Shehbaz A. Kureshi ( Kyoto University School of Medicine, Kyoto, Japan. )
Yoshiharu Yonekura ( Kyoto University School of Medicine, Kyoto, Japan. )
Yutaka Konishi ( Kyoto University School of Medicine, Kyoto, Japan. )
Kanji Torizuka ( Kyoto University School of Medicine, Kyoto, Japan. )
Inferior myocardial infarction is frequently associated with ST segment depression in the chest leads. In such a clinical setting it may be useful to examine lead aVR. If ST segment depression in chest leads is associated with ST elevation lead aVR, these precordial changes are probably not reciprocal but due to associated anterior subendocardial ischemia infarction : (JPMA 35: 365, 1985).
Anterior ST segment depression frequently occurs with inferior acute myocardial infarction (AMI) and is associated with greater global and regional left ventricular dysfunction,1,2 and a higher incidence of hospital and late complications and the presence of significant left coronary Artery disease3. ST segmain depression can be anterior wall subendocardial ischemia or infarction, or a reciprocal change of inferior or posterior wall injury. To distinguish between the two, it is useful to examine lead aVR the socalled “intracavitary” lead. If lead aVR shows ST segment elevation, the ST depression in the anterior precordial leads is probably due to subendocardial ischemia or infarction. We present the following case study as an illustration.
A 63 years old male was admitted for the evaluation of his unstable angina. He had pre. viously suffered inferior myocardial infarction. His resting electrocardiogram showed Q-waves in II, III and aVF and T-wave changes in aVL, V4, V5 and V6. On master two step exercise test ST was depressed significantly from V2-V6. ST depression was also seen in IT, III and aVF. Simultaneously ST in aVR was elevated (Fig-I).
Coronary angiographic findings showed total occlusion of right coronary artery in segment 1, left anterior descending segment 7 was also totally occluded and there was subtotal occlusion of left circumflex artery. Thallium-201 stress test using single photon emission computed tomography (SPECT) •showed perfusion defect in inferior, anterior and antero-septal segments. The defect in anterior and antero-septal segments was “filled in.” on delayed imaging indicating that it was reversible ischernia (Fig-2).
After one month of Aorto coronary by pass surgery the perfusion defects seen earlier in anterior and antero-septal segment were not visualised in the post operative state, only a fixed perfusion defect was seen in the inferior segment on a repeat thallium-201 stress test (Fig-3).
During the post operative stress test no apparent ST segment changes were seen. Also, there was no ST -elevation in aVR.
Several studies have shown that anterolateral ST segment depression during inferior AM! is associated with a higher rate of clinical complications. Although the significance of anterolateral ST depression in this clinical setting is established, the mechanism underlying it remains unclear. In a subgroup of these patients the antero-lateral ST depression may be reciprocal. The presence of ST elevation in a YR in a patient with inferior wall myocardial ihfarction and ST depression in precordial leads suggests that the ST depression is not reciprocal and it is associated with anterior wall ischaemia The examination of ST segment in aVR in patients with inferior M.I is useful clinically and can help identify patients with inferior AM! with increased risk.
1. Shah, P.K., Pichler, M., Berman, D.S., Maddahi, J., Peter, T., Sing, B.N. and Swan, H.J.C. Nonin vasive identification of high risk subset of patients with acute inferior myocardial infarction. Am. J. CardioL, 1980;46 :915.
2. Goldberg, H.L., Borer, J.S., Jacobstein, J.G., Kluger, J., Scheidt, S.S. and Alonso, D.R. Anterior S-T segment depression in acute inferior myocardial infarction indicator of posterolateral infarction. Am. J. Cardiol.,1981 ;48 : 1009.
3. Nasmith, J., Marpole, D., Homan, J., Stewart, S. and Sniderman, A. Clinical outcomes after inferior myocardial infarction. Ann. Intern. Med., 1982;96 :22.