Statin therapy: new therapy for cardiac microvascular dysfunction

See doi:10.1016/S1095-668X(03)00478-0for the article to which this editorial refers Cardiac syndrome-X is a clinical entity characterized by angina-like chest discomfort that is often prolonged in duration, normal coronary arteries as assessed by arteriography, non-inducible coronary vasospasm with ergonovine provocation and ST segment depression on treadmill exercise testing. The pathogenesis of cardiac syndrome-X has been ascribed to myocardial ischaemia that may be caused by microvascular dysfunction and increased sensitivity to intracardiac pain. Support for impaired myocardial perfusion in the aetiology of chest pain was provided in a case-control study of 20 patients with established syndrome-X and 10 matched controls that underwent cardiac magnetic resonance imaging at rest and after adenosine infusion.1In syndrome-X patients, adenosine infusion reduced the subendocardial to subepicardial myocardial perfusion index and provoked chest pain in 19 of 20 patients.The mechanisms that may contribute to microvascular dysfunction in syndrome-X include endothelial dysfunction, and abnormal vasoconstrictive responses of the microvasculature to nitric oxide and endothelin. Several lines of evidence support impaired nitric oxide production or endothelial release by coronary vessels of syndrome-X patients. Intracoronary infusions of acetylcholine induce a diminished vasodilator response in syndrome-X patients compared to controls or may induce myocardial ischemia in the absence of vasospasm in epicardial coronary arteries. The acetylcholine-induced ischaemia may result from a vasoconstrictor effect of acetylcholine on vascular smooth muscle cells. In contrast, intracoronary infusions of L-arginine, the precursor of nitric oxide, enhance coronary vasodilation in response to acetylcholine. Further, levels of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide, are increased in syndrome-X patients.2Therapeutic approaches for …