term outcome of hospital survivors was similar between groups (log-rank p=0.80). Conclusions: In our series, all three pre-transplant hemodynamic parameters reflecting PH had an additive value for prediction of early, severe RV failure and 30-day mortality. The simultaneous presence of all three risk factors was associated with unacceptably high rates of RV failure and early death. Long-term outcome of hospital survivors is not affected by baseline PH degree. 265 Primary Graft Failure in Heart Transplantation: The Need of a Working Definition J. Segovia, J.M. Barcelo, M. Gomez-Bueno, C. Garcia-Montero, C. Tellez, M. Cobo, L. Alonso-Pulpon Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain Purpose: Primary graft failure (PGF) is the leading cause of early mortality in heart transplantation (HTx). Homogeneous definition of PGF is lacking, what results in a wide range of incidence (9-25%) and mortality (13-88%). The aim of our study was to propose a specific working definition of PGF and apply it to the study of this entity in a consecutive series of 621 HTx. Methods and Materials: PGF is defined by: A) impairment of systolic graft function affecting the right, left or both ventricles, B)severe hemodynamic compromise manifested as hypotension and/or low cardiac output that requires 2 intravenous inotrope/pressors, in- cluding norepinephrine or epinephrine, or mechanical support [ei- ther intraaortic balloon (IABP) or ventricular assist device (VAD)], C) occurring in the first 24 hours after Htx, and D) without any other obvious cause of graft dysfunction. Results: PGF occurred in 56 of 621 HT, for an overall incidence of 9%. Isolated right ventricular graft failure occurred in 34 patients (60.7 %), and biventricular dysfunction in 22 patients (39.3 %). In addition to intravenous inotropic therapy, 37(66 %) patients required any type of mechanical support. Twenty-seven of 56 PGF patients (48.2%) received VAD (20 right-sided, 1 left- sided and 6 biventricular support), and 10 patients (17.8%) IABP. Early (30-day) mortality of patients with PGF was 80.4%, as compared with 9.9% in the remain- ing patients, p0.001. PGF accounted for 44.6% of all early deaths. Mortality for patients with mechanical support was 78.4%, while 19 medically treated patients showed a death rate of 84.2%, p=0.6. Long-term outcome of 11 hospital survivors was not different from the rest of the series (average annual mortality in the first 10 years 3.5% vs 3.0%, log-rank p=0.30). Conclusions: The proposed working definition of PGF was a useful, objective, interchangeable tool for the diagnosis of this syndrome. The incidence of PGF in our series was 9%. More than 60% underwent circulatory support device implantation but mortality rates were over 75% in all treatment groups. 266 Right Ventricular Dysfunction Immediately Post Transplant – A Marker for Poor Outcome? E. Shao 1 , M. Kawano 1 , N. Moradzadeh 1 , A. Ankrom 1 , K. Kiyosaki 1 , J. Patel 1 , M. Kittleson 1 , J. Moriguchi 1 , A. Ardehali 2 , J. Kobashigawa 11 David Geffen School of Medicine at UCLA, Los Angeles, CA; 2 David Geffen School of Medicine at UCLA, Los Angeles, CA Purpose: Right ventricular dysfunction (RVD) immediately post heart transplantation may be due to many causes. These include pulmonary hypertension, primary graft dysfunction, insufficient preservation, and inadequate cooling. Most patients with RVD do recover function after heart transplantation, but it is not clear as to whether their long- term survival is compromised. Methods and Materials: Between 1994 and 2008, we identified 115 patients out of 823 patients (14%) with RVD in the absence of left ventricular dysfunction. RVD was suspected by abnormal hemody- namics usually with high right atrial pressures (RAP12mmHG, mean RAP=14.6) in the presence of normal pulmonary artery systolic pressures (PAS30mmHG, mean PAS=22.8) and lower cardiac index (CI2, mean CI=1.5). RVD was then confirmed by echocardiogra- phy. All RVD was identified within the first week after transplant. The remaining 708 patients without RVD served as controls. Results: 5-year survival was significantly lower in the RVD group than the control group (70.3% vs. 78.7%, p=0.026). There was no differ- ence in 5-year freedom from cardiac allograft vasculopathy or 1-year freedom from rejection between the two groups (see table). The causes of RVD were pulmonary hypertension (65%) and primary graft failure (35%). The major causes of death were rejection (n=12), infection (n=10), and CAV (n=3) for the RVD group. Conclusions: Early RVD appears to have long ranging detrimental effects on 5 year survival. Further investigation into therapies to ameliorate this poor effect on outcome is warranted. 267 High Rates of False-Positive Hepatitis C Antibody Tests Can Occur after Left Ventricular Assist Device Implantation A.V. Srivastava 1 , B. Czerska 2 , C. Williams 2 , I. Alesh 2 , L. Krese 2 , M.A. Huang 2 , C. Drost 2 , C. Smith 2 , H. Nemeh 2 , C. Tita 2 , R. Brewer 2 , D. Lanfear 21 Yale University, School of Medicine, New Haven, CT; 2 Heart and Vascular Institute, Henry Ford Hospital, Detroit, MI Purpose: Testing for Hepatitis C is a routine part of evaluation for cardiac transplantation, and virus presence is an exclusion criteria at most centers. Left ventricular assist devices (LVAD) are often used as bridge to transplantation and are known to lead to immune activation. Methods and Materials: We collected data on consecutive patients undergoing Heartmate® LVAD implantation between 1/2006-2/2008 at a single center. Patients needed to survive to discharge and have Hepatitis C ELISA antibody tests, pre and post LVAD placement to be included. Positive Hepatitis C antibody tests led to confirmatory testing with the Radioimmunoblot assay (RIBA) and Hepatitis C RNA PCR. Results: 32 patients underwent implantation, of which 9 patients were excluded; 3 did not survive to discharge and 6 had incomplete data. Thus 23 patients made up the study cohort. 10 patients received Heartmate II and 13 patients received Heartmate XVE LVAD. All patients were Hepatitis C antibody negative prior to LVAD implanta- tion. 7 patients (30%) subsequently tested positive for Hepatitis C antibody. Ultimately, none were found to have actual Hepatitis C infection. 2 patients returned to negative serologic status upon serial testing. 5 remained continuously positive. Of these, 2 had negative Hepatitis C RIBA tests while 3 had at least one indeterminate RIBA. All 3 indeterminate RIBA tests had similar patterns; antibodies to the 5-1-1p/c100p antigen were present, but no antibodies to c33p, c22p, NS5, or hSOD were detected. No patient had detectable Hepatitis C RNA. Conclusions: About 30% of patients undergoing LVAD implantation developed false positive Hepatitis C antibody tests. Cardiac transplant The Journal of Heart and Lung Transplantation Abstracts S159 Volume 28, Number 2S