Coronary Vasomotor Tone: Implications in Ischemic Heart Disease

In the early 1950’s, the increase in myocardial oxygen demand was seen as the main mechanism responsible for episodes of angina pectoris [1]. The coronary stenosis was indeed considered as a fixed obstruction on the epicardial vessel, limiting the capacity of the coronary artery to augment coronary flow. Myocardial ischemia was assumed to occur for a given and very reproducible level of myocardial oxygen demands. However, this concept was progressively refuted by the development of coronary angiography. In 1959, Prinzmetal et al. [2] described a group of patients with typical angial pain which was provoked by large vessel coronary spasms, pointed out by coronary angiography. Moreover from angiographic studies [3], even severe atherosclerotic epicardial vessels appear to retain the capacity to dilate and to constrict. Pharmacological studies of isolated human coronary arteries [4] have also shown that severe atherosclerotic segments are not rigid structure.