Introduction
In 1959, Prinzmetal et al described a variant form of angina which appeared to be a separate disease entity to classical angina pectoris. The pathogenesis of classical stable angina pectoris has been accepted as the failure to meet the increased metabolic demand of the heart due to fixed atherosclerotic stenoses in the coronary arteries. The variant form was described to have spontaneous onset at rest and appeared unrelated to increased cardiac metabolic demand. Unlike classical angina, the variant form was associated with ST elevation corresponding to the distribution area of a major coronary artery in 12leads ECG recordings. Finally, they observed that the variant angina attacks were most likely to occur between midnight and early morning. This circadian variation is absent in classical angina and cannot be explained by atherosclerosis. It was hypothesized that the underlying pathology for this variant angina was spasm of a coronary artery.
In early 1970s,......
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