Effect of @entity4688 on ventricular remodeling and function during healing after @entity583 in the XXXX .

@entity4688 @entity235 @entity2814 @entity1184 @entity3371 @entity2554 @entity1188 @entity720 @entity439 @entity583 @entity67 @entity121
BACKGROUND: Ventricular remodeling after @entity583 involves changes in ventricular size, shape, structure, and matrix that impact on function. Prolonged @entity2814 inhibition after @entity1188 with @entity3371 reduces @entity67 and improves clinical outcome, but whether @entity4688 produces similar benefits is controversial. METHODS AND RESULTS: The effect of @entity4688 during healing between 1 day and 6 weeks after @entity583 on in vivo changes in ventricular size, shape, mass, and function (asynergy, or akinesis and dyskinesis, and ejection fraction), as determined by serial two-dimensional echocardiography, hemodynamics, postmortem topography (planimetered short- and long-axis ventricular contours), and collagen content (determined by levels of @entity720 , a marker for collagen), was measured in 25 instrumented @entity235 . The @entity235 were randomized 1 day after left anterior descending coronary artery ligation to a control group (no treatment) and a group receiving oral @entity4688 (2.5 mg BID). Compared with no treatment, @entity4688 produced a sustained lowering of left atrial pressure but no difference in heart rate and mean blood pressure over the 6 weeks. Also compared with no treatment, @entity4688 modified in vivo remodeling parameters between 1 day and 6 weeks, with less elongation of the asynergy-containing segment, a lower expansion index (ratio of endocardial lengths of @entity1188 to non- @entity1188 -containing segments demarcated by @entity121 ), less scar wall thinning, a lower thinning ratio (ratio of average thickness of infarcted wall to average thickness of the normal wall), smaller ventricular volume, less regional bulging and @entity439 frequency, prevention of the increase in ventricular mass, less total extent of asynergy, and higher volume ejection fraction. At postmortem examination, scar mass was similar in the two groups, but topographic maps with @entity4688 revealed less @entity1188 , and less noninfarct wall thickness. In addition, postmortem collagen content was similar in noninfarct zones of the two groups but lower in @entity1188 zones of the @entity235 given @entity4688 . CONCLUSIONS: Prolonged @entity4688 therapy, in a dose that did not lower blood pressure, during healing after anterior @entity1188 produced prolonged reduction of left ventricular preload in @entity235 . This diastolic unloading was associated with limitation of remodeling parameters ( @entity1188 expansion and thinning, progressive @entity2554 and @entity1184 , and regional bulging), less total asynergy, and improved left ventricular ejection fraction. Although @entity2814 inhibition was associated with lower collagen content in the @entity1188 area and altered scar topography, these effects did not impact negatively on overall remodeling and function.
