Complications of implanted cardiac rhythm devices

This editorial refers to ‘Rate, causes, and impact on patient outcome of implantable device complications requiring surgical revision: large population survey from two centres in Italy’ by P. Palmisano et al., on page 531 In this issue of the journal, Palmisano et al.1 present a large retrospective study of device-related complications in 2671 consecutive procedures in two centres (1511 primary implantations and 1034 elective device replacements) performed between January 2006 and March 2011 with a median follow-up of 27 months. All the procedures were performed by six electrophysiologists with a long (>10 years) experience with device therapy. Few acute complications were observed. Although 70% of the leads were implanted by direct puncture of the subclavian vein, the incidence of pneumothorax was remarkably low (0.31% per procedure-year) and slightly higher for pacing system upgrade. Cardiac tamponade (presumably at the time of implantation) occurred only in 3 (1.2%) of 242 patients receiving cardiac resynchronization therapy (CRT). Although not stated in the report, it is logical to assume that these cases involved coronary venous perforation which resulted in the death of one patient. The lead dislodgement rate for primary implantation was quite low at only 0.79% per procedure-year for pacemakers (including atrial leads), and was slightly higher for implantable cardioverter defibrillators (ICD). As expected, it was also slightly higher for pacing system upgrade, but substantially higher (3.31% per procedure-year) for CRT which is an acceptable rate of dislodgement of coronary venous leads. In terms of lead dislodgement, one might argue that the data show a trend favouring active-fixation over passive-fixation leads. It is strange that the report contains no mention of lead perforation which would be expected in at least 1% of the cases because contemporary small-diameter leads with active-fixation were probably used in the study. These leads are associated with a higher incidence of perforation presenting as a subacute or relatively late clinical problem.2 One wonders whether lead perforation was classified as lead dislodgement. Long-term lead failure was unusual and consistent with the prevailing recall from one of the manufacturers. Device infection occurred in 30 patients: 18 (60.0%) presented pocket infection, and 12 (40%) presented (40.0%) with systemic infection. The overall incidence of infection was low at 0.68% per procedure-year and was considerably lower for primary implantations. Three procedures are generally associated with a greater risk of infection compared with an initial pacemaker or ICD implantation: (i) CRT where the mechanism is probably related to the longer procedural times and use of multiple leads; (ii) elective device replacement; and (iii) system upgrade or revision. Infection following the procedures listed under (ii) and (iii) probably results from surgical manipulation of the thick fibrotic capsule containing a dormant bacterial colonization from the previous surgery in the absence of any sign of pocket infection. This study confirmed that the above three procedures were indeed associated with a much higher incidence of infection reflecting the general belief that repeat surgery involving the device pocket carries about a five times greater incidence of infection than a new implantation. The 12 patients with systemic infection were transferred to outside centres where all the hardware was extracted. In contrast, the 18 cases of pocket infection underwent extensive surgical revision of the pocket (with debridement and capsulectomy) without the complete removal of all the hardware. The old devices were returned to the revised pocket in 10 patients and new devices were connected to the pre-existing leads in eight patients. Relapse was observed after a median of 5 months in 8 (44%) patients. Then, a new pocket revision was again performed and in three cases, complete removal of the pacing system was eventually necessary. One cannot conclude that infection was eradicated in the 10 patients who did not require a second surgical revision and in the five cases, where a second pocket revision appeared effective because the follow-up was too short. It is likely that a longer follow-up would reveal relapse in most, if not all, cases that displayed no recurrence in the setting of the incomplete hardware removal. Device infection is a potentially lethal complication of device therapy with a higher mortality if all the hardware is not removed.3–5 Conservative management with antibiotics alone or in combination with incomplete hardware removal is often not optimal. It may work in isolated cases, and device removal is almost always needed. In terms of therapy, pocket infections should not be considered as a separate entity from endovascular infection. Both represent an infected system in contact with endocardium and bloodstream. Surprisingly, the authors reported only one death in a patient with systemic