Angiotensin-Converting Enzyme (ACE) inhibitors block conversion of Angiotensin I → Angiotensin II and are foundational drugs in cardiovascular medicine.
Primary Effects: • ↓ Vasoconstriction • ↓ Aldosterone • ↓ Sodium retention • ↓ Remodeling • ↓ Afterload and preload
ACE inhibitors are mortality-reducing drugs in heart failure and post-MI patients.
ACE inhibitors block:
Angiotensin I → Angiotensin II
Results:
• ↓ Angiotensin II (vasoconstrictor) • ↓ Aldosterone secretion • ↓ Sodium & water retention • ↓ Sympathetic activation • ↓ Ventricular remodeling • ↑ Bradykinin (vasodilation)
Net Hemodynamic Effect: • ↓ SVR (afterload) • Mild ↓ preload • Improved cardiac output (in HF)
• Lisinopril • Enalapril • Captopril • Ramipril • Benazepril • Perindopril • Fosinopril • Quinapril • Moexipril • Trandolapril
Most commonly used: • Lisinopril • Enalapril • Ramipril
• Mortality benefit • Reduced hospitalization • Prevents remodeling
Core component of GDMT.
• Prevents ventricular remodeling • Reduces mortality
• ↓ Intraglomerular pressure • ↓ Proteinuria
Due to ↑ bradykinin accumulation Occurs in ~5–20%
↓ Aldosterone → ↓ potassium excretion
Risk increases with: • Renal insufficiency • Potassium-sparing diuretics • ARBs • MRAs
Especially first dose (volume-depleted patients)
Rare but life-threatening More common in Black patients
Contraindication to future ACE inhibitor use.
• Mild ↑ creatinine expected • Significant rise suggests bilateral renal artery stenosis
• Pregnancy • Bilateral renal artery stenosis • History of ACE inhibitor–induced angioedema
ACE inhibitors: • ↑ Bradykinin • Cause cough • More angioedema
ARBs: • Block AT1 receptor directly • Do not increase bradykinin • Lower cough risk
→ Angiotensin Receptor Blockers
✔ Mortality benefit in HFrEF and post-MI ✔ First-line in many hypertensive patients ✔ Mild creatinine rise is expected ✔ Monitor potassium ✔ Switch to ARB if persistent cough
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