The results suggested that patients with AMI exhibited significantly increased expression of endothelial injury markers (von Willebrand factor, heart‑type fatty acid‑binding protein and cardiac troponin I) and miR‑133a in blood samples compared with patients without AMI.
Plasma VWF:Ag and VWF:GPIbR levels were significantly higher in patients with AMI than in CTL (P<.0001), whereas the ratios of ADAMTS13/VWF:Ag and ADAMTS13/VWF:GPIbR were significantly lower (P<.0001).
Engrafted hMSCs (4.1 +/- 0.3% of injected cells) expressed von Willebrand factor (16.9 +/- 2.7%) but no stringent cardiac or smooth muscle markers. hMSCs from patients with IHD engraft in infarcted mouse myocardium and preserve LV function 2 wk after AMI, potentially through an enhancement of scar vascularity and a reduction of wall thinning.
No association was found between the Sma I polymorphism and vWF plasma levels in controls, patients with acute ischemic stroke, or the AMI group (one-way ANOVA, P=.323, P=.315, P=.96).
The frequency of the -1185A/-1051G haplotype, associated with elevated VWF levels, was similar in the case and control groups, yielding a haplotypic odds ratio for MI of 0.93 (95% CI 0.77, 1.12, P = 0.43), and there was no significant association between the -1185A/-1051G haplotype and the risk of MI in any subgroup analysed.