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Articles by P. Kovoor
Total Records ( 3 ) for P. Kovoor
  S Zaman , G Sivagangabalan , A Narayan , A Thiagalingam , D. L Ross and P. Kovoor

Background— Methods to identify high-risk patients and timing of implantable cardioverter-defibrillator (ICD) therapy after ST-elevation myocardial infarction need further optimization.

Methods and Results— We evaluated outcomes of early ICD implantation in patients with inducible ventricular tachycardia. Consecutive patients treated with primary percutaneous coronary intervention for acute ST-elevation myocardial infarction underwent early left ventricular ejection fraction (LVEF) assessment. Patients with LVEF >40% were discharged (group 1); patients with LVEF ≤40% underwent risk stratification with electrophysiological study. If no ventricular tachycardia was induced, patients were discharged without an ICD (group 2). If sustained monomorphic ventricular tachycardia (≥200-ms cycle length) was induced, an ICD was implanted before discharge (group 3). Follow-up was obtained up to 30 months in all patients and up to 48 months in a subgroup of patients with LVEF ≤30% without an ICD. The primary end point was total mortality. Group 1 (n=574) had a mean LVEF of 54±8%; group 2 (n=83), 32±6%; and group 3 (n=32), 29±7%. At a median follow-up of 12 months, there was no significant difference in survival between the 3 groups (P=0.879), with mortality rates of 3%, 3%, and 6% for groups 1 through 3, respectively. In the subgroup of group 2 patients with LVEF ≤30% and no ICD (n=25), there was 9% mortality at a median follow-up of 25 months. In group 3, 19% had spontaneous ICD activation resulting from ventricular tachycardia.

Conclusions— Early ICD implantation limited to patients with inducible ventricular tachycardia enables a low overall mortality in patients with impaired LVEF after primary percutaneous coronary intervention for ST-elevation myocardial infarction.

  G Sivagangabalan , J Pouliopoulos , K Huang , M. A Barry , J Lu , S. P Thomas , D. L Ross , A Thiagalingam and P. Kovoor

Background— We assessed a novel simultaneous biventricular mapping and ablation approach for septal ventricular tachycardia (VT) in a chronic ovine infarct model.

Methods and Results— In 8 sheep with inducible VT, mapping and ablation were performed 9±3 months after percutaneously induced myocardial infarction, with left ventricular ejection fraction 23±8%. Scar was identified by EnSite Dynamic Substrate Mapping plus CARTO voltage mapping. Thirty VT episodes (cycle length, 235±42 ms) were mapped with simultaneous analyses using EnSite arrays deployed in both the left ventricle and the right ventricle. Short ablation lines were created perpendicular to the breakout pathway along the scar border in the ventricle with earliest activity. If septal VT was still inducible, this line was extended before ablation in the second chamber. The end point of noninducibility of VT was achieved in all animals. The mean difference in delay in noncontact breakout timing between the ventricles was shorter for VT with (n=18) than without (n=12) septal breakout (32±7.8 ms, P<0.001). In 5 of 6 animals, after ablation in one ventricle, septal VT was still inducible with a common breakout site in the second ventricle. After septal ablation in the second ventricle, VT was no longer inducible. In the 6 animals in which septal VT had been ablated, transmural septal ablation was identified at the scar border, with overlapping left ventricular and right ventricular ablation lesions present in 5 of 6 (septal thickness 8 to 17 mm) and left ventricular endocardial ablation being transmural in 1 of 6 (6 mm).

Conclusions— Biventricular scar and VT activation mapping correctly localizes septal VT pathways, directing ablation from one or both septal endocardial aspects. Creation of a transmural septal lesion at the scar border interrupting VT exit points is highly effective at ablating septal VT.

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