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1 fter MI and be associated with the degree of LV dilation.
2 emodeling, leading to myocardial rupture and LV dilation.
3 after myocardial infarction (MI) results in LV dilation, a major cause of congestive heart failure a
7 deletion of MMP9 have less left ventricular (LV) dilation after experimental MI than do sibling wild-
8 O-null mice experienced 35.1% (P<0.001) less LV dilation and a 52.2% (P<0.0001) improvement in LV fun
9 ilure model, TG hearts displayed accelerated LV dilation and a faster decline of shortening fraction.
11 P<0.001), causing lethal cardiomyopathy with LV dilation and depressed systolic function (percent fra
17 ed with saline control, would result in less LV dilation and fewer adverse clinical events between ba
21 esent project tested the hypothesis that the LV dilation and remodeling during the progression of CHF
22 to non-CIMR, CIMR animals exhibited greater LV dilation and significant reductions in posterior maxi
24 iated with increased LV function and reduced LV dilation and that end-systolic wall stress was reduce
25 lude alternative causes of left ventricular (LV) dilation and dysfunction, identify etiologies that m
29 ute MI improves global LV function, prevents LV dilation, and blunts the increase in constitutive mic
30 reserved LV systolic performance, diminished LV dilation, and decreased ventricular sphericalization.
33 ocyte infiltration, significant reduction in LV dilation, and marked preservation of LV function.
35 arly post-MI treatment with p1158/59 reduced LV dilation at day 7 post-MI by preserving LV structure
38 +/- 8%, MR was initially trace with limited LV dilation, but it became moderate with subsequent prom
39 ic constriction developed significantly less LV dilation by echocardiography and magnetic resonance i
40 eks after MI, untreated rats had significant LV dilation compared with sham-operated rats (LV diastol
41 -/-) mice developed a faster and more severe LV dilation compared with WT mice (P<0.05 for both end-s
44 tening or ejection fraction z-score <-2) and LV dilation (end-diastolic dimension [LVEDD] z-score >2)
46 5%; and 3% (n = 7) had frank DCM, defined as LV dilation, impaired contractile performance and LVEDD
48 These perturbations may be linked to more LV dilation in CIMR, which possibly reduced the effectiv
49 evice (CSD) was shown to prevent progressive LV dilation in dogs with heart failure (HF) and increase
51 Four weeks of TACE inhibition abrogated the LV dilation in the MHCsTNF mice and resulted in an incre
54 Longer durations of SVT caused progressive LV dilation, LV pump failure, and myocyte contractile dy
55 to have no prognostic impact over and above LV dilation, LV systolic dysfunction, and presence of LG
57 dil for 6 days before imaging did not reduce LV dilation or improve function compared with those in c
58 control mice; however, AC(VI) mice had less LV dilation (P < 0.001) and increased ejection fractions
62 LV function, cardiac myocyte shortening, and LV dilation that were at least partially reversible by r
63 concentric hypertrophy to left ventricular (LV) dilation that occurs in this line of transgenic mice
64 ) dysfunction versus geometric distortion by LV dilation, using models of acute and chronic segmental
65 lar collagen weave in the MHCsTNF2 mice with LV dilation was characterized by a diminished collagen c
68 myocardial infarction, BM(-/-) mice had more LV dilation, worse LV systolic and diastolic function, h
69 Ptges(-/-) mice develop more left ventricle (LV) dilation, worse LV contractile function, and higher
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