In stable IHD, antianginal drugs may be used to reduce the rate of occurrence and severity of angina attacks.
Nitrates cause vasodilation of the venous capacitance vessels by simulating the endothelium-derived relaxing 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.
Agents include nitroglycerin (glyceryl trinitrate) or pentaerythritol tetranitrate.
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.
Agents include either cardioselectives such as acebutolol or metoprolol, or non-cardioselectives such as oxprenolol or sotalol.
Calcium channel blockers
Calcium ion (Ca++) antagonists (Calcium channel blockers) 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.
Class III agent has negligible inotropic effect and causes almost no reflex tachycardia.
Examples include Class I agents ( verapamil), Class II agents ( amlodipine, nifedipine), or the Class III agent diltiazem.
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