Introduction: Implantable devices elicit fibrotic and inflammatory responses, which may result in reduced efficacy of the device. Prior literature has addressed thrombus formation and fibrous encapsulation of intravascular leads. This mechanism is at least in part different than subcutaneous fibrosis. However, there have been scarce reports of fibrosis related to subcutaneous leads. Case: A 74 year-old male with long standing ischemic cardiomyopathy and absence of pacing indication met indications for primary prevention S-ICD. After shared decision making, a device was implanted with defibrillation thresholds at 65 joules. He later presented with interventricular dyssynchrony (QRS 160 msec) and symptomatic heart block. Upgrade to a biventricular defibrillator was undertaken with removal of the S-ICD system. S-ICD coil manual traction failed to free the lead from the subcutaneous space of implantation. After extensive blunt dissection and removal of the coil, extensive coil ingrowth and fibrosis was noted (Figure 1). Conclusions: This case describes the occurrence and visually documents extravascular coil fibrosis and ingrowth into the SICD coil, similarly seen in intravascular ICD leads. The S-ICD coil is a necessary component of the shocking vector and extensive fibrosis may contribute to elevated shock impedance and failed defibrillation thresholds. In cases of elevated shock impedance, it is unknown whether failed defibrillation thresholds or elevated high voltage shock impedance is the result of the generator, coil, or both. Further research is warranted to ascertain whether failed defibrillation thresholds and increased shock impedance is due solely from the SICD generator pocket. Advances in coil technology and regenerative medicine may offer insights into mitigation of the inflammatory process.