Key result
STEMI was associated with significantly higher baseline sEPCR levels (172.0 vs. 107.1 ng/ml) and lower protein C activity (91.9% vs. 124.5%) compared to stable angina pectoris (P<0.001 for both).
Why the study?
The relationship between soluble endothelial protein C receptor levels and protein C activity in patients with STEMI was not well characterized.
Cross-Sectional (n=89)
Absolute Event Rate: 172% vs 107.1%
p-value: p=<0.001
Does not support immediate changes in STEMI management; leaves open whether sEPCR or protein C activity predicts thrombotic risk or guides therapy.
OBJECTIVES: In contrast to its membrane-bound form, soluble endothelial protein C receptor (sEPCR) expresses procoagulant activity through binding to protein C. We aimed to investigate the relationship between sEPCR levels and protein C activity in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: The study population included 60 STEMI patients who had undergone a primary percutaneous coronary intervention and 29 patients with stable angina pectoris (SAP) with significant coronary stenosis on angiography. Preprocedural sEPCR levels and protein C activity were determined in all study patients. RESULTS: In the STEMI group, the baseline sEPCR level was significantly higher (172.0±89.3 vs. 107.1±39.2 ng/ml, P<0.001) and protein C activity was significantly lower (91.9±26.4 vs. 124.5±16.2%, P<0.001) compared with patients with SAP. There was a significant negative correlation between protein C activity and sEPCR in the STEMI group (r=-0.38, P=0.002); however, no significant correlation was observed in the SAP group (r=0.02, P=0.91). Angiographic thrombus load and the incidence of no-reflow phenomenon were significantly higher in STEMI patients with protein C activity under the median level. CONCLUSION: The ratio of sEPCR levels to protein C activity is high, with a significant negative correlation in patients with STEMI. Lower protein C activity is associated with the development of no-reflow in STEMI patients. However, the sEPCR level has no relation to the development of no-reflow. The clinical significance of elevated sEPCR level in STEMI should be evaluated in larger studies.
No takes yet. Share an insight, caveat, or question.
Tanalp et al. (2013) conducted a cross-sectional in ST-segment elevation myocardial infarction (STEMI) (n=89). ST-segment elevation myocardial infarction (STEMI) vs. Stable angina pectoris (SAP) was evaluated on Baseline soluble endothelial protein C receptor (sEPCR) level (ng/ml) (p=<0.001). STEMI was associated with significantly higher baseline sEPCR levels (172.0 vs. 107.1 ng/ml) and lower protein C activity (91.9% vs. 124.5%) compared to stable angina pectoris (P<0.001 for both).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: