spontaneous increase in the electrocardiographic (ECG) R-wave voltage after acute myocardial infarction (MI) is a unique phenomenon, and regeneration of R-waves or disappearance of Q-waves after acute ischemic events has been reported. [1][2][3][4][5][6][7] With the prevalence of interventional therapy, it is thought that this phenomenon is increasing, but little is known regarding the physiological mechanism involved.Patients with acute MI always undergo echocardiography in order to evaluate changes in wall motion, left ventricular (LV) cavity, and LV function over time. Myocardial scintigraphy provides important information about myocardial perfusion and/or metabolism. Specifically, a combined study of myocardial metabolic tracer with perfusion tracer provides clues about the myocardial status in the healing stage of MI. [8][9][10] Perfusion -metabolism mismatch of the Circulation Journal Vol. 70, November 2006 perfusion/metabolic dual-tracers represents impaired but viable myocardium in the risk area, which is involved in functional recovery after revascularization in patients with acute MI. 11-13 Therefore, both examinations are cardinal diagnostic modalities for patients after acute MI.In this study, we performed dual-isotope scintigraphy and echocardiography, and compared the findings with ECG results to determine the physiological mechanism of the increase in ECG R-wave voltage during the acute to the subacute phase after revascularization in patients with acute MI.
Methods
PopulationOne hundred and seventy-one consecutive patients with first onset of acute MI who underwent emergency coronary revascularization, dual-isotope scintigraphy, and echocardiography between January 1998 and March 2004 were retrospectively examined. Acute MI was diagnosed by typical chest pain for >30 min, ECG ST-elevation of ≥0.1 mV (1 mm) in at least 2 contiguous leads, and a characteristic rise in plasma creatine kinase-MB activity. All patients underwent emergency coronary angiography (CAG) immediately after the ECG diagnosis and subsequent coronary revascularization. In the emergency CAG, antegrade flow was characterized using the Thrombolysis In Myocardial Background The physiological mechanism of the increase in the electrocardiographic (ECG) R-wave voltage after revascularization in patients with acute myocardial infarction (MI) needs to be elucidated.
Methods and ResultsOne hundred and thirty-eight MI patients (83: anterior MI, 45: inferior MI, 10: lateral MI) underwent ECG and echocardiography in both the acute and subacute phases after emergency revascularization, as well as a resting thallium-201/iodine-123 15-p-iodophenyl-3-(R,S)-methyl pentadecanoic acid myocardial scintigraphy in the acute phase. The total sum of the R-wave voltage (∑R) was calculated over multiple leads on ECG for each infarcted lesion. Scintigraphic defect on each tracer was expressed as the percentage (%) defect of the total left ventricular (LV) myocardium. The % defect-discordance on both images in the acute phase and the % increase in ∑R an...