The exact pathophysiology behind<unk>  has not been elucidated. Instead, a combination of different factors has been proposed to contribute to<unk> . In general, it is thought that an abnormality within a coronary artery causes it to become hyperreactive to vasoconstrictor stimuli. This abnormality can be located in one segment of the coronary artery, or it may be diffuse and present throughout the entire artery. If and when vasoconstrictor stimuli act upon the hyperreactive segment of the artery, then<unk>  can result. Ultimately, when large coronary arteries undergo<unk> , this can lead to either complete or transient occlusion of blood flow within the artery. As a result, ischemia to the tissues served by the artery can occur. Symptoms due to ischemia can follow. Some of the factors that have been proposed to contribute to<unk>  include the following: * Endothelial dysfunction * Certain vasodilatory agents exert their effects by working via the endothelium, the cells that make up the lining of blood vessels. Specifically, these agents work by enhancing the production of nitric oxide from endothelial nitric oxide synthase. Normally, nitric oxide then works to promote vasodilation in a blood vessel through its own mechanisms such as inhibiting the release of agents that cause vasoconstriction. * Endothelial dysfunction wherein there is a deficiency in the production of nitric oxide has been found to be associated with<unk>  in some but not all cases. Vasodilatory agents with mechanisms dependent on a functional endothelial nitric oxide synthase can cause vasoconstriction instead in the setting of endothelial dysfunction, leading to<unk> . * Chronic inflammation * Various markers of low-grade chronic inflammation have been found in cases of<unk> . * In addition to this, one of the risk factors for<unk>  is smoking. Chronic inflammation due to smoking has been shown to be damaging to endothelial cell function. * Oxidative Stress * Oxygen free radicals contribute to the pathogenesis of<unk>  through their damaging effects on vascular endothelial cells and degrading nitric oxide, an important vasodilatory agent. * Smooth Muscle Hypercontractility * At a cellular level, pathways that lead to enhanced myosin light chain phosphorylation promote vasoconstriction. Increased activity of Rho-kinase leading to enhanced myosin light chain phosphorylation has been implicated in the pathogenesis of<unk> .
Coronary vasospasm
Coronary ischemia
Coronary occlusion
Myocardial stunning
Cerebral vasospasm
Hyperdynamic circulation
Coronary steal
Coronary thrombosis