To the Editor:—

In a recent commentary, Fleisher stated that even if ST segment trend monitoring has identified accurately a significant ST segment change, ST segment depression may not represent myocardial ischemia in younger individuals or in those with a low probability of coronary artery disease (CAD). 1In support of this contention, the argument is made that structural CAD usually is absent in these patients when tested postoperatively. 2This argument seems to equate the presence of structural CAD with myocardial ischemia, which we define for this discussion to be inadequate myocardial blood flow or oxygen delivery to meet metabolic demands. Although it may be true that ST segment depression does not indicate the presence of CAD in low-risk patients and, therefore, represents a false positive predictor of CAD, it may not be possible to extrapolate these data to state that a myocardial oxygen imbalance or myocardial ischemia does not exist.

Even if CAD is unlikely in the obstetric population, insufficient evidence exists to dismiss ST segment depression during cesarean section as physiologically unimportant because hemodynamic perturbations known to affect myocardial perfusion frequently coexist during these clinical occurrences. It is common for the combination of diastolic hypotension and tachycardia to coexist immediately after delivery when rapid infusions of oxytocin are administered. It is possible that the combination of hypotension and tachycardia may decrease myocardial perfusion, even in the absence of CAD. Similarly, preoperative smoking was associated with ST segment depression in patients with a low risk of coronary artery disease, 3and the incidence of ST segment depression increased with indices of cardiac work and intraoperative carbon monoxide concentrations. This indicates that metabolic poisoning caused by smoking may be responsible for markers of ischemia such as ST segment depression in patients with a low risk of CAD. In addition, the possible contribution of endothelial dysfunction to occurrences of ST segment depression may be nearly impossible to establish during an intraoperative event. Even in the absence of angiographically demonstrable CAD, endothelial dysfunction may produce ischemia in response to what are normally vasodilator stimuli in the normal vessel. 4,5Endothelial dysfunction is an emerging concept that may explain symptoms of ischemic heart disease in angiographically normal patients.

Although it may be difficult or impossible to prove their contribution in any individual patient in a clinical perioperative setting, these metabolic, hemodynamic, or endothelium-related etiologies may potentially contribute to intraoperative ST segment depression. Although the existing literature has shown that, in low risk populations, intraoperative ST segment depression may not indicate structural CAD, the literature does not support the contention that myocardial ischemia does not exist in these situations, nor has it been shown that ST segment depression should go untreated or ignored in patients who have a low risk of CAD and may have other etiologies for myocardial oxygen imbalance.

Fleisher L: Real-time intraoperative monitoring of myocardial ischemia in noncardiac surgery. Anesthesiology 2000; 92: 1183–8
Fleisher L, Zielski M, Schulman S: Perioperative ST-segment depression is rare and may not indicate myocardial ischemia in moderate risk patients undergoing noncardiac surgery. J Cardiothorac Vasc Anesth 1997; 11: 155–9
Woehlck H, Connolly L, Cinquegrani M, Dunning M, Hoffmann R: Acute smoking increases ST depression in humans during general anesthesia. Anesth Analg 1999; 89: 856–60
Zeiher AM, Krause T, Schachtmyer V, Minners J, Moser E: Impaired endothelium-dependent vasodilation of coronary resistance vessels is associated with exercise-induced myocardial ischemia. Circulation 1995; 91: 2345–52
Egashira K, Inou T, Hirooka Y, Yamada A, Urabe Y, Takeshita A: Evidence of impaired endothelium-dependent coronary vasodilation in patients with angina pectoris and normal coronary arteries. N Engl J Med 1993; 328: 1659–64