Electrocardiographic pseudo-infarct patterns after implantation of cardioverter-defibrillators.

Postoperative electrocardiographic (ECG) changes are frequently present after insertion of implantable cardioverter-defibrillators (ICD) and may mimic perioperative myocardial infarction (MI). The purpose of this study was to assess the incidence and clinical significance of postoperative ECG changes in relation to clinical, laboratory, and implantation data. In 25 (16%) of 156 patients undergoing ICD implantation, significant ECG changes (> or = 50% reduction in R-wave amplitude in > or = 3 leads or new Q waves in > or = 2 leads) were present 1 to 3 days after the operation and persisted at hospital discharge in 12 (8%). Presence of thoracotomy, the total number of induced ventricular fibrillation episodes, and the number of defibrillation shocks required during defibrillation threshold (DFT) testing correlated with postoperative ECG changes. Other factors associated with a significant R-wave loss in the lateral precordial leads included left-sided pleural effusion, lung infiltrates or atelectasis, and large defibrillator patch electrodes over the left ventricle or the lateral chest wall. Myocardial necrosis documented by elevated cardiac enzymes occurred in 6 (5%) of 151 patients without significant ECG changes and in 3 (12%) with (p value not significant). However, postoperative ECG changes associated with elevated enzymes were indistinguishable from changes unrelated to necrosis. Therefore the sensitivity and specificity of the surface ECG for detection of MI after ICD placement is poor. Multiple factors such as thoracotomy, myocardial injury from DFT testing, electric insulation, or shielding of the heart may contribute to the development of electrocardiographic pseudo-infarct patterns.

Curative transcatheter radiofrequency current ablation for atrioventricular nodal reentry tachycardia.

BACKGROUND: To evaluate the efficacy of atrioventricular nodal modification by transcatheter ablation using radiofrequency energy in preventing electrically inducible and spontaneous symptomatic atrioventricular nodal reentry tachycardia, a prospective, nonrandomized, "before-after" trial was performed. Fifty consecutive patients with recurrent spontaneous symptomatic atrioventricular nodal reentry tachycardia referred to the Massachusetts General Hospital, Boston, were recruited. METHODS: A diagnostic intracardiac electrophysiologic study was performed to define the mechanism of each patient's supraventricular tachycardia. Thereafter, selective ablation of one or more slow atrioventricular nodal pathways was attempted in 47 patients, and in three patients selective ablation of a retrograde fast atrioventricular nodal pathway was carried out. Repeated programmed cardiac stimulation was performed 30 minutes after catheter ablation therapy and, where possible, before hospital discharge to evaluate the presence of electrically inducible supraventricular tachycardia. RESULTS: Electrically inducible atrioventricular nodal reentry tachycardia was eliminated in all 50 patients. No patient developed early heart block. During a mean (+/- SD) follow-up period of 8.9 +/- 5.3 months, three patients experienced a recurrence of spontaneous atrioventricular nodal reentry tachycardia and underwent a successful second ablation procedure. Two patients required permanent pacemaker implantation, one for symptomatic first-degree atrioventricular block and one for late complete heart block. CONCLUSIONS: Catheter ablation of slow atrioventricular nodal pathways by means of radiofrequency current is a safe and effective technique for eliminating electrically inducible and spontaneous atrioventricular nodal reentry tachycardia.