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Background Left ventricular assist devices are increasingly being used in patients with advanced heart failure as both destination therapy and bridge to transplant. We aimed to identify histomorphometric, structural and inflammatory changes after pulsatile- and continuous-flow left ventricular assist device placement. Methods Clinical and echocardiographic data were collected from medical records. Aortic wall diameter, cellularity and inflammation were assessed by immunohistochemistry on aortic tissue collected at left ventricular assist device placement and at explantation during heart transplantation. Expression of adhesion molecules was quantified by Western blot. Results Decellularization of the aortic tunica media was observed in patients receiving continuous-flow support. Both device types showed an increased inflammatory response after left ventricular assist device placement with variable T-cell and macrophage accumulations and increased expression of vascular E-selectin, ICAM and VCAM in the aortic wall. Conclusions Left ventricular assist device implantation is associated with distinct vascular derangements with development of vascular inflammation. These changes are pronounced in patients on continuous-flow left ventricular assist and associated with aortic media decellularization. The present findings help to explain the progressive aortic root dilation and vascular dysfunction in patients after continuous-flow device placement.

Purpose Galectin-3 (gal-3) is a novel biomarker implicated in cardiac fibrosis and is shown to correlate with the severity of heart failure (HF) and to independently predict mortality in HF. We investigated if hemodynamic improvement after left ventricular assist device (LVAD) implantation affects gal-3 levels. Methods and Materials Plasma samples were acquired from patients at time of LVAD implantation (HMII or Heartware, n=57), at 3 (n=17) and 6 months post-LVAD (n=14), and at explantation (n=23), as well as from healthy age and gender matched controls (n=30). Gal-3 was measured using a commercially available ELISA assay (BG Medicine, Waltham, MA). Data was analyzed with Prism 5. Events rates were calculated using the Kaplan-Meier method. Results At time of LVAD implantation, HF patients had significantly higher gal-3 levels compared to controls (29.2±14 ng/ml vs. 13±9 ng/ml; p figure 1 ] Conclusions Gal-3 levels are associated with HF state and predict survival on LVAD support. Distinct dynamics in gal-3 levels occur in patients following LVAD implantation with an initial decrease but subsequent increase. Gal-3 may serve as a new biomarker for risk assessment of patients before LVAD implantation.

Purpose Liver abnormalities have prognostic impact on the outcome of patients with advanced heart failure.We evaluated the Model of End-stage Liver Disease (MELD) score and its modified versions, established measures of liver dysfunction, as a tool to evaluate HTx urgency in ambulatory HF patients. Methods and Materials We retrospectively evaluated 343 patients undergoing HTx evaluation between 2005 and 2009. The prognostic effectiveness of MELD/MELDNa/MELD-XI for endpoint events defined as death/HTx/ventricular assist device (VAD) requirement was evaluated in our cohort and in subgroups of patients on and off oral anticoagulation. Results The MELD and MELDNa score were excellent predictors for 1 year endpoint events (AUC: 0.71 and 0.73, respectively). High scores (>12) were strongly associated with poor survival at one year (MELD: 69.3% vs. 90.4%, p Conclusions Assessment of liver dysfunction using the MELD scoring system provides additional risk information in patients with ambulatory heart failure.

judged as signs of possible LVAD indication. Lastly, in-hospital and 1-year outcome was analyzed and compared with outcome of LVAD implanted from 2007 to 2010 (C-LVAD). Results: 1244 pts were hospitalized for HF in one year. 191 were excluded due to age and 270 for other causes. 59 out of the remaining 783 pts had LVEF 0.35 and received inotropes, but only 38 (3%) were considered appropriate potential LVAD candidates after hospital chart review. Inhospital mortality was 5/38 (13%). Within 1-year, 8 pts underwent to heart transplant and 3 to LVAD with 10 surviving; 8/16 (50%) of medically managed pts died. In-hospital mortality after 2007-2010 C-LVAD implantation was 5/27 (18.5%). In 1-year, 3 pts were transplanted and only 1/20 pts remaining on LVAD died. Conclusions: Pts with HF characterized by low LVEF and the need for inotropes have a poor 1-year prognosis on medical therapy and would probably benefit from LVAD. The proportion of pts potentially candidates for LVAD is low with respect to the total population of HF, but the absolute number is high due to the prevalence of this syndrome.