189 Regulation of the Mitochondrial Proteins Mitofilin and Porin in Explanted Failing Human Hearts R.C. Gupta, S. Rastogi, M. Wang, P. Mohyi, H. N. Sabbah. Medicine, Henry Ford Hospital, Detroit, MI. Purpose: The concept that the failing heart is energy starved is supported by observations of abnormal energy production by the mitochondria respi- ratory chain. We previously showed that the physiologic processes of mitochondria biogenesis, fission and fusion are abnormal in the failing human heart and give rise to mitochondria hyperplasia, reduced organelle size and poor respiration. This study examined the regulation of two key mitochondrial proteins; porin (PO), the outer membrane protein that forms the aqueous channel for metabolite flux between mitochondria and cytosol, and mitofilin (MF), a critical organizer of mitochondria cristae morphology and thus indispensible for normal mitochondrial function. Methods and Materials: Studies were performed in LV tissue homoge- nate obtained from 6 normal (NL) donor human hearts, 6 explanted failing human hearts with dilated cardiomyopathy (DCM) and 6 explanted failing human hearts with ischemic cardiomyopathy (ICM). Protein expression of PO, MF and glyceraldehyde 3-phosphate dehydrogenase (GAPDH), a housekeeping protein, was measured with specific antibodies and Western blotting and bands quantified in densitometric units (du). Results: Compared to NL donor hearts, MF was significantly reduced in ICM and DCM hearts while expression of PO and GAPDH were un- changed (Table). Protein Expression in LV Myocardium NL-Donor DCM ICM PO (du) 0.40  0.03 0.40  0.02 0.41  0.02 MF (du) 0.43  0.03 0.20  0.01* 0.17  0.01* GAPDH (du) 1.63  0.02 1.61  0.03 1.62  0.03 PO/GAPDH 0.24  0.02 0.25  0.01 0.25  0.01 MF/GAPDH 0.26  0.02 0.12  0.01* 0.10  0.01* *p0.05 vs, NL-Donor. Conclusions: Downregulation of the key mitochondrial protein MF in LV myocardium of failing human hearts provides support to the concept of energy deprivation in heart failure and emphasizes the need for the devel- opment of therapeutics that target this critical abnormality. 190 Local Expression of Myocardial Galectin-3 Does Not Correlate with Its Serum Levels in Patients Undergoing Heart Transplantation A. Beiras-Fernandez, 1 J. Rothkopf, 2 S. Reinwand, 3 I. Kaczmarek, 2 S. Kreth, 3 F. Weis. 31 Thoracic and Cardiovascular Surgery, JW Goethe University, Frankfurt, Germany; 2 Cardiac Surgery, LM-University, Munich, Germany; 3 Anesthesiology, LM-University, Munich, Germany. Purpose: Galectins are a family of soluble lectins expressed on a variety of tissues that play many important regulatory roles in inflammation, immu- nity, and cancer. The up-regulation of galectin-3 in hypertrophied hearts, and the development of fibrosis have been shown in experimental studies. Increased galectin-3 levels are associated with poor long-term survival in chronic heart failure (CHF). We examined the relationship between plasma galectin-3 levels and the myocardial tissue expression of galectin-3 in patients with end-stage CHF. Methods and Materials: Expression of Galectin-3 was assessed by means of real-time PCR on left ventricle and atrial myocardium of patients (n12) with CHF undergoing heart transplantation. All patients gave informed consent. A control group consisting of left ventricle (n5) and right atrium (n5) muscle biopsies from patients with good ejection fraction (EF  65%) was designed. Serum expression of Galectin-3 was assessed by means of ELISA in serum from 20 patients in end-stage CHF and in 20 healthy volunteers, who served as control. Results: Expression of Galectin-3 was similar in the myocardium of pa- tients in comparison to the control group independently of the anatomical area (CHF vs. healthy ventricle: 1.73E-02 vs. 1.50 E-02; CHF vs. healthy atrium: 1.32E-02 vs. 1.16E-02). However, serum expression of Galectin-3 was significantly higher in the end-stage CHF patients compared to the healthy controls (13.02  10.6 vs. 3.7  1.3 ng/ml; p0.05). Conclusions: Plasma galectin-3 levels correlate with the ejection fraction and are elevated in patients with CHF. However, the myocardial expression of Galectin-3 does not correlate with the ventricular ejection fraction.Our data support the use of Galectin-3 as a marker of heart insufficiency, though the therapeutic potential of Galectin-3 in the treatment of heart failure may be limited. 