Author + information
- Hemal M. Nayak, MD∗ ()
- Department of Medicine, Section of Cardiology, Center for Arrhythmia Care, University of Chicago Medicine, Chicago, Illinois
- ↵∗Reprint requests and correspondence:
Dr. Hemal M. Nayak, Center for Arrhythmia Care, University of Chicago Medicine, 5841 South Maryland Avenue, MC 9024, Chicago, Illinois 60637.
- cardiac implantable electronic devices
- transvenous lead extraction
The rate of cardiac implantable electronic device (CIED) infection is outpacing the rate of implantation of these specialized devices (1). CIED infection is a serious condition that carries a high morbidity and mortality and is a significant cost burden to our health care system (2). Early recognition, antimicrobial therapy, and total system removal are the mainstays of therapy. Understanding the microbiology of CIED infection is important in correctly choosing the right antimicrobial agent and potentially offering earlier intervention.
In this issue of JACC: Clinical Electrophysiology, Hussein et al. (3) present the microbiological findings from a contemporary cohort of patients with CIED infection. A total of 816 patients, with confirmed CIED infection undergoing extraction between the years 2000 to 2011, comprised the study group. Patients were categorized into 2 groups: those with early versus late infection (defined as >1 year after pocket intervention). Patients were also characterized as having pocket or endovascular CIED infection. First, this is the largest series of patients with CIED infection reported. Second, patients were evaluated and cared for by electrophysiologists as well as infectious disease specialists. Involving infectious disease specialists in the care of these patients is particularly important in determining the selection and duration of intravenous antimicrobial therapy and the timing of transition to oral agents.
To determine the causative organism, blood cultures were obtained in all patients before extraction. Pocket swabs were sent when purulence was seen. The capsule was excised and lead tips and any attached fibrotic tissue were sent for culture. The authors did not send the explanted generators for culture, and instead, returned them to the manufacturer for quality assessment. Sending all infected tissue and hardware for culture is paramount in identifying the causative organism and is a class 1C recommendation in the most recent American Heart Association scientific statement on CIED infection and management (4). But because complete capsule excision is not uniformly done in the community as it was in this study, sending the generator (which has a large surface area) for culture is also recommended.
Despite a fairly extensive effort to determine the culprit organism, pathogens were identified in approximately 87% of patients. This left 13% with “culture-negative” infections and is higher than what has previously been reported in the published data (5). One possible explanation may have been antibiotic use before collection of blood cultures or empiric treatment with antibiotics in patients with subtle signs of CIED infection.
Staphylococcal species accounted for 68% of CIED infections and is consistent with previous reports in the published data (4). The most important finding in this study is the fact that methicillin-resistant staphylococci (MRS) were pathogens in 33.8% of all CIED infections and accounted for close to 50% of all staphylococcal infections. Additionally, 15% of CIED infections were due to methicillin-resistant Staphylococcus aureus. Although this may not seem surprising because of the nearly epidemic nature of MRS infection in the United States (6), it represents an 8-fold increase from what has previously been reported (5) and confirms findings from more recent, smaller retrospective studies (7).
Because CIED infection is associated with significant mortality, up to 18% in some studies of treated patients (2), recognition that MRS is the likely pathogen in a third of all CIED infections, necessitates the use of antibiotics such as vancomycin or daptomycin as first-line agents. This is particularly crucial for patients with Staphylococcus aureus bacteremia because of its high mortality in older patients (8). These antibiotics should be selected over traditional β-lactam agents (9). Antibiotic therapy can then be tailored on the basis of culture results.
Another important finding is that 50% of pocket infections occurred late or a full year after pocket manipulation and most were due to coagulase-negative staphylococci (CoNS). Unlike infections due to staphylococcus aureus, infections due to CoNS are more indolent and present with subtler findings. This suggests that CoNS infections were likely acquired during pocket intervention.
And finally, another important observation was that 22% of patients with endovascular infection had concomitant infections (abscesses at other sites, osteomyelitis) making the often exhaustive search for a source even more compelling.
One limitation of this study is that microbiological data were only obtained from patients with CIED infection who underwent extraction. Although system removal is recommended when at all possible, there likely were some patients with severe comorbidities who were deemed too high risk and not even referred. A number of these patients likely died before extraction was performed or even contemplated. One wonders whether these patients might have had even more virulent organisms including those that would have failed vancomycin therapy.
Notably, infections involving subcutaneous defibrillators were not included in this analysis though it is very probable that the vast majority of these infections would be due to staphylococcal species as well.
Another limitation is that data were derived from a single institution. More centers should report their experience with CIED infection and certainly more knowledge is needed concerning the duration of antibiotic therapy, incidence of antibiotic failure, clinical outcome after extraction, and best practices involving reimplantation.
Despite these limitations, Hussein et al. (3) should be commended in reporting their large experience and reiterating the importance of rising antibiotic resistance in CIED infection.
↵∗ Editorials published in JACC: Clinical Electrophysiology reflect the views of the authors and do not necessarily represent the views of JACC: Clinical Electrophysiology or the American College of Cardiology.
Dr. Nayak has reported that he has no relationships relevant to the contents of this paper to disclose.
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