Ultimately, when large coronary arteries undergo vasospasm, 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 coronary vasospasm 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 coronary vasospasm 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 coronary vasospasm. Chronic inflammation
Various markers of low-grade chronic inflammation have been found in cases of coronary vasospasm. In addition to this, one of the risk factors for coronary vasospasm 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 coronary vasospasm through their damaging effects on vascular endothelial cells and degrading nitric oxide, an important vasodilatory agent.
EKG findings
When coronary vasospasm causes an artery to undergo complete occlusion, an EKG might show evidence of ST-segment elevation in the leads indicative of that arterys territory. Transient ST-segment depression can also occur, usually in the setting of sub-total occlusion of an artery.Additional EKG findings in coronary vasospasm include evidence of arrhythmias that might be induced by ischemia: ventricular premature contractions, ventricular tachycardia, ventricular fibrillation, and more. History
Chest pain due to coronary vasospasm was described in the medical literature by Prinzmetal et al. in 1959. This discovery led to this type of angina being referred to in the literature as Prinzmetal angina. 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. Angina due to coronary vasospasm is also known as variant angina. References
Further reading


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