Abstract
guing finding that the presence of abrasion in the intracardiac part of the leads was strongly associated with infection. Insulation defect was frequent in their population (64%) and was significantly higher on leads extracted for an infectious indication (91%). In multivariate stepwise analysis incorporating patient age, number of leads, lead age, number of prior procedures, time from the last procedure, and the presence of any abrasion in the intracardiac part was independently associated with infection with an odds ratio of 4.9 (95% confidence intervals, 1.5ā15.4) for atrial leads and 21.7 (2.8ā167.8) for ventricular leads. To explain such as a significant association between lead defects and infection, we have to go back to the mechanisms of device infections. Mode of contamination Two distinct mechanisms of contamination exist: (i) haematogenous contamination with seeding of the device from a distant source of infection or during a bacteraemia, e.g. valvular endocarditis; and (ii) local contamination of the pulse generator or leads during implantation of the device or any subsequent procedure on the pulse generator site. We do not know the exact proportion of device infections induced by haematogenous contamination but we have many plausible arguments to believe that this is a rare mechanism of contamination compared with local contamination. Firstly, in haematogenous contamination, risk factors for infection mainly relate to the implant procedure particularly device replacement and multiple device revisions, early reintervention on the pulse generator site, procedure duration, pulse generator size and additional subcutaneous material, experience of the operator, and lack of antibiotic prophylaxis during the implant procedures. 2,3 Secondly, infection occurring early after a surgical intervention is directly attributable to the procedure. The majority of device-related infections are diagnosed in the 24 months following implantation. In our series of 544 patients with device infection, the median time to the occurrence of infection was 7 months, with 83% of infections occurring within 24 months after implantation (unpublished data). Thirdly, Staphylococcus epidermidis and the coagulase negative Staphylococcus (CoNS), known to be part of the normal skin microflora, are responsible for the great majority of infections. Da Costa et al. 4 have compared bacteria found on systematic skin cultures during pacemaker implantation procedures with the bacteria responsible for device infections during follow-up and have shown that devices were infected by bacteria present on the skin during the implantation procedure. Therefore, we cannot explain the association between lead abrasion and lead infection by a haematogenous contamination mechanism occurring preferentially on damaged leads.
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