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1 prevented the collagen deposition and caused cardiac rupture.
2 05, 3.16) were independently associated with cardiac rupture.
3 by a paradoxic increase in early deaths from cardiac rupture.
4 ocker use were independently associated with cardiac rupture.
5 hage necroptosis, impaired fibrogenesis, and cardiac rupture.
6  7 days (2.9%); 28 recurrent MIs (26.6%); 13 cardiac ruptures (12.4%); 4 pump failures (3.8%); 2 othe
7  promotes ischemic injury, increases risk of cardiac rupture, accentuates post-MI remodeling and left
8                              Recurrent MI or cardiac rupture accounts for a high proportion of sudden
9 lay normal cardiac function but are prone to cardiac rupture after acute myocardial infarction.
10 se deficiency prevented aldosterone-enhanced cardiac rupture after myocardial infarction.
11 hic characteristics of patients experiencing cardiac rupture after thrombolytic and adjunctive antico
12                   Although the scar prevents cardiac rupture, an excessive profibrotic response impai
13 m by oxidative activation of CaMKII, causing cardiac rupture and increased mortality in mice after my
14 =0.04), and postmortem examination confirmed cardiac rupture as the cause of most of the deaths.
15  had a catastrophic prognosis, with frequent cardiac rupture, as the result of markedly reduced colla
16                         Studies suggest that cardiac rupture can be accelerated by thrombolytic thera
17                                  CONCLUSIONS Cardiac rupture following thrombolytic therapy tends to
18 ming and prevalence as a cause of death from cardiac rupture in patients with acute myocardial infarc
19 ce restored inflammation resolution, reduced cardiac rupture incidence, and improved cardiac function
20                                              Cardiac rupture is a major lethal complication of acute
21 t ventricular (LV) pseudoaneurysms form when cardiac rupture is contained by adherent pericardium or
22                                              Cardiac rupture is preceded by left ventricular dilation
23                                   BACKGROUND Cardiac rupture is responsible for nearly 15% of all in-
24 showed compromised survival, higher rates of cardiac rupture, more severe left ventricular dilation,
25 ues of impaired healing or increased risk of cardiac rupture or failed to show any additional benefit
26 creased day 7 mortality because of increased cardiac rupture post-MI.
27          Cardiac pseudoaneurysm, a contained cardiac rupture, predisposes patients to further rupture
28 reased the incidence of early postinfarction cardiac rupture, promoting a matrix-degrading fibroblast
29 es in reperfusion strategies, mortality from cardiac rupture remains high.
30 ggests that thrombolytic therapy accelerates cardiac rupture, typically to within 24 to 48 h of treat
31                    Although the incidence of cardiac rupture was low (<1.0%), it was responsible for
32                               A diagnosis of cardiac rupture was made clinically in patients with sud
33 urred within 48 h of treatment Patients with cardiac rupture were older, of lower body weight and sta
34                                   No further cardiac ruptures were documented.
35          Of the Agtr2-/Y mice, 63.6% died of cardiac rupture, whereas 23.5% of the WT mice died of th
36 mice displayed 100% mortality resulting from cardiac rupture within 12 days after MI compared with ap