The Who, What, Why, When, How and Where of Vasospastic Angina

Abstract

Ischemic heart disease involves both "structural" and/or "functional" disorders of the coronary circulation. Structural atherosclerotic coronary artery disease (CAD) is well recognized, with established diagnostic and treatment strategies. In contrast, "functional CAD" has received limited attention and is seldom actively pursued in the investigation of ischemic heart disease. Vasospastic angina encompasses "functional CAD" attributable to coronary artery spasm and this "state of the art" consensus statement reviews contemporary aspects of this disorder. Patients with vasospastic angina typically present with angina at rest that promptly responds to short-acting nitrates and is associated with transient ischemic ECG changes. Although spontaneous episodes may be documented, provocative spasm testing may be required to confirm the diagnosis. It is important to diagnose vasospastic angina because it may be associated with major adverse events that can be prevented with the use of appropriate vasodilator therapy (eg, calcium-channel blockers) and the avoidance of aggravating stimuli (eg, smoking). Future studies are required to clarify the underlying pathophysiology, natural history and effective treatments for patients refractory to conventional therapy. (Circ J 2016; 80: 289 -298)

Acute Coronary Syndromes

“…Epicardial coronary vasospasm may occur in patients in whom coronary angiography does not demonstrate an obstructive atherosclerotic plaque 75 . In the CASPAR study, coronary angiography failed to show “culprit lesions” in about 30% of patients with suspected ACS 76.…”

Impact of Morning Onset on the Incidence of Recurrent Acute Coronary Syndrome and Progression of Coronary Atherosclerosis in Acute Myocardial Infarction

“…26 Among 61 patients with recurrent ACS in the present study, unstable angina caused by coronary spasm was noted in 1 patient with morning onset acute MI and in 1 patient with acute MI onset between 00:00 and 05:59 hours. Although we did not perform provocative testing for coronary spasm, patients with morning onset acute MI may have increased spasticity in the coronary arteries because coronary spasm is more likely to occur in the morning, 27 and coronary vasoconstrictor response to acetylcholine also increases in the morning. 28,29…”

Fluctuations in the amplitude of ST-segment elevation in vasospastic angina

“…[17] Long-acting calcium antagonists are the first-line therapy because they are very effective in reducing symptomatic VSA episodes. [18] Most importantly, a calcium antagonist is an independent determinant in preventing future major cardiovascular events for VSA patients. [19] Other pharmacological therapies which have been shown to relieve VSA and therefore might be considered include nicorandil, fasudil, and statins.…”

“…[12] Percutaneous coronary intervention is generally not useful in patients with VSA who have no obstructive coronary artery disease. [18] However, it may be considered in those with concomitant obstructive coronary artery disease. Nevertheless, these patients should have maintenance calcium antagonists and/or nitrate therapy after percutaneous intervention to prevent spasms in other sites in the coronary arteries.…”