Early identification of acute myocardial infarction by activated protein C--protein C inhibitor complex.

INTRODUCTION

Increased coagulation activity due to coronary thrombosis in a ruptured plaque should result in activation of the protein C anticoagulant system with formation of complexes between activated protein C (APC) and the protein C inhibitor (PCI), which reflects coagulation activity. We hypothesized that elevated APC-PCI concentration might allow earlier detection of ongoing myocardial infarction than traditional biochemical markers. We have evaluated a newly devised immunofluorimetric assay for measuring plasma concentration of APC-PCI complexes among patients with suspected acute coronary syndrome.

MATERIALS AND METHODS

Blood samples were taken from 340 patients (median 71 years, range 31-97) with suspected acute coronary syndrome at first presentation in the emergency department. Electrocardiogram was recorded and APC-PCI, Troponin I and Creatine kinase-MB concentrations were repeatedly measured 3 times at 6 h interval.

RESULTS

The 74 patients who were eventually diagnosed with myocardial infarction had a higher median level of APC-PCI complex than those without myocardial damage; 0.27 vs. 0.20 microg/L (p = 0.001). In a multivariate regression model, APC-PCI level in the fourth quartile (>0.32 microg/L) independently predicted myocardial infarction with an odds ratio of 3.7 (95% CI 1.4-9.6, p < 0.01).

CONCLUSION

Early APC-PCI elevation can be detected among patients with a normal first Troponin I and non-ST-elevation myocardial infarction and provides additional risk assessment in acute coronary syndrome.