The Return of Coronary Vasomotion After Bioresorbable Scaffold Implantation.

T he coronary artery endothelial lining maintains vascular tone and regulates blood flow. Mechanical forces such as increased shear stress trigger activation of endothelial cells, prompting generation of nitric oxide (NO) and prostacyclin, which promote vasodilation and increased flow. NO causes relaxation of vascular smooth muscle cells as well as inhibition of smooth muscle cell proliferation, inflammation, and thrombosis. As a counterbalance, the endothelium also produces vasoconstrictors such as endothelin-1. When the endothelium does not function normally, pathological vasoconstriction can occur due to direct smoothmuscle stimulation. An absence of functioning endothelium may lead to myocardial ischemia, thrombosis, repeated revascularization, inflammation, and atherosclerosis progression. Epicardial and microvascular coronary endothelial dysfunction independently predict worse functional capacity and acute cardiovascular events, even in the absence of obstructive coronary artery disease (1). Acetylcholine (ACh) causes release of NO and subsequent vasodilation in the presence of healthy endothelium. However, in the absence of endothelium or with dysfunctional endothelium, ACh acts directly on the smooth muscle cells causing vasoconstriction.