## Mechanism Analysis of Antianginal Drugs ### Nitrates (Option 1 — CORRECT) **Key Point:** Nitrates are prodrugs that require enzymatic bioconversion to release nitric oxide (NO), which activates guanylate cyclase and increases cGMP, leading to smooth muscle relaxation and vasodilation. ### Beta-Blockers (Option 2 — CORRECT) **Key Point:** Beta-blockers reduce myocardial oxygen demand (MVO₂) by decreasing: - Heart rate (negative chronotropic effect) - Contractility (negative inotropic effect) - Blood pressure (negative dromotropic effect) This reduction in MVO₂ is the primary antianginal mechanism. ### Calcium Channel Blockers (Option 3 — CORRECT) **Key Point:** CCBs produce dual benefit: - Direct coronary vasodilation (increase coronary blood flow) - Reduction in peripheral vascular resistance and afterload - Negative inotropic effect (especially non-dihydropyridines) ### Ivabradine (Option 4 — INCORRECT) **High-Yield:** Ivabradine is a selective inhibitor of the If (funny) current in the sinoatrial node. It **reduces** heart rate without affecting contractility or blood pressure — the opposite of what Option 4 claims. **Clinical Pearl:** Ivabradine is used in stable angina when beta-blockers are contraindicated or not tolerated. Its benefit comes from ↓ heart rate → ↓ MVO₂, NOT from increasing heart rate. **Warning:** Confusing ivabradine's mechanism is a common trap. It is a **heart rate-lowering** agent, not a rate-increasing agent. ## Summary Table | Drug Class | Primary Mechanism | Effect on HR | Effect on Contractility | Effect on BP | | --- | --- | --- | --- | --- | | Nitrates | ↑ cGMP via NO | ↑ (reflex) | ↑ (reflex) | ↓↓ | | Beta-blockers | ↓ MVO₂ demand | ↓ | ↓ | ↓ | | CCBs (non-DHP) | Vasodilation + ↓ demand | ↓ | ↓ | ↓ | | Ivabradine | Selective If inhibition | ↓↓ | — | — | [cite:KD Tripathi 8e Ch 31]
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