Key result
Ventricular rupture after myocardial infarction was associated with significant down-regulation of miR-150 and miR-155, and up-regulation of miR-146a in infarcted heart tissue compared to patients without rupture.
Population
Autopsy samples of infarcted heart tissue from 50 patients with myocardial infarction and normal hearts.
Design
Case-control
Authors
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May flag post-MI VR risk via miRNA profiling; leaves open prognostic utility and therapeutic targeting.
Observational (n=60)
No
p-value: p=0.022
Differential expression of miR-146a, miR-150, and miR-155 in MI patients with ventricular rupture suggests that innate immunity and intense inflammatory reactions play a role in its pathogenesis.
Zidar et al. (2011) conducted an observational in Myocardial infarction and ventricular rupture (n=60). Ventricular rupture vs. Myocardial infarction without ventricular rupture was evaluated on Expression of miR-146a, miR-150, and miR-155 in infarcted heart tissue (p=0.022). Ventricular rupture after myocardial infarction was associated with significant down-regulation of miR-150 and miR-155, and up-regulation of miR-146a in infarcted heart tissue compared to patients without rupture.
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