria 2 major 1major and 2 minor NYHA (functional classes) Class Function 1 yr mortality I Asymptomatic with ordinary activity 5% II Slight limitation of normal function 15% III Marked limitation of physical activities 30% IV Dyspneic at rest 60% ACC/AHA Stages of heart failure Stage A High risk for heart failure without structural disease, currently asymptomatic B Heart disease with asymptomatic LV dysfunction C Prior or current symptoms of Heart failure D Advanced heart disease and severely symptomatic or refractory 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) 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 How do you manage this patient? ASA B-Blocker ACE Spirnolactone Lasix Nitrates Hydralazine 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. Treatments 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! 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 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 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 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 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 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 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 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 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 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 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 ACE inhibitors Drug Target Dose Captopril 50 mg TID (SAVE trial) Enalapril 10 mg BID (Delahaye et al. 2000) Fosinopril 40 mg QD (drug info) Lisinopril Quinapril 40 mg QD (Packer et al. 1999 in ATLAS trial) 40 mg QD (drug info) Ramipril 10 mg QD (HOPE trial 2000) 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 Beta-Blockers Drug Target Dose Bisoprolol 10 mg QD (CIBIS – II trial) Carvedilol 25 mg BID (US Carvedilol HF study) 150 mg QD (50 TID or 75 BID) (Cleland 2003) 200 mg QD (MERIT-HF study) Metoprolol tartate Metoprolol succinate (XL) Atenolol 100 mg QD (Ansari et al. 2003) Relative contraindications for Bblocker use HR<60 Systolic<100 Signs of peripheral hypoperfusion PR interval>0.24 Second or third degree heart block Severe COPD Asthma history PVD 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 Specifically… ARBs They should be considered instead of ACE inhibitors due to intolerance. Class IIa recommendations: – In Stage C patients who are being treated with digitalis, diuretics, and a beta-blocker who cannot be given an ACE inhibitor because of cough or angioedema Specifically… diuretics Class I indications: – In Stage C and D patients who have evidence of fluid retention – In diastolic failure to control pulmonary congestion and peripheral edema