## Mechanism of Antianginal Action **Key Point:** Antianginal drugs work via two main mechanisms: decreasing myocardial oxygen demand (beta-blockers, calcium channel blockers, nitrates via preload reduction) or increasing oxygen supply (nitrates via coronary vasodilation). ### Isosorbide Dinitrate — Supply-Side Agent Isosorbide dinitrate is a long-acting organic nitrate that: 1. **Causes direct coronary vasodilation** — increases blood flow to ischemic myocardium 2. Dilates epicardial coronary arteries preferentially 3. Improves collateral circulation to ischemic zones 4. Also reduces preload (secondary oxygen-demand reduction) **High-Yield:** While nitrates have a dual mechanism, their *primary* and *unique* benefit is **direct coronary vasodilation** — the mechanism no other antianginal class possesses. ### Why Other Options Decrease Demand, Not Supply | Drug Class | Primary Mechanism | Effect on Supply | |---|---|---| | **Beta-blockers** | ↓ Heart rate, contractility, BP | No direct vasodilation | | **Calcium channel blockers** (e.g., amlodipine) | ↓ Contractility, HR, afterload | Peripheral vasodilation only; coronary effect minimal | | **Ivabradine** | ↓ Heart rate (I~f~ inhibition) | No effect on coronary flow | **Clinical Pearl:** In vasospastic (Prinzmetal's) angina, nitrates are the *gold standard* because they directly relieve coronary spasm — a supply-side problem. **Warning:** Do not confuse "nitrates dilate coronaries" with "all vasodilators increase supply." Amlodipine dilates peripheral vessels but does not preferentially increase coronary blood flow to ischemic zones.
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