Models of vasospasm: relationship of organic stenoses to sites of vasospasm.
This paper reviewed some possible mechanisms regarding coronary artery spasm. Since normal vasoconstriction cannot reduce luminal area sufficiently to decrease blood flow, amplification of the vasoconstriction response appears necessary. Hypercholesterol, platelets, and denudation probably hypersensitize the vessel, but may not cause hypershortening. Coronary atherosclerosis amplifies the effects of vasoconstriction and appears to be the primary factor in the pathogenesis of coronary artery spasm. Again, this paper has reviewed some potential mechanisms of coronary artery spasm. Additional studies are required to verify the exact cause of coronary artery spasm. For a more extensive review of coronary artery spasm, I recommend the articles by Maseri and Chierchia (1982), Freedman et al (1982), Yasue et al (1983), and Chierchia (1982).
D000818:Animals; D003324:Coronary Artery Disease / Q000150:complications*; D003329:Coronary Vasospasm / Q000209:etiology*; D004285:Dogs; D008955:Models, Cardiovascular; D013552:Swine