GROSS AND MICROSCOPIC CHANGES ASSOCIATED WITH A NONTHORACOTOMY IMPLANTABLE CARDIOVERTER DEFIBRILLATOR

The pathology associated with an investigational transvenous defibrillating and sensing lead is described. The lead system had delivered a total of 865 J from the time of implantation to the time of patient death from a noncardiac cause 7 months after implantation and 1 month after his last defibrillator shock. There was mild, superficial fibrous thickening on the endothelial surface of the superior vena cava adjacent to the proximal spring electrode, which did not extend into the vessel wall. The distal portion of endocardial lead was embedded in the interventricular septum near the apex of the right ventricle, surrounded by fibrous thickening, and partially covered by endocardial tissue. Microscopically, there was a thick bed of fibrous connective tissue surrounding the lead with extensive interstitial fibrous connective tissue radiating into the adjacent myocardium. Since this pattern is different from the more generalized fibrotic scarring produced by myocardial infarction, we speculate that the mechanism for the observed interstitial fibrosis is replacement fibrosis following acute myocyte injury that resulted from prior defibrillator shocks and possibly from the trauma produced by the lead compressing adjacent myocardium during systole. Potential effects on device efficacy of these fibrotic changes at the bioelectric interface include their representing a new arrhythmia substrate, the possibility that fibrosis could increase both defibrillation and pacing thresholds, and that the inflammatory reaction may cause deterioration of intracardiac electrograms and interfere with sensing and tachycardia recognition.