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Background: Listing status for heart transplantation (Tx) patients was changed in 1999 from Status 1 and 2 to Status 1A, 1B and 2. Because the selection process was modified in favor of seriously ill patients, it was not clear whether this change would affect survival or other aspects of transplant management. Methods: We examined outcomes in 551 patients transplanted at our institution between 1986 and 2002 (pre-1999: n = 419; post-1999: n = 132) to determine the effects of change in listing protocol on transplant outcome. Results: Using Cox proportional hazard analysis, survival was not different between pre-1999 (pre) and post-1999 (post). Overall waiting-list times were longer post-1999 (pre: 134 ± 10.5 days, post: 172 ± 15.6 days; p = 0.044), and were longer post-1999 for blood groups A (177 vs 123 days), B (96 vs 84 days) and O (229 vs 172 days), but were shorter post for blood group AB (42 vs 68 days). Survival was not affected by age (pre: 53.7 ± 0.52 years, post: 53.1 ± 1.04 years; hazard ratio [HR] 1.00; 95% confidence interval [CI] 0.996 to 1.023; p = 0.181), male gender (HR 1.132; 95% CI 0.822 to 1.56; p = 0.447) or waiting-list time. Serum creatinine was similar between the 2 groups (pre: 1.25 ± 0.02, post: 1.26 ± 0.04; p = 0.794), whereas pulmonary artery (PA) diastolic pressure was increased post-1999 (pre: 24.9 ± 0.46, post: 27.0 ± 0.74; p = 0.023). Survival was not affected by PA pressure (HR 1.00; 95% CI 0.986 to 1.014; p = 0.976), but an elevated pre-transplant creatinine reduced survival (HR 1.484; 95% CI 1.139 to 1.933; p = 0.003). Conclusions: The change in listing status implemented in 1999 caused an increase in wait times for patients with blood types A, B and O, and shortened wait time for type AB; however, no differences occurred in overall post-transplant survival after the change in listing protocol. Age, gender and PA pressure had no effect on survival in either time period, whereas pre-transplant serum creatinine decreased survival in both patient groups. [Copyright &y& Elsevier]

Background: Thrombin potently activates platelets via interaction with the protease-activated receptor 1. SCH 530348 is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin via antagonism of the protease-activated receptor 1. Because SCH 530348 does not interfere with other pathways for hemostasis, it is possible that SCH 530348 reduces thrombosis with less increase in bleeding than do other potent antiplatelet agents., Study Design: TRA 2 degrees P-TIMI 50 is a phase III, randomized, double-blind, placebo-controlled, multinational clinical trial designed to evaluate the efficacy and safety of SCH 530348 during long-term treatment of patients with established atherosclerotic disease receiving standard therapy (up to 27,000). Eligible patients with a history of myocardial infarction, ischemic stroke, or peripheral arterial disease are randomized 1:1 to SCH 530348 2.5 mg daily or matched placebo until the end of study. Randomization is stratified by the qualifying disease and planned use of a thienopyridine. The primary end point is the composite of cardiovascular death, myocardial infarction, stroke, or urgent coronary revascularization. The major secondary end point is the composite of cardiovascular death, myocardial infarction, or stroke. The evaluation of long-term safety includes bleeding defined by the GUSTO and TIMI criteria. Recruitment began in September 2007. The trial will continue until 2,279 primary end points and 1,400 secondary end points are recorded with expected completion in 36 to 44 months from first enrollment., Conclusions: TRA 2 degrees P-TIMI 50 is evaluating whether a new approach to platelet inhibition via interruption of thrombin-mediated platelet activation reduces major cardiovascular events with a favorable safety profile in patients with established atherosclerosis.