Background—
Electrophysiological study (EPS) after myocardial infarction may have a role in identifying patients at risk of sudden cardiac death. It has been shown previously that inducible very fast ventricular tachycardia (VT; cycle length [CL], 200–230 ms) is predictive of arrhythmia recurrence; however, its significance early after reperfusion in ST-segment–elevation myocardial infarction is unknown.
Methods and Results—
Consecutive patients with ST-segment–elevation myocardial infarction treated with primary percutaneous coronary intervention with a left ventricular ejection fraction ≤40% underwent early EPS with an implantable-cardioverter defibrillator implanted for inducible VT, but not for a negative EPS. The end point was the cumulative incidence of death or first arrhythmic event (defined as resuscitated cardiac arrest or spontaneous ventricular tachyarrhythmia). A total of 1721 patients with ST-segment–elevation myocardial infarction underwent early left ventricular ejection fraction assessment (median, 4 days after myocardial infarction) with a left ventricular ejection fraction ≤40% in 24%. EPS was performed in 290 eligible patients with no arrhythmia or ventricular fibrillation/flutter (CL<200 ms) induced in 203 patients (EPS negative, group 1), monomorphic VT induced in 87 patients, consisting of very fast VT in 67% (group 2; n=58), and standard VT (CL>230 ms) in 33% (group 3; n=29). Kaplan–Meier 4-year cumulative incidence of death or arrhythmia was 8.2±2.3%, 33.1±7.1%, and 37.0±10.2% in groups 1, 2, and 3, respectively (
P
<0.001).
Conclusions—
The majority of inducible VT in patients who have been reperfused early after ST-segment–elevation myocardial infarction is very fast VT (CL, 200–230 ms). This very fast VT incurs at least a similar risk of arrhythmia or death as inducible standard VT (CL>230 ms) and a significantly higher risk than patients with a negative EPS.
Patients receiving early reperfusion for STEMI had faster inducible and spontaneous VT and fewer spontaneous recurrences. This may be due to changes in the myocardial substrate as a result of early coronary artery reperfusion.
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