Single Versus Multidrug Regimen for Surgical Infection Prophylaxis in Left Ventricular Assist Device Implantation.

Infection is a serious complication of left ventricular assist device (LVAD) therapy. However, an optimal antimicrobial surgical infection prophylaxis (SIP) regimen for LVAD implantation is not well established. We retrospectively reviewed all adults who underwent continuous-flow LVAD implantation from February 2007 to March 2015 at Mayo Clinic Rochester. Left ventricular assist device infection (LVADI) was defined using criteria published by the International Society for Heart and Lung Transplant. Patients excluded from the analysis included those who did not have HeartMate II or HeartWare device, patients with incomplete documentation of SIP, and those with an actively treated infection at the time of LVAD implantation. We compared risk of LVAD-specific and LVAD-related infections and all-cause mortality between SIP regimens at postoperative day 90 and 1 year using Kaplan-Meier time-to-event analyses. During study period, 239 adults underwent continuous-flow LVAD implantation at our institution where 199 patients received single-drug and 40 received multidrug SIP regimen. Median patient age was 62 years. Left ventricular assist device infection occurred in three patients (1.5%) in the single-drug group versus two patients (5.0%) in the multidrug group at 90 days (p = 0.4). There was no difference in infection-free (p = 0.4) and overall survival (p = 0.9) between two groups at 1 year. In conclusion, there was no clear benefit of using multidrug regimen as it did not impact infection-free survival or all-cause mortality compared with single-drug regimen. Prospective clinical trials are needed to further define the optimal SIP regimen for LVAD implantation.

Cardiovascular implantable electronic device infections in left ventricular assist device recipients.

BACKGROUND: Most patients with left ventricular assist devices (LVADs) have concomitant cardiovascular implantable electronic devices (CIEDs). However, clinical presentation and outcome of CIED infection in the setting of LVAD has not been previously described. METHODS: We retrospectively reviewed 247 patients who underwent LVAD implantation at Mayo Clinic campuses in Minnesota, Arizona, and Florida, from January 2005 to December 2011. Demographic and clinical data of patients who met criteria for CIED infection were extracted. RESULTS: Of 247 patients with LVADs, 215 (87%) had CIED at the time of LVAD implantation and six (2.8%) subsequently developed CIED infections. Three patients developed CIED lead-related endocarditis and the other three had pocket infection. All three instances of CIED pocket infection were preceded by device generator exchange, whereas all three patients with CIED lead-related endocarditis had prior LVAD-related infections. Causative pathogens included Pseudomonas aeruginos (1), coagulase-negative staphylococci (2), methicillin-resistant Staphylococcus aureus (1), a gram-positive bacillus (1), and culture negative (2). All patients underwent complete CIED removal along with antimicrobial therapy. The three patients with CIED lead-related endocarditis and prior LVAD infections received chronic suppressive antibiotic therapy, and one patient had LVAD exchange. All but one remained alive at the last follow-up with a median duration of 15 months (7-46 months) from the time of CIED infection. CONCLUSION: Patients who are receiving LVAD therapy and develop CIED infection should be managed with complete CIED removal. Chronic suppressive antibiotic therapy is warranted in cases that have concomitant LVAD infection.

Methicillin-susceptible Staphylococcus aureus endocarditis isolates are associated with clonal complex 30 genotype and a distinct repertoire of enterotoxins and adhesins.

BACKGROUND: Using multinational collections of methicillin-susceptible Staphylococcus aureus (MSSA) isolates from infective endocarditis (IE) and soft tissue infections (STIs), we sought to (1) validate the finding that S. aureus in clonal complex (CC) 30 is associated with hematogenous complications and (2) test the hypothesis that specific genetic characteristics in S. aureus are associated with infection severity. METHODS: IE and STI isolates from 2 cohorts were frequency matched by geographic origin. Isolates underwent spa typing to infer CC and multiplex polymerase chain reaction for presence of virulence genes. RESULTS: 114 isolate pairs were genotyped. IE isolates were more likely to be CC30 (19.5% vs 6.2%; P = .005) and to contain 3 adhesins (clfB, cna, map/eap; P < .0001 for all) and 5 enterotoxins (tst, sea, sed, see, and sei; P ≤ .005 for all). CC30 isolates were more likely to contain cna, tst, sea, see, seg, and chp (P < .05 for all). CONCLUSIONS: MSSA IE isolates were significantly more likely to be CC30 and to possess a distinct repertoire of virulence genes than MSSA STI isolates from the same region. The genetic basis of this association requires further study.