Chronic Heart Failure Basics General Chronic Heart Failure can be classified multiple ways, most commonly by Ejection Fraction Heart Failure with Preserved Ejection Fraction (HFpEF) HFpEF is the most common cause of Chronic Heart Failure 50% of patients hospitalized with CHF Exertional dyspnea, orthopnea, lower extremity edema, but normal or near normal LVEF with objective evidence of diastolic dysfunction (abnormal LV filling pressures) by echo LV diastolic dysfunction due to impaired relaxation w/EF >50% Impaired Diastolic Filling, Decreased compliance Decrease in SV and Increase in EDP Significantly Increased LVEDP associated with Decrease in LVEDV Increased afterload, increased LV thickness, decreased LV size, decreased Compliance – Decrease in Ventricular distensibility that impairs ventricular filling during diastole (EF ≥50) Decreased LV Compliance, Decreased Lusitropy Normal CO w/ increased LVEDV/RVEDP, tachycardia, S4 Increased venous hydrostatic pressure Recurrent pulmonary flash edema 2/2 hypertensive cardiac remodeling (LVH) with left atrial dilation, orthopnea, and elevated BNP Mcly due to myocardial hypertrophy RF: Chronic hypertension (concentric LVH), Obesity & sedentary lifestyle (myocardial interstitial fibrosis), CAD & related RF (T2DM) Commonly due to Pericardial Tamponade, Constrictive Pericarditis, Restrictive or Hypertrophic Cardiomyopathies 1) Hypertension w/Left Ventricular Hypertrophy (90%) Chronic Hypertension (Concentric LV Hypertrophy) Primary (HCM), Secondary (Hypertension), Age, Fibrosis LVH shows Severe dip in V1 and rise in V6 2) Restrictive Cardiomyopathy (<9%) Amyloid/Sarcoid, Hemochromatosis Obesity/Sedentary lifestyle (myocardial interstitial fibrosis) Preserved systolic dysfunction, bi-atrial dilation, pulmonary hypertension in a pt with refractory HF Kussmaul’s sign Lack of typical inspiratory decline in CVP Associated with an S3 Treatment Eval for Transplant w/Advanced HF specialist Heart Failure with Reduced Ejection Fraction (HFrEF) 1) Ischemic Heart Disease/Cardiomyopathy (Impaired Contractility) IHD/CAD = 60-75% of HF cases in developing world Decreased cardiac output due to impaired contractility A compensatory rise in NE, Renin, and ADH Increases SVR Coronary Artery Disease (CAD) Chronic Volume Overload (MR, AR, Shunting) Chronic Lung Disease (Cor pulmonale, Pulmonary vascular disorders) 2) Dilated Cardiomyopathies (Impaired Contractility) 30%, Defect in force generation, transmission, myocyte signaling Genetic (20-50%) (Cytoskeleton mutation) Non-Genetic (Myocarditis, Peri-partum, Toxic (alcohol), Idiopathic) Infiltrative Disorders 3) Valvular Heart Disease 15% Toxic/drug-induced damage (Metabolic disorder, Viral) Chagas disease Rate and Rhythm disorders (Chronic Arrythmias) 4) Hypertension 80% die from Cardiovascular Causes (MC Cause of death) Worsening HF (Cardiogenic Shock, Low Output State) 40% Sudden Cardiac Death (VTach (most common), Bradyarrhythmia) Hypertension contributes to 75% of patients, also DM Valvular heart disease also contributes (EtOH, Hypertension, Drugs) Systolic Heart Failure (Contractile Failure) Compliance (C) = EDV/EDP EDV not easily measured, thus use EF = SV/EDV measured via TTE Characterized by decreased CO/CI, increased SVR, and increased LVEDV Decreased CO (insufficient ventricular contractility, EF will be low) Decrease in SV and Increase in EDP Decreased CO, increases A-a O2 and decreases renal perfusion Increased EDP associated with Increase in EDV Decreased Compliance (EF ≤40%), Increased HR