Early diagnosis of the site of infarction and the infarct-related coronary artery in patients with acute inferior myocardial infarction.

Abstract

We evaluated the relationship between the site of infarction and the infarct-related coronary arteries from electrocardiograms (ECGs) recorded early after the onset of chest pain in patients with an initial acute inferior myocardial infarction (IMI). The subjects were 80 patients (mean age 57 +/- 12 years) with IMI admitted within 6 hours from the onset of chest pain. This was prior to the thrombolytic era. We analyzed the ECGs on admission, at 24 hours and at 4 weeks. All patients underwent left ventriculography and coronary angiography at 4-6 weeks from the onset of the IMI. Left ventricular ejection fraction (EF) and regional area changes were measured. The infarct-related coronary artery was determined by the site of the asynergy. Patients were allocated into 2 groups according to the infarct-related artery, i.e. right (RCA, n = 52) and left circumflex (LCX, n = 28). Parameters measured were ST elevation, amplitude and width of R wave and R/S ratio in leads V1 and V2, and amplitude of U waves in leads V1 to V3. We defined the U wave as a prominent positive U wave (PPU) if it was > 0.5 mm (50 microV) in height. A significantly greater number of patients with PPU showed asynergy in posterolateral segments compared to those without PPU. The EF was significantly lower in patients with PPU than in those without (46 +/- 12% vs 54 +/- 13%, p < 0.05). Patients with PPUs eventually showed ECG evidence of posterior infarction (increased R wave duration and R/S ratio > or = 1 in lead V1 or V2) by 4 weeks compared to those without PPUs. Also a significantly greater number of patients with PPUs developed posterior infarction shown by left ventriculograms than those without PPUs. As to the infarct-related coronary arteries, a significantly greater number of patients with LCX disease showed concomitant posterior infarction than those with RCA disease. Also, a significantly greater number of LCX patients showed PPUs and ST elevations in leads V5 and V6 than those with RCA disease. The sensitivity of PPUs and ST elevations in leads V5 and V6 suggesting LCX disease was 60% and the specificity was 98% with a predictive accuracy of 87%. Therefore, we conclude that PPUs in leads V1-3 and ST elevations in leads V5 and V6 are specific markers for the diagnosis of LCX-related infarction in the setting of evolving IMI.