Pain due to atherosclerosis causing incomplete coronary artery occlusion. Pain onset with strenuous activity or emotional strain due to increased myocardial oxygen demand.
Pain due to atherosclerotic plaque rupture and subsequent embolization causing incomplete coronary arterial occlusion.
Variant (Prinzmetal's) Angina
Pain due to transient vasospasm causing coronary artery vasoconstriction.
Nitrates cause vasodilation of the venous capacitance vessels by stimulating 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.
They are contraindicated in variant angina and can precipitate heart failure. They are also contraindicated in severe asthmatics due to bronchoconstriction, and should be used cautiously in diabetics as they can cause hypoglycemia
Calcium channel blockers
Calcium ion (Ca++) antagonists (Calcium channel blockers) are used in the treatment of chronic stable angina, and most effectively in the treatment of variant angina (directly preventing coronary artery vasospasm). They are not used in the treatment of unstable 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.