Objectives: This study tested the hypothesis that plasma heparin cofactor II (HCII) activity independently predicts cardiovascular events in patients after acute myocardial infarction (AMI) and attempted to elucidate the role of HCII in atherothrombosis.
Background: HCII inhibits thrombin activity by binding to dermatan sulfate and has been shown to be a novel and independent risk factor for atherosclerosis. However, there is limited data on the relation between plasma levels of HCII after AMI and future cardiovascular events.
Methods: A total of 110 consecutive patients (aged 63+/-11 years) with AMI were followed up for 42+/-12 months. Plasma HCII activity was determined from blood samples collected immediately after hospitalization. The primary end point was the combined occurrence of major adverse cardiovascular events (MACE), including rehospitalization because of unstable angina, nonfatal MI, revascularization with either percutaneous coronary intervention or coronary artery bypass grafting, ischemic stroke, and cardiovascular death.
Results: All patients were divided into three groups: a high-HCII group (>122%, n=35), a normal-HCII group (>98% and <or=122%, n=41), and a low-HCII group (<or=98%, n=34). The high-HCII group had reduced MACE compared with the other groups, although the difference was not significant (P=0.150). Enhanced plasma HCII activity was, however, significantly associated with decreased MACE in the nondiabetic patients (P=0.034). In a Cox multivariate regression analysis that included all patients, plasma HCII activity was an independent predictor of future MACE (P=0.029).
Conclusion: The results indicate a potential association between plasma HCII activity and future cardiovascular events after AMI. Moreover, HCII activity seems to play a pivotal role in atherothrombosis.