BARK1 were determined by quantitative RT-PCR and imuno- histochemical analysis in each group. Results: The results at 120 minutes of reperfusion are described in the table. BARK1 B2AR Failing Control LVPDP(%) 50  6* 89  5** 63  6 84  4 CF(%) 78  4 90  4 87  3 80  3 Data = Mean  SEM. Pretreatment values were defined as 100%. LVPDP = Left ventricular peak developed pressure, CF = Coronary flow, *p  0.05 compared to Failing. **p  0.05 compared to Control, ANOVA post hoc Tukey. In summary, B2AR overexpression restored the myoprotective effects of IPC in failing hearts, and BARK1 abolished the myoprotective effects of IPC in normal hearts. Conclusion: These data indicate that BAR signal transduction pathway may be involved in IPC mechanisms and that B2AR gene transfer is effective in restoring the myoprotective effects of IPC in the failing hearts. 289 THE EFFECT OF OPEN LABEL UT15 OR BOSENTAN ON HOSPITALISATION DAYS IN PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION (PAH) A.M. Keogh, K.M. Brown, C.A. Corrigan, C. Allada, Y. Ten, St. Vincent’s Hospital, Sydney, Australia Two novel therapies, bosentan (endothelin antagonist) and UT15 (prostacycline analogue), have been shown in random- ised trials to be efficacious in patients with PAH of varying etiologies. Following end of randomised trial, 49 Class III-IV patients (bosentan n=12 and UT15 n=37), were entered to open label therapy at a single centre and survived to followup 30 Sept 2001, allowing comparison of the effect of these two therapies on hospitalisation. Etiology of PAH was primary (24), scleroderma/SLE (7), Eisenmengers (7), embolic (7) and other (4). There were 29 females, 20 males: mean age at start of open label drug 4916 years. Mean time from symptoms to diagnosis was 1517 months for bosentan, and 3398 months for UT15, reflecting the inclusion of Eisenmengers in the UT15, but not bosentan trial. Hospitalisation days, adjusted for months of followup were compared for the time from symptom onset to start open label drug, and from start open label drug to the followup date. Results: Time from symptom onset to start drug was shorter for bosentan than UT15 (4640 months vs 78122 months, p0.05), and time on drug to followup was also shorter (6.50.5 months vs 15.97.2 months, p0.001). When hospital days were adjusted for duration of disease, the mean total days/month for the index disease before and after start open label bosentan were 0.186 and 0.051 (76% reduction), and for UT15 0.146 and 0.182 (25% increase). For all cause hospitalisation, including index disease, but also ulceration and amputation, mean total hospital days/ month before and after start open label bosentan were 0.188 and 0.064 (66% reduction), and for UT15 0.207 vs 0.321 (55% increase). In addition, 17% of bosentan and 70% of UT15 patients were admitted to commence drug, resulting in trial-related hospital days of 0.581.38 vs 2.542.08, p=0.0044 respectively. Conclusions: Bosentan, but not UT15, appears to reduce time- adjusted hospitalisation rates in patients with PAH, both for the index disease and for inter-related causes. 290 CORRELATIONS BETWEEN BASIC FIBROBLAST GROWTH FACTOR (bFGF), VASCULAR ENDOTHELIAL GROWTH FACTOR (VEGF), AND CLINICAL FEATURES OF PULMONARY ARTERIAL HYPERTENSION (PAH) J.D. Rich, 1 J. Benisty, 2 V.V. McLaughlin, 1 J. Folkman, 2 S. Rich, 1 1 Rush Heart Institute, Rush-Presbyterian-St. Lukes Medical Center, Chicago, IL; 2 Harvard Childrens Hospital, Boston, MA PAH is the result of abnormal pulmonary vascular growth. Elevations in bFGF and VEGF have been noted in animal models, but growth factors that cause PAH in humans are unknown. We measured serum and urine bFGF and VEGF in 76 stable pts with PAH (primary pulmonary hypertension (PPH)=51, collagen vascular disease (CVD)=15, congenital heart disease (CHD)=10), and 10 controls. Growth factors were correlated against age, gender, etiology, NYHA Functional Class, current medications, and hemodynamics. Results: Pts with PAH had significant elevations in serum bFGF (6.914.1 vs. 0.530.7 ng/ml) and VEGF (72.916.6 vs. 21.92.5 pg/ml) from controls (p0.01). There were differences in bFGF levels based on etiology (PPH=8.9, CHD=3.9, CVD=1.9) (p0.01) (Figure), with highest levels in pts with the highest PA pressures (p=0.04). Elevations in VEGF were con- fined to those with PPH (PPH=92.8, CHD=27.1, CVD=37.4) (p0.01), with the highest values in pts with the lowest cardiac outputs (p=0.05). Urinary bFGF and VEGF were elevated only in pts with PPH, and correlated poorly with serum levels. Conclusion: bFGF may play an important role in the myointimal proliferation noted in PAH. In contrast, VEGF, which has been associated with plexiform lesions in PPH, may increase as a result of localized angiogenesis in response to tissue hypoxia. The molecular pathways responsible for PPH appears to differ from those in other forms of PAH. 291 HOW TO IMPROVE PREDICTION OF WAITING LIST MORTALITY IN HEART TRANSPLANT CANDIDATES? J.M. Smits, 1 M.C. Deng, 2 J. De Meester, 3 M. Hummel, 4 F. Schoendube, 5 H.H. Scheld, 5 H.C. van Houwelingen, 6 1 Eurotransplant, Leiden, Netherlands; 2 Columbia University, New York, NY; 3 Onze Lieve Vrouw Clinic, Aalst, Belgium; 4 Berlin Heart Center, Berlin, Germany; 5 University Hospital, University of Muenster, Muenster, Germany; 6 LUMC The Journal of Heart and Lung Transplantation Abstracts 159 Volume 21, Number 1