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 results: One 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 (SigmaR) 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 SigmaR and the absolute increase in LV ejection fraction from the acute to the subacute phase (DeltaEF) were also calculated. The SigmaR in the subacute phase was significantly greater than that in the acute phase (p<0.0001). The % increase in SigmaR significantly correlated with the DeltaEF (r=0.57, p<0.0001). The % increase in SigmaR also correlated with the % defect-discordance (r=0.68, p<0.0001).
Conclusions: The increase in the ECG R-wave voltage reflects not only the improvement in myocardial perfusion but also the presence of salvaged myocardium after revascularization in acute MI patients.