191 Modulation of the Myocardial Expression of Neuregulin-1 and Its Receptor ErbB4 in Patients with Chronic Heart Failure J. Rothkopf, 1 F. Weis, 2 I. Kaczmarek, 1 S. Kreth, 2 A. Beiras-Fernandez. 3 1 Cardiac Surgery, LM-University of Munich, Munich, Germany; 2 Anesthesiology, LM-University of Munich, Munich, Germany; 3 JW- Goethe University, Frankfurt, Germany. Purpose: Neuregulin-1 (NRG-1) is a cardioactive paracrine growth factor released by microvascular endothelial cells that has cardioprotective effects in animal models of heart failure. ErbB4 is a member of the ErbB family that serve as receptor for NRG-1. Administration of NRG-1 has been shown to improve LV function in chronic heart failure (CHF) experimental models. Our aim was to determine whether CHF is associated with changes in expression and distribution of NRG-1 and its receptor erbB4 in human myocardium. Methods and Materials: Expression of Neuregulin-1 and its receptor ErbB4 was assessed by means of real-time PCR on left ventricle and atrial myocardium of patients with CHF undergoing heart transplantation (n12). All patients gave informed consent. Biopsies (n 40) of the explanted hearts were obtained and divided according to the anatomical origin (Left Ventricle, Atrium). A control group consisting of left ventricle (n5) and right atrium (n5) muscle biopsies from patients with good ejection fraction (EF  65%) was designed. Results: Expression of ErbB4 was significantly down-regulated in the left ventricle of patients in comparison to the control group and up-regulated in atrium (CHF vs. healthy ventricle: 8.66E-05 vs. 3.35E-04; CHF vs. healthy atrium: 1.20E-04 vs. 6.20E-05). Expression of Neuregulin-1 was signifi- cantly up-regulated in the left ventricle and in both left and right atrium of patients in comparison to the control group (CHF vs. healthy ventricle: 2.4E-04 vs. 2.45E-05; CHF vs. healthy atrium: 5.34E-04 vs. 2.83E-04). Conclusions: Neuregulin-1 and its receptor ErbB4 show different expres- sion patterns in patients with end-stage CHF and in patients with conserved EF. Reduced heart function originated a higher expression of Neuregulin-1 in cardiomyocytes and a decrease on the expression of ErbB4. Our results confirm the modulation of the NRG-1/ErbB4 signalling in human heart failure. 192 Safety and Efficacy of Ixmyelocel-T, an Expanded Patient-Specific Mixed Cell Product, in Dilated Cardiomyopathy (IMPACT-DCM) R.R. Bunge, 1 A.N. Patel, 2 B.L. Hamman, 4 O.M. Lattouf, 3 N.G. Smedira, 5 R.L. Bartel, 6 S. Watling, 6 B.A. Bruckner. 11 Cardiovascular Surgery, The Methodist Hospital DeBakey Heart & Vascular Center, Houston, TX; 2 Cardiothoracic Surgery, University of Utah, Salt Lake City, UT; 3 Cardiothoracic Surgery, Emory Crawford Long Hospital, Atlanta, GA; 4 Cardiothoracic Surgery, Baylor University Medical Center, Dallas, TX; 5 Thoracic and Cardiovascular Surgery, Cleveland Clinic Foundation, Cleveland, OH; 6 Aastrom Biosciences Inc., Ann Arbor, MI. Purpose: Intramyocardial injection of ixmyelocel-T was assessed in pa- tients with ischemic dilated cardiomyopathy (IDCM) and non-ischemic dilated cardiomyopathy (NIDCM) in IMPACT-DCM, a Phase 2 trial. The objectives included: (1) safety and tolerance of ixmyelocel-T; and (2) preliminary signals of efficacy via symptomatic, functional and structural assessments. Methods and Materials: Forty patients diagnosed with IDCM or NIDCM, NYHA Class III/IV heart failure and an overall mean left ventricular ejection fraction (LVEF) of 30% and with no treatment options were enrolled. Patients were randomized to either a single administration of S72 The Journal of Heart and Lung Transplantation, Vol 31, No 4S, April 2012