In year 1959 Prinzmetal et al reported 32 patients of angina which occurred at rest unlike William Heberden classical angina which was associated with exertion
Clinical characteristics of Prinzmetal angina are.
Exertion did not precipitate angina and stress tests was typically negative in these patients
ST elevation was noted during pain as opposite to classical angina where ST depression is present.
Angina occurred during same time of the day.
These angina episodes sometimes associated with arrhythmias and sometimes progressed to MI.
The basic pathology of Variant angina is spasm of epicardial coronary arteries.
These patients classical have chest pain which occurs at rest at a same time of day more commonly early morning hours, transient ST changes, relived promptly by nitrates
As these patients are prone for arrhythmias they may also present with syncope and cardiac arrest.
Among conventional risk factors for atherosclerosis only cigarette smoking is associated with Prinzmetal angina.
Waxing and waning, circadian nature of chest pain should make clinician to consider about this disease. Episode of Prinzmetal angina may come in clusters.
Ambulatory ECG monitoring :As ECG changes are transient to pick ECG changes, ambulatory ECG monitoring is done during hot phases i.e. when cluster of chest recur.
Exercise stress is negative
Coronary angiography: Normal coronaries are not mandatory for Prinzmetal angina diagnosis. Spasm of insignificant epicardial disease with ST elevation also produce Prinzmetal angina.
Provocative coronary artery test
o Intracoronary acetylcholine is administered in incremental doses temporary pacing is needed frequently to overcome acetylcholine induced bradycardia. For RCA incremental doses of 25-50micrograms and LCA incremental boluses of 25-100micrograms are given
o Some use 60micrograms of intracoronary Ergonovine slowly either into RCA or LCA
o Others give intracoronary Ergonovine every 5 minutes in incremental fashion i.e. 30-300micrigrams
o Test is considered positive if inducible coronary spasm is presence, assessed on the basis of chest pain, ECG changes and/or severe coronary constriction.
STEMI: Prompt response to nitrates suggest variant angina
Mixed pattern angina: In this both exercise and rest angina are present due obstructive coronary artery disease and also spasm of coronary artery disease respectively
Tako-tsubo cardiomyopathy: this also can present with transient ST changes at rest. Differencatation will be by apical ballooning of Tako-tsubo cardiomyopathy. Some people speculate Tako-tsubo cardiomyopathy is also due to spasm of epicardial vessels
Coronary microvascular disorders: Normal epicardial vessel with rest angina, suggest variant angina or microvascular disease, this can be differentiated demonstration epicardial spasm of epicardial vessels in variant angina.
o With Rest angina transient ST elevation and improvement or resolution symptoms with sublingual nitrates.
o Rest angina.
o Reversible ST changes (elevation or depression), and/or
o Spontaneous/provoked coronary spasm on angiography. (90% sensitivity and 99% specificity in the provoked spasm on angiography)
1. Stop smoking
2. Short acting nitrates
3. Calcium channel blockers
4. Potassium channel openers, nicorandil
5. Rho kinase inhibitor, fasudil
1. Significant morbidity and mortality 5year infract free survival is 60-95%
2. Calcium channel blockers and associated coronary obstructive and multi vessel disease also effect infarct free interval.
3. Caucasian have poorer outcomes than their Japanese counterparts, which in part may be due to the increased prevalence of coronary artery disease.