Antianginal

Drugs used are nitrates such as glyceryl trinitrate or pentaerythritol tetranitrate; Beta blockers, either cardioselectives such as acebutlol or metoprolol, or non-cardioselectives such as oxprenolol or sotalol; or Ca plus plus antagonists, either Class I agents (eg. verapamil), Class II agents (eg. amlodipine, nifedipine) or the Class III agent (diltiazem).

Nitrates cause vasodilation of the venous capacitance vessels by simulating the endothelium derived relaxant factor (EDRF). Used to relieve both exertional and vasospastic angina by allowing venous pooling, reducing the pressure in the ventricles and so reducing wall tension and oxygen requirements in the heart. Short-acting nitrates are used to abort angina attacks that have occurred. While longer-acting nitrates are used in the prophylactic management of the condition.

Beta blockers are used in the prophylaxis of exertional angina by reducing the work the heart is allowed to perform below the level that would provoke an angina attack. They cannot be used in vasospastic angina and can precipitate heart failure.

Ca⁺⁺ antagonists are used in the treatment of both exertional and vasospastic angina. In vitro, they dilate the coronary and peripheral arteries and have negative inotropic and chronotropic effects - decreasing afterload, improving myocardial efficiency, reducing heart-rate and improving coronary blood flow. In vivo, the vasodilation and hypotension trigger the baroreceptor reflex[?]. Therefore the net effect is the interplay of direct and reflex actions. Class I agents have the most potent negative inotropic effect and may cause heart failure; Class II agents do not depress conduction or contractility; the Class III agent has negligible inotropic effect and causes almost no reflex tachycardia.