Does late revascularization alter the evolution of the signal-averaged electrocardiogram in patients with a recent transmural myocardial infarction?

BACKGROUND AND OBJECTIVES

Early infarct-related artery patency associated with thrombolytic therapy decreases the incidence of signal-averaged electrocardiogram (SAECG) derived late potentials following acute Q wave myocardial infarction. The purpose of this prospective study was to follow the development of SAECG abnormalities in patients with persistent occlusion of the infarct-related artery, and to compare the course of those who subsequently had successful late percutaneous transluminal coronary angioplasty and coronary artery bypass grafting surgery with the course of those who were not revascularized.

METHODS

Baseline (24 +/- 25 days after myocardial infarction) SAECG studies were acquired from 39 patients just before revascularization of the infarct-related artery (group 1) and from 32 nonrevascularized patients (group 2). Late potentials were found in 19 group 1 patients and in 13 group 2 patients (not significant). Follow-up studies were done 103 +/- 63 days after baseline acquisition.

RESULTS

There were no differences between the two groups in the change in filtered QRS (fQRS), in low amplitude signal duration under 40 microV (LAS), or in the root mean square voltage of the last 40 ms (RMS). No difference was found in the frequency of resolution of late potentials (21.0% in group 1 versus 38.5% in group 2). Patients in whom late potential resolution occurred had less abnormal LAS than patients with persistent late potentials, and less abnormal RMS. In addition, the magnitude of change in the fQRS, LAS and RMS was significantly greater in patients with late potential resolution than in those with late potential persistence.

CONCLUSIONS

Late revascularization of an occluded infarct-related artery does not appear to enhance resolution of late potentials compared with conservative medical therapy. Resolution occurs in patients with less severe SAECG abnormalities. This may reflect a difference in arrhythmogenic substrate.