To the Editor:—
The excellent review detailing approaches to the prevention of perioperative myocardial ischemia 1includes a number of assertions and implications that conflict with published studies. First, the authors define coronary perfusion pressure as the difference between aortic diastolic pressure (DBP) and left ventricular end-diastolic pressure. I have been unable to find any peer-reviewed documentation stating that DBP is the upstream pressure for coronary perfusion pressure. This seems illogical because flow into the coronary arteries, coronary blood flow, is at or near its nadir at DBP. 2,3Presumably, this statement crept into textbooks because of the high coronary blood flow during ventricular diastole. However, the observed nadir in coronary blood flow at DBP is expected because DBP corresponds to the onset of ejection, which occurs during ventricular systole when coronary blood flow is impeded because left ventricular intracavitary and intramyocardial pressures are at least as high as aortic root pressure. Moreover, to use the left ventricular end-diastolic pressure as the downstream pressure for coronary perfusion pressure, one must assume that there is a vascular waterfall across the left ventricle. Although this seems logical, and early data seemed to confirm this, later studies that incorporated the effects of vascular compliance did not confirm an arterial waterfall. 4It is an area of some controversy, but most data do not support this concept. Consequently, the authors’ definition of coronary perfusion pressure does not seem to be supported by data.
Second, it is interesting that no prospective study has shown that intraoperative management of ischemia affects the myocardial infarction rate in the immediate postoperative period. This may be the result of difficulties in designing and implementing such studies, or it may be that such interventions do not affect this outcome, which is plausible for the following reasons. There is abundant evidence that the majority of events that constitute the acute coronary syndromes are related to plaque rupture or ulceration. 5Plaques that are vulnerable to such disruption tend not to be at the sites of high-grade stenoses, but high-grade stenoses cause stable angina and are at the sites of rate-related ischemia, which is not part of the acute coronary syndromes. Consequently, the regions at risk for a postoperative myocardial infarction might differ from those that generate rate-related ischemia. Therefore, rate-related ischemia might be totally unrelated to the risk of postoperative myocardial infarction, i.e. , this type of ischemia may be the equivalent of stable angina induced with exercise, which occurs frequently in patients with high-grade stenoses but rarely causes infarction. In contrast, unstable angina, which is part of the acute coronary syndromes, reflects transient occlusion or embolization from an unstable plaque and may be unrelated to rate-related ischemia. This is not to say that such ischemic episodes should not be treated, especially because stress or exercise seems capable of disrupting vulnerable plaques. However, if the ST-T depression seen in the acute perioperative period is the equivalent of stable angina, failure of treatment to alter perioperative myocardial infarction rates and difficulties in predicting the risk of an adverse outcome would be expected. Perhaps we should focus more on preventing plaque rupture or alterations in the coagulation system that might predispose to thrombosis at the sites of unstable plaques.
