Coronary artery spasm

Abstract

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 A(2) antagonists all failed to reduce significantly the number of anginal attacks, although they appeared to be effective in some patients. 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.

Mechanisms of I/R-Induced Endothelium-Dependent Vasodilator Dysfunction

“…A third possibility is release of inflammatory mediators the produce hyperreactive vasoconstrictor responses that limit NO-dependent dilation in arterial vessels, as has been observed in atherosclerotic plaques (Sato, Shirai, Hontani, Shinooka, Hasegawa, Kichise, et al, 2017). Similar responses have been suggested to play a role in vascular smooth muscle hyperreactivity associated with variant angina (Lanza & Maseri, 2000). This explanation may not pertain to our observations because atherosclerosis is not present.…”

Smooth muscle cell–extrinsic vascular spasm arises from cardiomyocyte degeneration in sarcoglycan-deficient cardiomyopathy

“…In Prinzmetal variant angina or primary coronary artery vascular spasm there is damage to cardiac tissue in the presence of minimal to no atherosclerotic disease. In Prinzmetal vasospasm, VSM is unusually hyperreactive, leading to spasm and tissue infarction (24,25). Using a model of focal degeneration that leads to cardiomyopathy, we now demonstrate that vascular spasm arises from a cardiomyocyte-intrinsic process.…”

Hyperventilation-induced ST segment elevation mimicking acute myocardial infarction in a comatose patient with tracheostomy

“…Respiratory alkalosis by hyperventilation is an effective stimulus for coronary artery spasm, and has been proposed as a part of the diagnostic workup for Prinzmetal's angina [1][2][3][4].…”

“…Hyperventilation and/or cold-pressor test have been proposed as valuable methods for reproducing the spasm, even during stress-echocardiography [1][2][3][4].…”