Plasma level of triglyceride-rich lipoprotein remnants is closely associated with the activation of coagulation factor VII in patients with myocardial infarction

Remnant-like particles, which have been recognized to be atherogenic deriva tives of chylomicrons and very low density lipoproteins, can be measured us ing a new assay kit. The purpose of the present study was to investigate th e association of remnant-like particles with the coagulation system that ha s an important role in the pathogenesis of myocardial infarction. We assaye d blood levels of total cholesterol, triglyceride, HDL-cholesterol, apolipo proteins, remnant-like particles-cholesterol, remnant-like particles-trigly ceride, fibrinogen, factor VII antigen, activated factor VII, and tissue fa ctor in 111 patients with a history of myocardial infarction and 128 contro l subjects. In simple regression analysis, plasma levels of remnant-like pa rticles-cholesterol and remnant-like particles-triglyceride showed a signif icant positive correlation with the levels of activated factor VII (r=0.319 , p<0.001, and r=0.286, p=0.002, respectively) and the activated factor VII /factor VII antigen ratio (v=0.241,p=0.011, and r=0.249, p=0.008, respectiv ely) in patients with myocardial infarction. In contrast, there were no sig nificant differences between remnant-like particles and activated factor VI I in control subjects. In stepwise multivariate regression analysis, the si gnificant determinants of activated factor VII were remnant-like particles- cholesterol (10.2%), apolipoproteins A-I (5.1%), and E (7.1%); for the acti vated factor VII/factor VII antigen ratio, remnant-like particles-triglycer ide (6.2%), age at blood sampling (5.1%), and apolipoprotein A-I (4.0%) in patients with myocardial infarction. However, the significant determinants of activated factor VII and the activated factor VII/factor VII antigen rat io were HDL-cholesterol (9.9% and 9.2%, respectively) in control subjects. It is concluded that remnant-like particles may be a risk factor for myocar dial infarction by activating the extrinsic coagulation pathway. (C) 2000 E lsevier Science Ltd. All rights reserved.