What is the underlying mechanism of coronary vasospasm?

Coronary vasospasm is primarily characterized by hyperreactivity of the coronary arteries to vasoconstrictor stimuli. This condition can lead to significant constriction of the coronary vessels, reducing blood flow to the heart muscle. The smooth muscle cells within the coronary arteries react excessively to certain triggers — such as stress, cold exposure, smoking, or the use of certain drugs — leading to transient narrowing of the arteries.

The underlying mechanism involves an imbalance in the regulatory factors that control vascular tone. Normally, there are vasodilators, such as nitric oxide, that help keep these blood vessels open, and vasoconstrictors, like endothelin-1, which promote narrowing. In cases of vasospasm, there is an enhanced sensitivity or exaggerated response to these vasoconstrictor stimuli, resulting in significant narrowing of the arteries and, consequently, reduced blood flow and potential ischemic symptoms.

In contrast, scenarios such as increased blood flow to coronary arteries, thrombosis, or aneurysm formation do not directly explain the mechanism of vasospasm. Increased blood flow is more related to the supply-demand balance in coronary perfusion rather than spasm. Thrombosis typically leads to blockage rather than intermittent spasm, and aneurysm formation