Key result
Plasma EMMPRIN levels were significantly higher in STEMI (39.4 ng/mL) and NSTEMI (37.1 ng/mL) patients than in stable CAD (27.5 ng/mL) or controls (24.5 ng/mL) (p<0.001).
Why the study?
Are plasma EMMPRIN levels elevated in patients with acute myocardial infarction compared to those with stable CAD or healthy controls?
Case-Control (n=176)
Are plasma EMMPRIN levels elevated in patients with acute myocardial infarction compared to those with stable CAD or healthy controls?
Odds Ratio: 1.25 (95% CI 1.16–1.34)
Absolute Event Rate: 39.4% vs 24.5%
p-value: p=<0.001
Plasma EMMPRIN levels are significantly elevated in acute myocardial infarction and correlate with markers of myocardial injury and inflammation, suggesting a potential role in diagnosis and pathogenesis.
May support EMMPRIN as AMI biomarker; leaves open diagnostic utility and mechanistic role pending prospective studies.
Purpose The purpose of this study was to determine whether the plasma levels of soluble extracellular matrix metalloproteinase inducer (EMMPRIN) differed among the patients with ST-elevation myocardial infarction (STEMI), non-STEMI (NSTEMI) and stable coronary artery disease (CAD) and the healthy controls, and to identify the factors associated with the differences in plasma levels of this this protein among patients in these groups. Methods Plasma EMMPRIN levels were compared among four age- and sex-matched groups of patients with STEMI, NSTEMI and stable CAD and healthy controls (n=44 per group), then logistic regression and correlation analyses were conducted for the whole acute myocardial infarction (AMI) patients group. Results EMMPRIN levels were significantly higher in the STEMI (39.4±9.2ng/mL) and NSTEMI (37.1±10.5ng/mL) groups than in either the stable CAD (27.5±4.7ng/mL) or control (24.5±5.8ng/mL) groups (p<0.001 for each comparison), whereas the differences between the STEMI and NSTEMI groups, and between the stable CAD group and the controls, was not significant. Moreover, in the whole AMI patients group, the elevation of EMMPRIN was independent of the other variables (Odds ratio=1.25, 95% confidence intervals=1.16-1.34, p<0.001), and EMMPRIN levels were correlated significantly and positively with the plasma levels of peak creatine kinase-MB (r=0.22, p<0.05), peak cardiac troponin T (r=0.27, p<0.05) and admission C-reactive protein (r=0.26, p<0.05), and correlated significantly and inversely with left ventricular ejection fraction (r=-0.22, p< 0.05). Conclusion EMMPRIN seems to play a role in the pathogenesis of AMI and its measurement in the plasma may play a role in the diagnosis of this disease.
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Akkuş et al. (2016) conducted a case-control in Acute myocardial infarction and stable coronary artery disease (n=176). Plasma EMMPRIN levels vs. Stable CAD and healthy controls was evaluated on Plasma EMMPRIN levels (OR 1.25, 95% CI 1.16-1.34, p=<0.001). Plasma EMMPRIN levels were significantly higher in STEMI (39.4 ng/mL) and NSTEMI (37.1 ng/mL) patients than in stable CAD (27.5 ng/mL) or controls (24.5 ng/mL) (p<0.001).
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