Is Your Patient Taking Calcium Channel Blockers?
This Post is adapted from the Canadian Pharmacists Association (CPhA) Drug Monograph: Calcium Channel Blockers
- Migraine prophylaxis: Verapamil
- Muscle cramps: Diltiazem
- This monograph focuses on the calcium channel blockers (CCBs) affecting the cardiovascular system.
- CCBs (also referred to as slow channel blockers, calcium entry blockers or calcium antagonists) are a chemically and pharmacologically heterogeneous group of drugs, but physiologically they all share the ability to selectively antagonize the calcium ion movements that are responsible for the excitation-contraction coupling in the cardiovascular system.
- There are two main classes of CCBs:
- Dihydropyridines (amlodipine, felodipine, nifedipine and nimodipine)
- Nondihydropyridines which include diltiazem (a benzothiazepine) and verapamil (a phenylalkylamine). Flunarizine is an antihistamine with calcium channel blocking activity.
- CCBs exert their effect at the voltage-gated (or slow) calcium channels of the plasma membrane. CCBs block transmembrane influx of calcium through the slow channel into the cardiac muscle and vascular smooth muscle, without significantly affecting the transmembrane influx of sodium through the fast channel. This results in a reduction of free calcium ions in the muscle tissue and no change in serum calcium concentrations. The effects on the cardiovascular system include depression of mechanical contraction of myocardial and smooth muscle and depression of both impulse formation (automaticity) and conduction velocity.
- The different pharmacologic profiles for these agents are in part based on their ability to bind to different receptor sites at the calcium channel.
- Dihydropyridines are strong vasodilators, acting via relaxation of vascular smooth muscle cells. They have little direct effect on myocardial contractility or SA/AV nodal conduction. However, they cause tachycardia and increased cardiac output via reflex sympathetic activity. These drugs also cause peripheral edema, presumably through precapillary vasodilation.
- The nondihydropyridines (diltiazem and verapamil) have an increased effect on AV nodal conduction compared to that of the dihydropyridines; while they also cause vasodilation via relaxation of vascular smooth muscle, their vasodilatory effects are only one-tenth the magnitude of nifedipine’s. All CCBs interfere somewhat with blood coagulation by inhibiting platelet aggregation.
- Risk of additional hypotensive effect in patients with angina or arrhythmias using antihypertensive drugs.
- Gingival Hyperplasia: Amlodipine, diltiazem, felodipine, nifedipine and verapamil have been implicated in drug-induced gingival hyperplasia.
- The reported prevalence of clinically significant hyperplasia varies widely but is generally felt to be from 3 to 10%.
- Males are 3 times as likely as females to develop clinically significant gingival hyperplasia (a link to androgen metabolism has been suggested). Good dental hygiene is crucial in minimizing this adverse effect.
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