Effects of pre-, peri-, and postmyocardial infarction treatment with omapatrilat in XXXX : survival, @entity943 , ventricular function, and remodeling.

@entity35 @entity583 @entity943 @entity1184
We showed previously that the vasopeptidase inhibitor (VPI) omapatrilat improves @entity583 ( @entity583 ) survival, but the mechanisms involved and whether these effects are sustained remained to be determined, and are the subject of this study. @entity35 (n = 272) received omapatrilat (20 mg x kg-1x day-1) starting 7 days before @entity583 and continued peri- and @entity583 , or no treatment (control). One group of @entity35 had continuous ambulatory ECG and blood pressure recordings started 6 h before @entity583 and continued until 24 h after @entity583 , when survival was evaluated, and the @entity35 were killed, and @entity583 size was evaluated. A second group had left ventricular (LV) remodeling evaluated by echocardiography at 30 days and, at 38 days, had cardiac hemodynamics and morphology done and survival evaluated. Survival 24 h after @entity583 (n = 255) improved with omapatrilat (60% vs. 46% for control; P = 0.0378). Over the next 37 days, there was no further improvement with omapatrilat but the early benefit was sustained. Omapatrilat reduced @entity583 size 24 h after @entity583 (36 +/- 2 vs. 42 +/- 2 mm2 for controls; P = 0.034). Omapatrilat reduced ventricular @entity943 score 1-12 h after @entity583 . Omapatrilat decreased blood pressure, but not during the first 24 h after @entity583 . Omapatrilat reduced LV diastolic and systolic dimensions and LV and right ventricular weights compared with control large @entity583 , indicating a decrease in reactive @entity1184 . Improvement in cardiac remodeling was accompanied by improved cardiac hemodynamics. Thus this study indicates that pre-, peri-, and @entity583 treatment with the VPI omapatrilat is beneficial in survival, @entity943 , LV remodeling, and cardiac function.