infection, but it is unclear as to whether it was due to infection or a complication of lead extraction. Without longer follow-up, the zero mortality in the patients with pocket infection should not be considered as the result of successful pocket revision with the partial hardware removal. The authors justified their treatment of all cases of pocket infection with surgical revision (without complete system removal) because both participating centres were not qualified for lead extraction and the routine transfer of patients with device infection to centres with expertise in lead extraction was not possible during the study. On the other hand, they admitted that complete pacing system removal was the only effective way to eradicate device infection completely. Furthermore, they referred all patients with a systemic infection for lead extraction.1 In 2009, the Heart Rhythm Society published a document on the standard of care of device infections.5 Any infection (including erosion which must be considered as being infected by contamination) with the possible exception of an isolated Gram-negative blood culture or the infection of a superficial incision (such a stitch abscess) should be approached with: (i) complete system removal including debridement of the fibrotic capsule and infected material; (ii) use of intravenous antibiotics; and (iii) reimplantation at another site (one side to the other) at a separate surgery at a time determined by the clinical course. Non-septic cutaneous decubitus results from a disproportion between a device volume or shape and the dimension of the pocket. The continuous pressure weakens the skin layers over the device so that the pacemaker eventually migrates through the skin and becomes infected by contamination. Palmisano et al.1 observed decubitus rarely (after only 10 procedures) and acted in a timely manner to correct the problem so as to prevent device erosion with resulting infection. This complication was treated with local skin excision and pocket replacement without device removal. In one case, the surgical revision was complicated by pocket infection. Management of anticoagulation in device surgery has been a challenging clinical problem that requires balancing the risk of acute thromboembolic events with bleeding. Current guidelines still recommend suspending warfarin and using heparin-based ‘bridging’ therapy. Cessation of warfarin with bridging heparin anticoagulation is associated with a higher incidence of bleeding complications and longer hospital stay. Recent studies and a meta-analysis of related reports have shown that uninterrupted warfarin therapy during cardiac rhythm device implantation is associated with a significantly lower risk of haemorrhagic complications than heparin-based bridging therapy.6–11 Since the aim of discontinuing warfarin therapy is to reduce bleeding and haematoma formation, these findings suggest that warfarin therapy should be continued during implantation. Uninterrupted warfarin therapy with a therapeutic international normalized ratio (INR) in patients with moderate-to-high thromboembolic risk is safe, simple, helps avoid heparin (low-molecular-weight heparin) therapy and is cost effective. On the day of surgery, the INR should be <3.0 and ideally between 2 and 2.5. This approach applies to primary implantations and should not be extrapolated to patients undergoing other types of device procedures, although early experience suggests that the same approach may be applicable to CRT implantation.7 It also makes sense to use uninterrupted warfarin therapy for simple device replacement. Thus, reducing the dose of warfarin (to achieve an INR ≤ 1.6 as in this study) coupled with bridging heparin therapy (which caused the expected increase in bleeding and haematoma) in patients with a high risk of thrombo-embolic complications should no longer be considered the standard of care. The official guidelines should be upgraded to advocate uninterrupted warfarin therapy for device implantation and finally do away with the unsatisfactory practice of heparin bridging. Antiplatelet therapy with aspirin does not increase the incidence of haematoma and it can be continued perioperatively. Clopidogrel with or without aspirin is associated with an increase in bleeding and haematoma formation and should be ideally discontinued >4 days before surgery to increase the safety of the procedure because even a ‘benign’ haematoma can become infected and create a far more serious problem. In this study, clopidogrel was discontinued 3 days before surgery which was somewhat sooner than the usual recommendation of 5 days raising the possibility that the protocol might not have eliminated all antiplatelet activity. It would be interesting to analyse the incidence of bleeding in this group of patients (3 days off clopidogrel) compared with patients certain to have had no antiplatelet drug therapy. Finally, withdrawal of clopidogrel is contraindicated in patients with recent coronary or intravascular stents. Conflict of interest: none declared.