Heart Failure Guidelines Patrice M. Schneider RN BSN Heart Failure Coordinator South Jersey Heart Group Lourdes Cardiology Services Background NHLBI estimates that @ any given time: 35% of pts with heart failure are NYHA I 35% of pts with heart failure are NYHA II 25% of pts with heart failure are NYHA III 5% of pts with heart failure are NYHA IV Therefore > 85% pf pts with heart failure are treated primarily in the ambulatory setting CONGESTIVE HEART FAILURE Scope of the Problem in U.S. Prevalence of CHF: Worldwide Incidence of > 3,000,000 in U.S. >15,000,000 CHF: Most > 400,000/year in U.S. common hospital discharge diagnosis in patients over 65 years old Mortality Cost All of CHF: of CHF: Approx 200,000/yr in U.S. > $ 7 Billion/yr for Hospital Care of above are likely to increase with population aging Etiology of Heart Failure What causes heart failure? The loss of a critical quantity of functioning myocardial cells after injury to the heart due to: Ischemic Heart Disease Hypertension Infections (e.g., viral myocarditis, Chagas’ disease) Toxins (e.g., alcohol or cytotoxic drugs) Valvular Disease Prolonged Arrhythmias Peripartum Idiopathic Cardiomyopathy Classification of HF: Comparison Between ACC/AHA HF Stage and NYHA Functional Class ACC/AHA HF Stage NYHA Functional Class A B C D High risk of developing HF Structural heart disease but without symptoms of HF Structural heart disease with HF symptoms, either prior or current Refractory HF requiring specialized interventions I II–III IV Asymptomatic HF Mild and Moderate HF Severe HF No symptoms Symptoms upon Symptoms mild to moderate at rest exertion Challenging Tradition NYHA class changes over time Increasing evidence that heart failure is a cellular disease Despite symptomatic improvement neurohormonal, cytokine and cellular changes continue to occur and allow heart failure to progress Ejection Fraction (EF) does not correlate with functional capacity (NYHA class) Classification of HF: Comparison Between ACC/AHA HF Stage and NYHA Functional Class ACC/AHA HF Stage NYHA Functional Class A B C D High risk of developing HF Structural heart disease but without symptoms of HF Structural heart disease with HF symptoms, either prior or current Refractory HF requiring specialized interventions I II–III IV Asymptomatic HF Mild and Moderate HF Severe HF No symptoms Symptoms upon Symptoms mild to moderate at rest exertion Stages of Heart Failure Evaluation of The Patient With Cardiomyopathy Historical Data ECG Findings Biochemical parameters Levels of various neurohormones Measurement of effect of NH activation Hemodynamic parameters Etiology Duration of symptoms Initial After tailored therapy Exercise Capacity Trends Risk of sudden deterioration Etiology of Cardiomyopathy Abnormal loading conditions Valvular disease Hypertention Shunts Chemotherapeutics Cobalt/heavy metal Acohol familial Muscular dystrophies Mitochondrial disorders Hypertrophic ARVD Ischemia Tachycardia High PVC burden Viral Thyroid disease Peripartum Idiopathic HIV Toxins Genetic Insults Unclear etiology Infiltrative Hemachromatosis Sarcoidosis amyloid Historical Data & Prognosis Duration of illness Shorter duration of illness associated with a greater likelihood of spontaneous improvement Patients with recent onset (<6-7 months require close clinical surveillance) But signs of hemodynamic instability Or end organ underperfusion Stevenson AM J Med 1987 Steimle JACC 1994 New York Heart Association Functional Classification I. No limitations of physical activity, no symptoms with ordinary activities II. Mild/slight limitation, symptoms with ordinary activities III.Moderate/marked limitation, symptoms with less than ordinary activities IV. Severe limitation, symptoms of heart failure at rest Symptoms: Dyspnea or fatigue Adapted from Criteria Committee of the New York Heart Association, 1994. Exercise Capacity NYHA (Gradman Card Clinics 1994) Annual mortality NYHA I NYHA II NYHA III NYHA IV 5% 3-25 % 10-45% 50-77% Some overlap II/III likely related to differences in classification from center to center, subjective interpretation, II, predominantly better than III Exercise Capacity 6 minute walk test (6MWT) Assess day-to-day efforts at submax exertion Measures distance an individual able to traverse over 6 minute period In moderate heart failure 6MWT has been shown to be Inversely related to QOL score Inversely related to NYHA Predictive or mortality in moderate HF In Severe HF (< 300 meters) Correlate to Peak VO2 Predictive of 6 month event-free survival But not long term (>6 month) survival Cahalin Chest 1996 Prognosis and CMP Trends Serial determination of LVEF may enhance prognostic value Mortality @ 1 year <-5 Survival based on change in EF 1.0 > 10 .50 <-5 29% >10 13 % * 24 48 Months V-HeFT I and II data 72 Prognosis and CMP Trends Decrease in EF Decrease in exercise capacity Increase in left ventricular diastolic dimension Risk of sudden Deterioration Non-revascularizable coronary lesion with a high ischemic burden Increase in number of arrhythmic events Treatment Chronic Systolic Heart Failure Vasodilator Therapy Ace-inhibitors & H/I B-Blockers Aldosterone Inhibitors ARBs CRT OHT DT Reduction in Mortality with ACE-I & B-Blocker therapy SOLVD II/III 16% 3 yr CONSENSUS IV 40 % 1 yr ACE-I MERIT HF II/III 34 % 1 yr US CARVEDILOL COPERNICUS II/III IIIB 65% ½ yr B-Blocker 35% 10 mos Which BB should we use? US CARVEDILOL Trial Coreg Target 25 mg bid Caveats > 70 kg: 50 mg bid Able to decrease vasodilator to allow uptitration to maximal dose MERIT-HF Trial Metoprolol Succinate Target: 150 mg daily Caveat Metoprolol Tartrate is inferior (however it was underdosed in the trial) CIBIS II Trial Bisoprolol Target: approximately 7.5 mg daily Asthmatics Carvedilol Dose-Response Trial (MOCHA): Effect on Ejection Fraction and Morbidity Changes in LVEF Cardiovascular hospitalizations 8 0.4 6 5 4 3 2 Mean number/subject LVEF (EF units) 7 0.3 0.2 0.1 1 0 Placebo 6.25 mg bid 12.5 mg bid Carvedilol 25 mg bid 0 Placebo 6.25 mg bid 12.5 mg bid 25 mg bid Carvedilol Patients receiving diuretics, ACE inhibitors, ± digoxin; follow-up duration 6 months; placebo (n=84), carvedilol (n=261). Adapted from Bristow et al, 1996. P<.05 vs placebo Mortality in the placebo arm of Val-HeFT by treatment group: 23-month mean follow-up Mortality 40 Sudden death 31.6 % 30 Pump Failure 6.1 22.5 20 4.5 12.3 19.4 8.9 11.9 10 13.2 6.1 0 ACEI-/BB- ACEI+/BB- Slide courtesy of J. Cohn 2.5 7.5 7.4 3.0 2.0 ACEI-/BB+ HF Therapy 11.9 ACEI+/BB+ ARBs ELITE II 3152 NYHA III-IV Val-HeFT 5010 NYHA II-IV CHARM –added 2548 II-IV Losartan 50 mg QD vs Capoten 50 mg TID No difference in mortality, well tolerated Pitt et al. Lancet 2000;355;1582-1587 Valsartan 160 mg BID vs placebo No Death difference in mortality Significant decrease in morbidity & mortality Hospitalizations for CHF* CohnCardiac et al. NEJM arrest2001;345:1667-75 Intravenous therapy Triple therapy adverse effect on mortality Candesartan 24 mg QD vs Placebo all on ACE-I Significant decrease in CVd and HF admit McMurray The LANCET 2003:362;767 Where Does Hydralazine/Isosorbide Fit in? ACE-I or ARB intolerant ACE-I or ARB are supperior But if intolerant due to Cough Hyperkalemia, renal insufficiency Angioedema BIDIL (V-HeFT Trial) AA who still have NYHA II-IV HF despite ACE/ARB and BB ON TOP of baseline therapy, not instead of 3 times a day Aldosterone Inhibitors RALES Trial 1663 NYHA III-IV 25 mg Aldactone vs Placebo Progressive HF SCD 35% reduction in hospitalization Significant improvement in NYHA functional class Pitt et al. NEJM 1999;341:709 6632 pts 3-14 d after AMI, EF < 40% And sign of HF Or DM with or without signs of HF 30% reduction in death* EPHESUS Trial 50 mgQD Eplerenone vs placebo Significant reduction in: Death 14 % v 17% CVd/hosp 27% v 30% SCD 4.9% vs 6% Pitt NEJM 2003;348:1309 Ventricular Resynchronization Sinus node Ventricular dyssynchrony 30 - 50% CHF patients with IVCD As QRS widens AV node Mortality increases Electrical delay translates to mechanical delay/dyssynchrony Improved A-V synchrony Interventricular synchrony Intraventricular synchrony Positive remodeling Reduction in heart failure and all-cause morbidity and mortality Conduction block Stimulation therapy Abraham WT and Hayes DL, Circulation 2003; 108:2596-2603 Chronic Heart Failure NYHA I ACE-inhibitor- SOLVD Prevention Trial NYHA II/III ACE-I – SOLVD, V-HeFT II Hydralazine/ISDN – V-HeFT B-Blocker – MERIT-HF, US Carvedilol, Angiotensin Receptor Blocker- Val-HeFT, CHARM NYHA IV ACE-I- CONSENSUS B-Blocker- COPERNICUS Aldosterone Blocker – RALES Resynchronization therapy (EF <35%, QRS > 130ms) ACE-I SAVE Trial B-Blocker CAPRICORN Trial Eplerenone EPHESUS Trial NYHA III/IV Post-AMI Mechanism of Death in HF SCD 64% Other 24% HF 12% Other 15% SCD 59% NYHA II HF 26% NYHA III HF = mortality secondary to worsening heart failure SCD = sudden cardiac death MERIT-HF Study Group. Lancet 1999 SCD 33% Other 11% HF 56% NYHA IV Ultimate Goal Delay progression of heart failure or death to the point where good quality and quantity of life is achieved