Calciumchannel blockers

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Calcium-channel blockers (less correctly called 'calcium-antagonists') interfere with the inward displacement of calcium ions through the slow channels of active cell membranes. They influence the myocardial cells, the cells within the specialised conducting system of the heart, and the cells of vascular smooth muscle. Thus, myocardial contractility may be reduced, the formation and propagation of electrical impulses within the heart may be depressed, and coronary or systemic vascular tone may be diminished. Calcium-channel blockers differ in their predilection for the various possible sites of action and, therefore, their therapeutic effects are disparate, with much greater variation than those of beta-blockers. There are important differences between verapamil, diltiazem, and the dihydropyridine calcium-channel blockers (amlodipine, felodipine, isradipine, lacidipine, lercanidipine, nicar-dipine, nifedipine, and nimodipine). Verapamil and dilti-azem should usually be avoided in heart failure because they may further depress cardiac function and cause clinically significant deterioration.

Verapamil is used for the treatment of angina (section 2.10.1), hypertension (section 2.5), and arrhythmias (section 2.3.2). It is a highly negatively inotropic calcium channel-blocker and it reduces cardiac output, slows the heart rate, and may impair atrioventricular conduction. It may precipitate heart failure, exacerbate conduction disorders, and cause hypotension at high doses and should not be used with beta-blockers (see p. 133). Constipation is the most common side-effect.

Nifedipine relaxes vascular smooth muscle and dilates coronary and peripheral arteries. It has more influence on vessels and less on the myocardium than does verapamil, and unlike verapamil has no anti-arrhythmic activity. It rarely precipitates heart failure because any negative inotropic effect is offset by a reduction in left ventricular work. Short-acting formulations of nifedipine are not recommended for angina or long-term management of hypertension; their use may be associated with large variations in blood pressure and reflex tachycardia. Nicardipine has similar effects to those of nife-dipine and may produce less reduction of myocardial contractility. Amlodipine and felodipine also resemble nifedipine and nicardipine in their effects and do not reduce myocardial contractility and they do not produce clinical deterioration in heart failure. They have a longer duration of action and can be given once daily. Nife-dipine, nicardipine, amlodipine, and felodipine are used for the treatment of angina (section 2.10.1) or hypertension. All are valuable in forms of angina associated with coronary vasospasm. Side-effects associated with vasodilatation such as flushing and headache (which become less obtrusive after a few days), and ankle swelling (which may respond only partially to diuretics) are common.

Isradipine, lacidipine, and lercanidipine have similar effects to those of nifedipine and nicardipine; they are indicated for hypertension only. Nimodipine is related to nifedipine but the smooth muscle relaxant effect preferentially acts on cerebral arteries. Its use is confined to prevention and treatment of vascular spasm following aneurysmal subarachnoid haemorrhage.

Diltiazem is effective in most forms of angina (section 2.10.1); the longer-acting formulation is also used for hypertension. It may be used in patients for whom beta-blockers are contra-indicated or ineffective. It has a less negative inotropic effect than verapamil and significant myocardial depression occurs rarely. Nevertheless because of the risk of bradycardia it should be used with caution in association with beta-blockers.

Unstable angina Calcium-channel blockers do not reduce the risk of myocardial infarction in unstable angina. The use of diltiazem or verapamil should be reserved for patients resistant to treatment with beta-blockers.

Withdrawal There is some evidence that sudden withdrawal of calcium-channel blockers may be associated with an exacerbation of angina.

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