LETTTER TO THE EDITOR
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Shozo Kusachi, MDa
a First Department of Internal Medicine,Okayama University Medical School,2-5-1, Shikata-cho Okayama 700-8558 JapanE-mail: skusachi@ccews2.cc.okayama-u.ac.jp
Kohichiro Iwasaki, MD and
Hisosuke Yamaji, MD
Our series presented all the characteristics of acute myocardial infarction (AMI), including elevated creatine kinase (CK), hemodynamic deterioration, associated with acute left main coronary artery (LMCA) obstruction, not LMCA stenosis (1). Patients in the reports published by Sclarovsky et al. (2,3) showed manifestations of unstable angina. Therefore, we do not believe that 12-lead electrocardiogram (ECG) findings in our patients (LMCA AMI patients) can be compared with findings in their patients (LMCA unstable angina patients). For this reason, our study did not refer to the reports by Sclarovsky et al. (2,3). In our patients, ST-segment depression was found in leads V5 and V6 in 38% (6/16) and 44% (7/16) of patients, respectively, whereas lead aVR ST-segment elevation was found in 88% (14/16) of patients. Moreover, lead aVR ST-segment shift was not correlated with ST-segment depression in lead V5 or lead V6. Stepwise multivariate 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.
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References
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1. Yamaji H, Iwasaki K, Kusachi S, et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography: ST segment elevation in lead aVR with less ST segment elevation in lead V1. J Am Coll Cardiol. 2001;38:1348–1354[Abstract/Free Full Text]
2. Sclarovsky S, Davidson E, Strasberg B, et al. Unstable angina: the significance of ST segment elevation or depression in patients without evidence of increased myocardial oxygen demand. Am Heart J. 1986;112:463–467[CrossRef][Medline]
3. Sclarovsky S, Rechavia E, Strasberg B, et al. Unstable angina: ST segment depression with positive versus negative T wave deflections—clinical course, ECG evolution, and angiographic correlation. Am Heart J. 1988;116:933–941[CrossRef][Medline]
4. Engelen DJ, Gorgels AP, Cheriex EC, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol. 1999;34:389–395[Abstract/Free Full Text]
5. Iwasaki K, Kusachi S, Kita T, et al. Prediction of isolated first diagonal branch occlusion by 12-lead electrocardiography: ST segment shift in leads I and aVL. J Am Coll Cardiol. 1994;23:1557–1561[Abstract]
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