[Early diagnosis of the site of infarction and the infarct-related coronary artery in patients with acute inferior myocardial infarction].
J Hosokawa
Abstract
J Hosokawa
Abstract
We evaluated the site and infarct-related arteries from electrocardiograms (ECGs) recorded early after the onset in cases of inferior infarction (IMI). The subjects were 80 patients with IMI admitted within 6 hours from the onset. We analyzed the ECGs on admission, at 24 hours, at 4 weeks. All patients underwent ventriculography and coronary angiography at 4-6 weeks from the onset. Regional wall motion and ejection fraction (FF) were measured. The infarct-related artery was decided on by the site of the asynergy. Patients were allocated into 2 groups according to the infarct-related artery; ie right (RCA, n = 52) and left circumflex (LCX, n = 52). Parameters measured were leads showing ST elevation (ST increases), width of R waves and R/S ratio in V1,2. Amplitude of U waves in V1-3. We defined U greater than or equal to 0.5mm as abnormal (GU). A significantly greater number of patients with GU showed asynergy in posterolateral and posterobasal segments compared to those without GU. The EF was significantly lower in patients with GU. As to the infarct-related arteries, a significantly greater number of patients with LCX disease showed concomitant posterior infarction (PMI) than those with RCA disease. Also a significantly greater number of those with LCX disease showed GU and ST increases in V5,6 than those with RCA disease. Therefore, we conclude that GU in V1-3 is a new marker suggesting posterolateral and posterobasal damage, and GU in V1-3, ST increases in V5,6 and electrocardiographic PMI are specific markers for the diagnosis of LCX related infarction.
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We evaluated the site and infarct-related arteries from electrocardiograms (ECGs) recorded early after the onset in cases of inferior infarction (IMI). The subjects were 80 patients with IMI admitted within 6 hours from the onset. We analyzed the ECGs on admission, at 24 hours, at 4 weeks. All patients underwent ventriculography and coronary angiography at 4-6 weeks from the onset. Regional wall motion and ejection fraction (FF) were measured. The infarct-related artery was decided on by the site of the asynergy. Patients were allocated into 2 groups according to the infarct-related artery; ie right (RCA, n = 52) and left circumflex (LCX, n = 52). Parameters measured were leads showing ST elevation (ST increases), width of R waves and R/S ratio in V1,2. Amplitude of U waves in V1-3. We defined U greater than or equal to 0.5mm as abnormal (GU). A significantly greater number of patients with GU showed asynergy in posterolateral and posterobasal segments compared to those without GU. The EF was significantly lower in patients with GU. As to the infarct-related arteries, a significantly greater number of patients with LCX disease showed concomitant posterior infarction (PMI) than those with RCA disease. Also a significantly greater number of those with LCX disease showed GU and ST increases in V5,6 than those with RCA disease. Therefore, we conclude that GU in V1-3 is a new marker suggesting posterolateral and posterobasal damage, and GU in V1-3, ST increases in V5,6 and electrocardiographic PMI are specific markers for the diagnosis of LCX related infarction.
Key concepts: Asynergy, Medicine, Cardiology, Internal medicine, Myocardial infarction, Ejection fraction, Infarction, Right coronary artery