User:CRH16/Coronary vasospasm

Pathophysiology
The exact pathophysiology behind coronary vasospasm has not been elucidated. Instead, a combination of different factors have been proposed to contribute to coronary vasospasm. Some of these factors include endothelial dysfunction, chronic inflammation, oxidative stress, and smooth muscle hypercontractility. 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 acts upon the hyperreactive segment of the artery, then vasospasm can result.

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. Subsequently symptoms due to ischemia can follow.

Signs and Symptoms
Coronary vasospasm can occur without chest pain or any other symptoms, leading to episodes of silent or asymptomatic myocardial ischemia. When chest pain does occur, it is often accompanied by additional symptoms of sweating and nausea and vomiting. Episodes of syncope are possible as well.

EKG findings
When coronary vasospasm causes an artery to undergo complete occlusion, the EKG might show evidence of ST segment elevation in the leads indicative of that artery's territory. Transient ST segment depression can also occur, usually in the setting of sub-total occlusion of an artery.

EKG findings in coronary vasospasm also include evidence of arrhythmias which might be induced by ischemia: ventricular premature contractions, ventricular tachycardia, ventricular fibrillation, and more.