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 derivatives of chylomicrons and very low density lipoproteins, can be measured using a new assay kit. The purpose of the present study was to investigate the association of remnant-like particles with the coagulation system that has an important role in the pathogenesis of myocardial infarction. We assayed blood levels of total cholesterol, triglyceride, HDL-cholesterol, apolipoproteins, remnant-like particles-cholesterol, remnant-like particles-triglyceride, fibrinogen, factor VII antigen, activated factor VII, and tissue factor in 111 patients with a history of myocardial infarction and 128 control subjects. In simple regression analysis, plasma levels of remnant-like particles-cholesterol and remnant-like particles-triglyceride showed a significant 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 (r=0.241, p=0.011, and r=0.249, p=0.008, respectively) in patients with myocardial infarction. In contrast, there were no significant differences between remnant-like particles and activated factor VII in control subjects. In stepwise multivariate regression analysis, the significant determinants of activated factor VII were remnant-like particles-cholesterol (10.2%), apolipoproteins A-I (5.1%), and E (7.1%); for the activated factor VII/factor VII antigen ratio, remnant-like particles-triglyceride (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 ratio 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 myocardial infarction by activating the extrinsic coagulation pathway.
Saigo
M
M
First Department of Internal Medicine, Kagoshima, 890-8520, Sakuragaoka, Japan.
Abe
S
S
Ogawa
M
M
Biro
S
S
Minagoe
S
S
Maruyama
I
I
Toda
H
H
Kiyonaga
K
K
Atsuchi
Y
Y
Tahara
M
M
Mawatari
K
K
Tei
C
C
D000328:Adult; D000368:Aged; D001059:Apoproteins / Q000097:blood; D001324:Autoantigens / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001774:Blood Chemical Analysis; D001779:Blood Coagulation Factors / Q000276:immunology / Q000378:metabolism; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D002914:Chylomicrons / Q000097:blood; D004789:Enzyme Activation; D015942:Factor VIIa / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D012044:Regression Analysis; D014280:Triglycerides / Q000097:blood*
D001059:Apoproteins; D001324:Autoantigens; D015415:Biomarkers; D001779:Blood Coagulation Factors; D002914:Chylomicrons; D008055:Lipids; D008074:Lipoproteins; D014280:Triglycerides; D002784:Cholesterol; D015942:Factor VIIa