Heart failure (HF) is classified by ejection fraction (EF) into heart failure with reduced ejection fraction (HFrEF, EF ≤40%, systolic failure) and heart failure with preserved ejection fraction (HFpEF, EF ≥50%, diastolic failure). In HFrEF, myocyte loss (post-MI necrosis, viral myocarditis, alcohol toxicity) reduces contractile mass. The remaining myocytes undergo eccentric hypertrophy (sarcomeres added in series), causing ventricular dilation. Reduced stroke volume activates the renin-angiotensin-aldosterone system (RAAS), increasing sodium/water retention, and the sympathetic nervous system (SNS), increasing heart rate and contractility—initially compensatory but eventually maladaptive. Chronic neurohormonal activation causes progressive fibrosis, further dilation, and worsening function. In HFpEF, the ventricle maintains contractile force but develops concentric hypertrophy (sarcomeres added in parallel) from chronic pressure overload (hypertension, aortic stenosis). The thickened, stiff ventricle has impaired relaxation and reduced compliance, requiring elevated filling pressures. Diastolic dysfunction causes pulmonary congestion despite normal EF. Natriuretic peptides (BNP, ANP) are released by myocardial stretch, promoting vasodilation and natriuresis as a counter-regulatory mechanism.