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 characteristics of the infarct containing the reentry circuit. RF lesions in these infarcts in humans have not been characterized.

METHODS AND RESULTS

Catheter mapping and ablation of VT originating from an anterior wall infarct was performed 8 days and again 12 hours prior to death. Pacing identified a region of abnormal conduction where RF ablation terminated 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 superficial thrombus and early coagulation necrosis without inflammation. Older lesions showed coagulation necrosis, sparse neutrophil infiltrate, minimal granulation tissue, hemorrhage, and mixed inflammatory infiltrate along the lumen without re-endothelialization.

CONCLUSION

In this patient, RF lesions had sufficient depth but not width to interrupt the thin, but potentially broad, sheets of myocytes in the reentry circuit. In thinned areas, RF lesions can extend to the epicardium. Selecting sites with abnormal electrograms confines RF lesions to the infarct region. Inflammation and hemorrhage could conceivably cause delayed effects of RF.