Dyslipidemia shifts the tissue factor/tissue factor pathway inhibitor balance toward increased thrombogenicity in atherosclerotic plaques: evidence for a corrective effect of statins

Atherosclerosis. 2007 Dec;195(2):e117-25. doi: 10.1016/j.atherosclerosis.2006.10.012. Epub 2006 Dec 28.

Abstract

Background: Tissue factor (TF) is a key mediator of atherosclerotic plaque thrombogenicity and may be regulated by plaque TF pathway inhibitor (TFPI). High atherogenic lipoproteins are a well-known arterial risk factor, but their effects on the TF/TFPI balance in atherosclerotic plaques, as well as those of widely used lipid-lowering agents such as statins, are incompletely understood.

Objectives: We analyzed the TF/TFPI balance in carotid plaques from 86 patients, according to the presence of dyslipidemia and statin therapy.

Results: In patients with untreated dyslipidemia (ApoB/ApoA1 ratio >0.7) (D+) (n=44), TF antigen (TF) tended to be higher than in those without dyslipidemia (D-) (n=16). In patients with statins (S+) (n=26), TF was lower than in D+ (p=0.02) and similar to that of D- patients. TFPI antigen was higher in D- than in D+ and S+ patients (p<or=0.02). As a result, the TF/TFPI (mol/mol) ratio was higher in D+ than in D- or S+ patients (p<or=0.005). TF activity correlated to TF/TFPI ratio (p<0.0001), and was higher in the D+ than in the D- and in the S+ patients (p=0.02). Among analyzed clinical risk factors and biological parameters, including CRP, dyslipidemia was the only independent predictor for low plaque TFPI and high TF/TFPI ratio. Histochemistry showed that TF and TFPI were mainly expressed in macrophage-rich regions surrounding the lipid-rich core in the three groups.

Conclusions: These results indicate that dyslipidemia is associated with a shift of the TF/TFPI balance and of TF activity toward higher plaque thrombotic potential. Statins correct this equilibrium mainly by decreasing plaque TF together with blood atherogenic lipoproteins.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Apolipoprotein A-I / analysis
  • Apolipoproteins B / analysis
  • Carotid Artery Diseases / physiopathology*
  • