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Purpose Heart failure (HF) patients often have comorbid conditions that confound management and adversely affect prognosis. The purpose of this study was to determine whether the obesity paradox is also present in hospitalized HF patients in an integrated healthcare system. Data sources A cohort of 2707 patients with a primary diagnosis of HF was identified within an integrated, 20‐hospital healthcare system. Patients were identified by ICD‐9 codes or a left ventricular ejection fraction ≤40% dating back to 1995. Body mass index (BMI) was calculated using the first measured height and weight when hospitalized with HF. Survival rates were calculated using Kaplan Meier estimation. Hazard ratios for 3‐year mortality with 95% confidence intervals were assessed using Cox regression, controlling for age, gender, and severity of illness at time of diagnosis. Conclusions Three‐year survival rates paradoxically improved for patients with increasing BMI. Survival rates for the larger three BMI quartiles were significantly better than for the lowest quartile after adjusting for severity of illness, age, and gender. Implications for practice While obesity increases the risk of developing HF approximately twofold, reports involving stable outpatients suggest that obesity is associated with improved survival after the development of HF. This finding is paradoxical because obesity increases the risk and worsens the prognosis of other cardiovascular diseases.

The use of continuous-flow left ventricular assist devices (LVAD) have markedly improved outcomes in patients with advanced heart failure (HF). The HeartWare LVAD is a miniaturized centrifugal pump implanted within the pericardial space. Implantable cardioverter-defibrillators (ICDs) are susceptible to oversensing of extracardiac signals (electromagnetic interference [EMI]). We report two cases of EMI in patients that received a HeartWare LVAD as destination therapy for advanced HF. The patients were 75 and 78 years old, both with severe ischemic dilated cardiomyopathy (ejection fraction < 0.20) and New York Heart Association class 4 heart failure. Both patients had a St. Jude Medical Unify ICD with a 7 Fr dual coil St. Jude Medical Durata ICD lead. In both patients, the lead location was in the right ventricular apex with an inferior orientation. Both patients experienced immediate ICD therapies after LVAD placement, requiring the tachytherapies to be disabled. ICD programming changes to increase sensitivity and the detection windows were ineffective. Both patients underwent ICD system revision. In one patient, the existing lead was moved to an anteroseptal location that stopped the EMI. In the other patient, the ICD system was changed to allow a separate right ventricular sensing lead in an anteroseptal location and a dual coil ICD lead placed in an apical location, a strategy used to obtain an acceptable defibrillation threshold. The patients have had no subsequent EMI detected on clinical and remote monitoring. Patients with a right ventricular apical ICD lead placement that undergo placement of a HeartWare LVAD are susceptible to EMI and inappropriate ICD therapies. These cases suggest the primary mechanism is proximity of the ICD lead to the device and as such relocation to an anteroseptal location can overcome the problem. These data suggest that all patients that receive a HeartWare LVAD with an ICD should have the device carefully checked at maximum LVAD output to determine if EMI may be present. ASAIO Journal 2013;59:136-139. Key Words: left ventricular assist device, electromagnetic interference, improper ICD shocks, end-stage heart failure.

Methods: Over a 45-month period 125 LTx were performed in this centre. CMV serostatus of donor (D) and recipient (R) was determined at time of transplant. CMV mismatches (MMϭDϩR-) received 3 months prophylaxis with oral ganciclovir (GCV). CMV positive recipients (CMVϩ) were followed up with weekly quantitative CMV-PCR, but received no prophylaxis. CMV DϪ/RϪ LTx served as control group. All patients were followed with sequential lung function testing and surveillance bronchoscopy to identify infection and episodes of acute rejection. Results: Over a study period of 10 -54 months, 25 patients developed BOS according to the ISHLT criteria. Of 31 MM recipients, three developed BOS, one of which had CMV disease. Of 49 CMVϩ recipients, eight developed BOS, two of whom had CMV disease. Of the 45 CMV DϪ/RϪ group, none had evidence of CMV disease or infection. 14 patients in this group developed BOS, a significantly higher incidence compared to the other groups (pϽ0.05) using Fisher's exact test. Conclusions: In our series CMV-viraemia does not appear to be associated with BOS. Indeed, surprisingly the highest incidence of BOS occurred in what is generally considered the lowest risk group. The incidence of BOS was not affected by GCV treatment, acute rejection episodes or bacterial infection. The low incidence of CMV disease might be explained by our CMV protocol: only MM LTx receive GCV prophylaxis, but we also perform QPCR surveillance for IgGϩ LTx (since 2000) and introduced a viral load cut-off of Ͼ1.0x10 4 copies/ml for commencing pre-emptive therapy (GCV for 2/52) in 2001. 383Baseline values are given in parentheses.