Anatomic and hemodynamic effects of catheter-delivered ablation energies in the ventricle.
Twenty dogs were studied to characterize the anatomic, hemodynamic and pathologic effects of catheter-delivered cardioversion (CDCV) in the left ventricle. Five dogs each received 1 CDCV of either 50, 100, 200 or 300 J at the left ventricular apex. The injury occurred at the posteroinferior apex. Structural integrity of the ventricle remained intact. Energy doses of 50 and 100 J resulted in focal subendomyocardial injury. Higher energy levels resulted in localized transmural injury. There was a linear dose-related correlation between the volume of injury and delivered energy. Electrocardiographic changes were seen immediately in all dogs. Fifteen dogs had acute, transient ventricular arrhythmias. One dog died with refractory arrhythmias. Minimal hemodynamic changes were associated with the CDCV. Unique histopathologic changes were observed. Thus, local tissue destruction can be produced with CDCV. The extent of injury is dose-related and is associated with minimum hemodynamic changes. The lesion may be acutely arrhythmogenic.
D000818:Animals; D002114:Calcinosis / Q000209:etiology; D002404:Catheterization / Q000009:adverse effects* / Q000379:methods; D004285:Dogs; D004554:Electric Countershock / Q000009:adverse effects* / Q000379:methods; D004719:Endomyocardial Fibrosis / Q000209:etiology; D005549:Foreign-Body Reaction / Q000209:etiology; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D013997:Time Factors