Pathophysiology
Clinical meaning
Heart Failure Advanced centers on progressive myocardial dysfunction. In systolic HF (HFrEF, EF <=40%), cardiomyocyte loss from ischemia, toxins, or genetic causes reduces contractile force. Compensatory neurohormonal activation (RAAS, sympathetic nervous system, natriuretic peptides) initially maintains cardiac output but chronically causes adverse remodeling: ventricular dilation, interstitial fibrosis, and further myocyte apoptosis. Elevated angiotensin II promotes vasoconstriction, aldosterone-mediated sodium/water retention, and myocardial fibrosis. Sustained sympathetic activation causes beta-receptor downregulation and direct myocyte toxicity. B-type natriuretic peptide (BNP) is released from stretched ventricular myocytes.