What is the primary therapy for RAAS inhibition in heart failure?

• A. ARBs
• B. ARNIs
• C. ACE inhibitors
• D. MRAs

Answer: (C)

Blocking the RAAS is a cornerstone of heart failure therapy because activation of this system drives vasoconstriction, sodium and water retention, and adverse cardiac remodeling that worsen symptoms and survival. An ACE inhibitor stops the conversion of angiotensin I to angiotensin II, lowering angiotensin II levels. That leads to dilation of arteries and veins, reduced afterload and preload, less aldosterone release, decreased sodium and water retention, and less remodeling of the heart. These effects translate into fewer hospitalizations, improved symptoms, and a mortality benefit in patients with reduced ejection fraction heart failure. Because of this proven benefit, starting an ACE inhibitor is the standard primary approach to suppress the RAAS in heart failure, provided there are no contraindications such as significant kidney dysfunction, hyperkalemia, or risk of angioedema. If an ACE inhibitor isn’t tolerated, an ARB offers similar RAAS blockade without the bradykinin-related cough, and a newer combination of neprilysin inhibition with an ARB (ARNI) has shown even better outcomes in eligible patients and is often preferred when possible. Mineralocorticoid receptor antagonists provide additional mortality benefit by blocking aldosterone’s effects and are added after initial RAAS blockade in many patients.