Coronary artery spasm
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Attacks of variant angina usually respond promptly to sublingual administration of short-acting nitrates (nitroglycerin, 0.3 to 0.4 mg, or isosorbide dinitrate, 5 to 10 mg), which may be repeated after 3 to 5 minutes if pain persists. In the rare cases resistant to sublingual nitrates, sublingual nifedipine (5 to 10 mg) or, when readily available, intravenous nitrates (nitroglycerin or isosorbide dinitrate, 2 to 10 mg) or calcium antagonists (verapamil, 5 to 10 mg, or diltiazem, 0.15 mg/kg) can be given.
All attempts to prevent ischemic attacks by means of specific receptor blockade in patients with vasospastic angina have been unsatisfactory. This may be either because the doses of the blockers used were insufficient or, more likely, because the blockade of a single receptor-agonist interaction leaves receptors for other vasoconstrictor stimuli unopposed and therefore capable of eliciting spasm. Thus, for instance, alpha-adrenergic, serotoninergic, and thromboxane A2 antagonists all failed to reduce significantly the number of anginal attacks, although they appeared to be effective in some patients [1–3].
Until the actual causes of the coronary smooth muscle hyperreactivity to constrictor stimuli are known, treatment of vasospastic angina is based on the use of nonspecific vasodilators. Indeed, the mainstay of pharmacologic treatment of coronary artery spasm is calcium channel blocking agents together with nitrates to cover the periods in which spasm is most likely to occur.
These powerful vasodilating agents, at their usual doses, are able immediately and completely to control the recurrences of ischemic attacks in as many as 80% of patients. Moreover, some studies have shown that use of calcium antagonists significantly improves clinical outcome in patients with variant angina [4,5].
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References and Recommended Reading
- 11.Beltrame JF, Shigetake S, Maseri A, et al.: Racial heterogeneity in coronary artery vasomotor reactivity: difference between Japanese and Caucasian patients. J Am Coll Cardiol 1999, 33:1442–1452. An article that advances the intriguing hypothesis that there are racial differences (between Caucasian and Japanese patients) in coronary vasoreactivity and characteristics of coronary artery spasm responsible for clinical variant angina.PubMedCrossRefGoogle Scholar
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