Abstract
The pathogenesis of coronary vasospasm has been of interest since originally proposed by Latham in 1845 (1). Prinzmetal et al. (2) described a “variant” form of angina pectoris and reintroduced the concept of coronary spasm as an important factor in some instances of rest angina. Gensini et al. (3) used coronary angiography to document for the first time appearance of spontaneous vasospasm associated with angina, in a patient with mild atherosclerotic coronary artery disease, as well as the resolution of this vasoconstriction and chest pain with administration of nitrates. Later, Guazzi et al. (4) and Maseri et al. (5) demonstrated that in “variant” angina, in contrast to typical angina, there is no increase in myocardial metabolic demand before the episodes of chest pain. Additional studies have suggested that spasm-induced decreases in myocardial perfusion are not only responsible for “variant” angina, but also lead to unstable angina, myocardial infarction and sudden death (6–7).
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References
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Lopez, J.A., Harrison, D.G., Armstrong, M.L., Heistad, D.D. (1990). Hemodynamic Consequences of Changes in the Artery Wall During Atherogenesis. In: Glagov, S., Newman, W.P., Schaffer, S.A. (eds) Pathobiology of the Human Atherosclerotic Plaque. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3326-8_31
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