Electrocardiographic Differentiation of the ST-Segment Depression of Acute Myocardial Injury Due to the Left Circumflex Artery Occlusion from that of Myocardial Ischemia of Nonocclusive Etiologies

P with symptoms of acute myocardial ischemia and ST-segment elevation can be presumed to have complete occlusion of a coronary artery, which is most often thrombotic in origin.1,2 In contrast to patients with ST-segment elevation in whom thrombolytic therapy has been shown to be beneficial,3–5 no such benefits have been demonstrated in patients with ST-segment depression. Among patients with acute myocardial ischemic syndromes presenting with STsegment depression, some have complete thrombotic occlusion. Many patients with complete acute thrombotic occlusion of the left circumflex (LC) artery have only ST-segment depression on their standard 12-lead electrocardiograms.6,7 These patients, if accurately distinguished from the remainder of the population with ST-segment depression, might be as likely to benefit from thrombolytic therapy as those with STsegment elevation. Complete acute occlusion of a major coronary artery typically produces a ST-segment deviation pattern specific for the location of the occlusion.8 Conversely, nonocclusive ischemia produces a diffuse ST-segment depression pattern that is not specific for the myocardial location of the ischemia.9,10 To differentiate the ischemia of acute LC occlusion from nonocclusive ischemia we retrospectively studied the pattern of isolated ST-segment depression in 2 populations: (1) those undergoing percutaneous transluminal coronary angioplasty (PTCA) of the LC coronary artery, and (2) those undergoing exercise tolerance testing (ETT). • • • The following 2 patient populations were retrospectively identified: (1) acute LC occlusion model consisting of 104 consecutive patients undergoing elective PTCA at our institution, who had continuous 12-lead electrocardiographic monitoring by ST100 monitor (Mortara Inc, Milwaukee, Wisconsin) during this procedure, and (2) nonocclusive ischemia model consisting of 200 patients who had ETT at our institution. Patients undergoing elective LC PTCA were subgrouped into 3 groups based on the pattern of STsegment deviation relative to the baseline, at the time of balloon inflation: (1) those who had ST-segment elevation of $100 mV in $1 lead (except aVR); (2) those who did not have $100 mV of ST-segment elevation or depression in any lead, and (3) those who had $100 mV of ST-segment depression in $1 lead but no ST-segment elevation of $100 mV in any lead (‘‘isolated’’ ST-segment depression). Only those in subgroup 3 are included in this study. The ST-segment depression patterns in the nonocclusive ischemia model were analyzed based on the electrocardiographic recording with the greatest STsegment depression relative to the baseline. To minimize the inclusion of patients with ST-segment changes due to nonischemic causes (false–positives), those who did not have $200 mV ST-segment deviation in any lead were excluded. The data for following baseline demographic and coronary risk factors were obtained: age, gender, history of systemic hypertension or diabetes mellitus, multivessel coronary artery disease, and left ventricular ejection fraction measured by cardiac catheterization. Thirty-six of 104 (35%) patients with LC occlusion during PTCA had ST-segment elevation of $100 mV in $1 lead, and 31 (30%) had no ST-segment deviation in any lead. There were 37 study patients (35%) with isolated ST-segment depression. Of the 200 patients with nonocclusive ischemia 74 (37%) met the criteria of having $200 mV ST-segment depression during ETT. None