Cyclooxygenase-2 inhibitors and cardiovascular thromboembolic events.

iate discriminant analysis did not select V5 or V6 as leads in which ST-segment shift distinguished patients with acute LMCA obstruction from patients with acute obstruction of the left anterior descending coronary artery (LAD). Therefore, we do not consider ST-segment depression in leads V5 and V6 to be a characteristic finding in “LMCA AMI patients.” The findings of our patients indicated that lead aVR ST-segment elevation is not a mirror image of ST-segment depression in leads V5 and V6. Engelen et al. (4) reported that lead aVR ST-segment elevation was observed in acute obstruction of the LAD proximal to the major septal branch but not in acute LAD obstruction distal to the major septal branch. They concluded that lead aVR ST-segment elevation associated with proximal LAD obstruction was caused by transmural ischemia of the basal part of the septum. Our findings were completely in agreement with the findings by Engelen et al. (4). Our previous study (5) clearly demonstrated that isolated diagonal branch occlusion caused ECG abnormalities in leads I and aVL, while less frequently causing changes in the precordial leads compared with those caused by acute LAD obstruction, indicating that leads I and aVL represent myocardium perfused by the diagonal branch. Acute LMCA obstruction causes ischemia in myocardium perfused by the diagonal branch. Our finding that ST-segment elevation in lead aVL was observed in high incidence in LMCA AMI patients was completely in agreement with our previous study (5). The ST-segment elevation in leads aVL and I in LMCA AMI patients was caused by ischemia in myocardium perfused by the diagonal branch associated with acute LMCA obstruction.