HISTOLOGIC EVOLUTION OF RADIOFREQUENCY LESIONS IN AN OLD HUMAN MYOCARDIAL INFARCT CAUSING VENTRICULAR-TACHYCARDIA

Introduction: Radiofrequency (RF) ablation of ventricular tachycardia (VT) late after myocardial infarction may be difficult due to characte ristics of the infarct containing the reentry circuit, RF lesions in t hese infarcts in humans have not been characterized. Methods and Resul ts: Catheter mapping and ablation of VT originating from an anterior w all infarct was performed 8 days and again 12 hours prior to death, Pa cing identified a region of abnormal conduction where RF ablation term inated VT. This region contained strips of myocytes sandwiched between endocardial fibrosis and dense scar, RF lesions ranged from 2 x 2 mm to 5 x 10 mm and were up to 3 mm in depth, Acute lesions showed superf icial thrombus and early coagulation necrosis without inflammation. Ol der lesions showed coagulation necrosis, sparse neutrophil infiltrate, minimal granulation tissue, hemorrhage, and mixed inflammatory infilt rate along the lumen without re-endothelialization. Conclusion: In thi s patient, RF lesions had sufficient depth but not width to interrupt the thin, but potentially broad, sheets of myocytes in the reentry cir cuit, In thinned areas, RF lesions can extend to the epicardium, Selec ting sites with abnormal electrograms confines RF lesions to the infar ct region, Inflammation and hemorrhage could conceivably cause delayed effects of RF.