Ghostbusters should come back to lead extraction arena in order to fight with ghosts: authors reply

We appreciate the interest of Dr Canpolat in our article.1,2 Persistence of residual fibrous tissue after transvenous lead extraction (TLE) has been described variously over the last few years.3–5 Focusing on pathophysiological mechanism for development of ‘ghost’, Andreas et al. described the histopathology of an inhomogeneous highly mobile structure in the right atrium after TLE, as organized thrombus in a case report.6 Immunohistochemical analysis of 17 extracted leads revealed that a fibrous capsule surrounding the lead was partially or completely covered with a monolayer of CD34 expressing endothelial cells.7 Endothelialization of the fibrous encapsulation indicates a functionalization of blood-contacting surfaces around leads, thus providing a mechanism for long-term persistence of foreign materials in the blood.7 On the other hand, granuloma tissue and vasculogenesis were present in the encapsulating tissue of 56 extracted leads, particularly in patients with device-endocarditis and pocket infection.8 Two observational studies2,5 demonstrated a significant association between device-related endocarditis before TLE and development of ghost after TLE. Interestingly, in both studies, ghosts were never observed among the remaining non-infected patients. Besides fibrosis, device-endocarditis might act as a drive for ‘ghost’ development. Histopathological analysis of ‘ghosts’ series in patients undergoing surgical extraction could directly clarify whether these masses were inflammatory or non-inflammatory fibrous tissue, mixture of fibrous tissue, and thrombus or endocarditic vegetations. In our study, at univariate analysis, oral anticoagulant therapy did not differ among the two groups 10% ghost group vs. 28% no ghost group, P = ns). Thus, an association between oral anticoagulant therapy and development of ghost could not be evaluated. In our population, only two patients (0.9%) presented with pulmonary embolism after TLE, both in ghost group, with a mean length of ghost of 21 and 32 mm, respectively. Further studies need to evaluate whether the mean length of ghost could predict embolic events after TLE. Twenty patients (9.2%) died at a median follow-up of 11 months: 15 (75%) of sepsis, 2 (10%) of advanced heart failure, and 3 (15%) of sudden death. After adjusting for preoperative endocarditis and systemic infection at admission, the presence of ‘ghost’ was an independent predictor of mid-term mortality. As Dr Canpolat points out the presence of ‘ghost’ after TLE is not an innocent phenomenon. Thus, accurate echocardiographic and clinical surveillance should be continued in this high-risk subgroup of patients after TLE. Therapeutic strategies as prolonged elective antibiotic therapy and surgery should be considered, as indicated by recent ESC guidelines on endocarditis.9 Conflict of interest: none declared.