Why angina pectoris in aortic stenosis.

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The mechanism of angina pectoris in aortic stenosis is unclear. In their report in this issue of Circulation , Julius et al1 describe several hemodynamic factors in patients with angina pectoris that differ from those in persons without angina in the presence of aortic stenosis. Those patients with aortic stenosis and angina pectoris had lower left ventricular (LV) mass, increased LV peak systolic pressure, increased systolic-diastolic wall stress, smaller left coronary artery diameter, and lower coronary flow reserve compared with persons without angina. The authors conclude that myocardial ischemia and angina pectoris in aortic stenosis are due to inadequate LV hypertrophy, with high systolic and diastolic wall stresses causing reduced coronary flow reserve. Although these factors do differ between the groups of patients with and without angina pectoris in aortic stenosis, there is such great overlap between the groups that these hemodynamic measurements do not correlate specifically with angina pectoris in individuals. Furthermore, it is difficult to explain ischemia on the basis of limited coronary flow reserve when, in fact, there is remaining coronary flow reserve, as indicated by average flow reserves of 1.5 and 1.9 in those with and without angina, ie, 50% to 90% increases in blood flow after dipyridamole administration. Given the wide range of variability and overlap between the groups, it is difficult to ascribe myocardial ischemia to differences in coronary flow reserve when flow reserve was so markedly reduced in both groups. Coronary flow reserve is so comparably reduced in both groups with so much overlap that explaining angina pectoris on the basis of reduced flow reserve is unconvincing. Although the authors have contributed valuable information to this question, their conclusions remain moot. There is a missing link that the authors do not address which is a more specific mechanism for myocardial ischemia and …