The renin-angiotensin-aldosterone system (RAAS) plays a central maladaptive role in heart failure progression. Decreased cardiac output activates the RAAS: renin from juxtaglomerular cells converts angiotensinogen to angiotensin I, which is converted by angiotensin-converting enzyme (ACE) to angiotensin II. Angiotensin II causes potent vasoconstriction (increasing afterload), stimulates aldosterone release (promoting sodium/water retention and myocardial fibrosis), activates the sympathetic nervous system, and promotes pathological cardiac remodeling (myocyte hypertrophy and interstitial fibrosis). ACE inhibitors (enalapril, lisinopril, ramipril) block the conversion of angiotensin I to angiotensin II. They also prevent the breakdown of bradykinin (a vasodilator), which contributes to their vasodilatory effect but also causes the characteristic dry cough (10-20% of patients) and rare but life-threatening angioedema. ACEi reduce preload, afterload, aldosterone secretion, and cardiac remodeling, producing mortality reduction of 20-30% in HFrEF. ARBs (losartan, valsartan, candesartan) block the angiotensin II type 1 (AT1) receptor directly, providing RAAS inhibition without bradykinin accumulation — they are used when ACEi-intolerant due to cough but NOT for angioedema (cross-reactivity possible). Sacubitril/valsartan (ARNI — angiotensin receptor-neprilysin inhibitor) combines the ARB valsartan with sacubitril, which inhibits neprilysin (neutral endopeptidase),...