[Coronary vasomotion in myocardial ischemia]

Coronary vasomotion can be characterized with respect to its localization in the coronary vascular tree as segmental (epicardial, collateral, resistive), with respect to its localization in the myocardium as transmural (subendocardial vs subepicardial), or with respect to its mediators (myogenic, metabolic, endothelial, neuronal, humoral). Coronary vessels exhibit a marked coronary dilator reserve which can be recruited to maintain regional myocardial blood flow and contractile function distal to coronary stenoses. Even in the presence of myocardial ischemia, coronary vessels retain a significant dilator reserve which can only be recruited pharmacologically. A critical reduction in blood flow at the level of epicardial coronary arteries is the underlying cause for a range of pathophysiological processes that extends from changes in the hemodynamic severity of a fixed stenosis to dynamic coronary stenosis, and finally to true spasm. These pathophysiological processes differ in the quantitative contribution of active coronary vasoconstriction and fixed mechanical obstruction to the initiation of myocardial ischemia; the mediators of epicardial coronary constriction are largely unclear. Significant alpha 2-adrenergic coronary constriction of the resistive vessels, predominantly in the subendocardium, contributes to the initiation of poststenotic myocardial ischemia during sympathetic activation and exercise in experimental studies. Intracoronary alpha-blockade with phentolamine also attenuates exercise-induced myocardial ischemia in patients with stable angina. Experimental analyses of regional myocardial blood flow and contractile function in ischemic myocardium reveal that a discrepancy between O2-supply (flow) and O2-demand (function) does not exist on a hemodynamic level. Regional myocardial blood flow and function are instead adequately reduced in ischemic myocardium. Thus, absolute regional myocardial blood flow--as a result of coronary vasomotion and blood flow redistribution--is the significant determination of myocardial ischemia.