[1] In 1959, Prinzmetal et al. described a type of chest pain resulting from coronary vasospasm, referring to it as a variant form of classical angina pectoris.
[5] There are cases of coronary vasospasm that occur without any symptoms at all, leading to episodes of silent or asymptomatic myocardial ischemia.
Shorter episodes of occlusion can lead to what is referred to as silent myocardial ischemia due to its asymptomatic nature.
[1] Longer episodes of occlusion can lead to stable or unstable angina, myocardial infarction, and sudden cardiac death.
[1] Unlike classical angina pectoris, traditional cardiovascular risk factors are not thought to be significantly associated with coronary vasospasm.
[9] For example, cocaine use can trigger vasospasm in coronary arteries through its actions on adrenergic receptors causing vasoconstriction.
[11] Exercise, cold weather, physical activity or exertion, mental stress, hyperventilation are additional precipitating factors.
[6] Features such as chest pain at rest, a diurnal variation in tolerance for exercise with a reduction in tolerance for exercise in the morning, and responsiveness of chest pain to calcium channel blockers as opposed to beta blockers can be important clues.
[3][20] A following study further distinguished this angina from classical angina pectoris due to the fact that the results showed that the patients with chest pain due to coronary vasospasm lacked evidence of atherosclerosis on cardiac catheterization.
[20] During the 70’s and 80’s, intense research[21] headed by Dr. Robert A. Chahine resulted in the delineation of Spasm's role in Prinzmetal's angina, allowing for easy identification and effective treatment.