Calcium channel blockers are a heterogeneous group of compounds used in a variety of cardiovascular disorders such as stable angina pectoris, vasospastic angina, hypertension, hypertrophic cardiomyopathy, and supraventricular arrhythmias.
This topic review will present the major issues regarding the use of calcium channel blockers in the patient with stable angina and the evidence that these drugs are effective. Their role, compared with other drugs, in the overall management of angina is discussed separately. (See "Stable ischemic heart disease: Overview of care".)
MECHANISM OF ACTION
Calcium influx into the myocyte initiates a series of events essential for contractility. Calcium entry into the myocyte first triggers intracellular calcium release; the released calcium then binds the regulatory protein troponin, resulting in a calcium-troponin complex which allows actin and myosin to interact and contract. The sequence of events is the same in vascular smooth muscle cells, except that a calcium-calmodulin complex instead of calcium-troponin permits the interaction between actin and myosin. The net effect is vasodilatation; the ensuing fall in blood pressure decreases cardiac work and may contribute to the efficacy of these drugs in the patient with angina.
Calcium channel blockers work by blocking the initial calcium influx into myocytes and vascular smooth muscle cells, preventing the cascade of events detailed above. The available calcium channel blocking agents block receptors on the L-type calcium channel which gives rise to a slowly inactivating high threshold current in cardiac cells.
CARDIOVASCULAR AND ADVERSE SIDE EFFECTS
The currently available calcium channel blockers may be categorized into four groups based upon different chemical structures: