[Analysis of functional changes in ventricular late potentials for risk assessment of ventricular tachycardias after myocardial infarct].

BACKGROUND: Electrophysiological abnormalities during ischaemia and increased heart rate may influence the detection of ventricular late potentials in the surface electrocardiogram. Whether the analysis of functional changes adds information to the risk stratification of patients prone to ventricular tachycardia is unclear.

METHODS: We therefore retrospectively investigated 100 selected patients (25 with documented, sustained ventricular tachycardia (< 230/min) ( = VT group), 25 resuscitated from ventricular fibrillation (VF group) and 50 without ventricular arrhythmias (phi VT/VF group)) in the chronic phase after myocardial infarction. Late potential analysis was performed at rest, during atrial pacing at a rate of 100/min and 120/min (n = 60), during and after occlusion of the coronary artery for coronary angioplasty (PTCA) (n = 70), and immediately after maximum exercise using selective signal averaging.

RESULTS: At rest in 72% of patients in the VT group, in 32% of the VF group, and in 6% of the phi VT/VF group late potentials could be found. During atrial pacing in 80% of patients in the VT group, in 72% of the VF group, and in 10% of the patients in the phi VT/VF group and during ischaemia because of occluded coronary artery in 86% of patients in and the VT group, 70% of the VF group, and in 20% of the patients of the phi VT/VF group late potentials were present. Immediately after maximum exercise which let both ischaemia and increased heart rate, late potentials were detectable in 92% of patients in the VT group, 80% of the VF group, and in 14% of patients in the phi VT/VF group. Similar results could be achieved by using the Holter-ECG after exact correction of recorder tape speed variations. 62% of patients with only by ischaemia, increased heart rate or exercise provokable late potentials and all patients with preexistent not by PTCA extinguished late potentials developed recurrent ventricular tachycardias during the one year follow-up period. Patients without late potentials (n = 50) and patients with preexistent by PTCA extinguished late potentials (n = 11) had no recurrent ventricular tachycardias. Cycle length of recurrent and clinical tachycardia in patients with preexistent not by PTCA extinguished late potentials (n = 18) were significantly longer than in patients with only provokable late potentials (n = 21).

CONCLUSIONS: Analysis of functional changes of ventricular late potentials with exercise or in Holter ECG recordings promises considerable improvement of postinfarction risk stratification especially in patients prone to ventricular fibrillation.