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.
Diagnosis & workup
Diagnostics & workup: - BNP >100 pg/mL or NT-proBNP >300 pg/mL supports diagnosis (age-adjusted cutoffs) - Transthoracic echocardiography for EF, chamber dimensions, wall motion, valvular function - 12-lead ECG for Q waves, LBBB, arrhythmia, LVH (present in ~90% of HF) - Chest X-ray: cardiomegaly (CTR >0.5), cephalization, Kerley B lines, pleural effusions - BMP including sodium (dilutional hyponatremia = poor prognosis), potassium, creatinine - Iron studies (iron deficiency present in ~50% of HF patients) - Coronary angiography or stress testing to evaluate ischemic etiology