Heart Failure with Improved Ejection Fraction (HFimpEF) Diagnosis A Simple, Evidence-Based Approach to Help Guide Diagnosis of Heart Failure With Preserved Ejection Fraction H2pEF risk score Assesses likelihood of HFpEF and is used to discriminate cardiac vs. non-cardiac causes of dyspnea Obesity (2 points), Afib (3 points), age >60 (1 point), 2 Antihypertensives (1 point), Echo E/e’ ratio >9 (1 point) and Echo PAS pressure >35 (1 point) Echo Normal LV cavity size, increased LV wall thickness, LAE, abnormal diastolic function, elevated PAS pressure >35 BNP may be normal in obese or only exertional symptoms Prognosis HFpEF Cause of Death (broader than HFrEF): Cardiovascular Worsening HF (RHF, Restrictive cardiomyopathy) Sudden Death (Non-arrhythmic, Tachycardia, Bradycardia) Myocardial Infarction Vascular (Aortic Aneurysm, PE) Cerebrovascular (Intracranial hemorrhage, Stroke) Non-Cardiovascular Renal (ESRD, renal venous congestion) Resp (Failure, pulmonary hypertension, COPD) Infection/sepsis Multisystem (Organ failure) Mortality Due to progressive HF and arrhythmias 5-year rate of 36% 10-year rate of 63% HFrEF 30-40% die within 1 year of diagnosis and 60-70% die within 5 years On GDMT of ARNI/BB/MRA/SGLT2i Estimated 7.9, actual 4.9 years gained for a 50 y/o with HFrEF Estimated 5.0, actual 3.3 years gained for a 70 y/o with HFrEF Poor Prognostic Factors for HFrEF Higher NYHA functional Class Exam Resting Tachycardia Presence of an S3 gallop Elevated JVP Hypotension: BP <100/60 Labs: Hyponatremia Elevated pro-BNP levels, high NE and catecholamines, elevated troponins Renal insufficiency Low maximal oxygen consumption (peak VO2) ECG: QRS >120ms, LBBB pattern Echocardiography Moderate to severe mitral regurgitation Severe LV dysfunction Concomitant diastolic dysfunction Reduced RV function Pulmonary Hypertension Other: Anemia Atrial Fibrillation Diabetes Mellitus HFpEF Management Diuresis Caution in diastolic HF w/diuretics Afterload reduction as needed Reduce hospitalization ACEI/ARB = no mortality benefit BP control Treat exacerbating conditions (CAD, OSA, Afib) Exercise training/cardiac rehabilitation Improves functional capacity and overall quality of life Treatment to improve long-term survival in HFrEF Chronic Stable HF Optimization Initial Optimized Therapy ARNI/ARB/ACEI NHYA I-IV with LVEF ≤40% Either Entresto OR ACEI/ARBs Beta-Blockers (3 specific ones) Step 2 of Optimized Therapy Step 3 of Optimized Therapy Supplementary Agents Diuretics Isosorbide Dinitrate + Hydralazine (Bidil) Additional therapy if asymptomatic or RAS Blocker Intolerance Also, in worsening systolic CHF, reduce mortality in AA Improves symptoms and may improve mortality Digoxin Persistent symptoms despite other therapy Reduces hospitalizations, no mortality benefit (0.5-0.8) Avoid CCBs Add Amlodipine/felodipine if high BP (no mortality improvement) No anticoagulation unless AFib or prior VTE 40% complicated by Afib Aggressive rhythm control Catheter ablation of AF (improves morbidity and mortality) Persistent Severe HF symptoms on maximal GDMT Heart Transplant Evaluation 1 year survival is near 90%, 12 year median survival Generally 65-70 w/o T2DM w/End organ damage, Cancer in the past 5 years, GFR >30, No other survival decreasing illnesses, good social support and adherence LVAD (Left Ventricular Assist Device) EF <25% and NYHA IV symptoms on maximal therapy with either 1-2 year predicted mortality or inotrope dependency who still want aggressive restorative care Other Management Heart Failure GDMT