Park, Soon J.

Background: Concerns exist regarding orthotropic heart transplantation (OHT) in hepatitis C (HCV) seropositive recipients. The UNOS national registry was accessed to evaluate HCV recipient sero-positivity and outcomes. Method: Retrospective analysis of the UNOS registry (2000-2014) to evaluate recipient profile and clinical outcome of HCV sero-positive (HCV+ve) and sero-negative (HCV -ve) pts. Early and late adjusted survival and adverse events at follow-up were compared. Results: From 23,507 patients (mean age 52 yrs; 75% male), 481 (2%) were HCV +ve (mean age 52 yrs; 77% male). Annual proportion of HCV +ve recipients was comparable over the study period (range 1.3-2.7%; p=0.2). The HCV +ve cohort had more African American (22% vs 17%; p=0.01), pts with a prior LVAD (21 vs 14%; p<0.01 and more hepatitis B core Ag+ve recipients (17% vs 5%; p<0.01). However, ECMO (p=0.7), inotropic (p=0.2), and intra-aortic balloon pump (p=0.7) support, serum creatinine (p=0.7) and serum bilirubin (p=0.7) were similar. Proportion of Status 1A pts was similar (24% HCV+ vs 21% HCV -); however wait-time for HCV + recipients was longer (mean 23 vs 19 days; p<0.01). Among donor variables, age (p=0.8), hepatitis B status (p=0.4) and CDC high risk status (p=0.9) were comparable. At a median follow up of 4 years, 67.1% patients were alive, 28.4% died and 1.1% were re-transplanted (3.4% missing). Overall survival was worse in the HCV+ cohort (64.3 vs 72.9 % and 43.2 vs 55% at five and ten years; p<0.01). Late renal [OR 1.2(1-1.6); p = 0.02] and liver dysfunction [OR 4.5 (1.2-15.7); p=0.01] occur in HCV +ve recipients. On adjusted analysis, HCV sero-positivity is associated with poorer survival [HR0.6 (0.5-0.8); p<0.01]. Conclusion: A small proportion of patients receiving a heart transplant in the United States have hepatitis C. In spite of comparable pre-operative hepatic function, hepatitis C sero-positive recipients develop late liver dysfunction and have poorer long-term survival.

Renal function improves early after left ventricular assist device (LVAD) implantation but later decline has been observed. We sought to determine the occurrence and evaluate possible causes for this decline. In 62 consecutive patients with HeartMateII LVAD with available calculated glomerular filtration rate (GFR, ml/min/1.73 m2) 1 year after implant, GFR was assessed repeatedly and possible predictors for decline from 3 to 12 months were investigated. Post-mortem renal specimens for patients supported with an LVAD were evaluated. GFR 54.5 ± 19.5 at admission increased to 66.4 ± 22.3 preoperatively and to 79.2 ± 30.1 ~1 month after implantation. Subsequently at ~3 months GFR declined to 74.7 ± 25.4, at ~6 months to 68.8 ± 23.1, and ~1 year after implant to 63.9 ± 17.7. Glomerular filtration rate at 1 year was significantly lower (p < 0.0001, p < 0.0001, p = 0.005) than GFR 1, 3, and 6 months after implant. Early rise in GFR after surgery was not associated with late decline. Shorter bypass time (β = −0.09, p = 0.048) and higher albumin 3 months after LVAD (β = 14.4, p = 0.025) were significantly associated with less later decline in GFR. Arteriosclerosis was identified in autopsy renal specimens. In conclusion, early gains in renal function after LVAD implant are not sustained in many patients. Patient, device, and operative factors may influence long-term renal function in these patients.

BackgroundMost 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.MethodsWe 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.ResultsOf 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.ConclusionPatients 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.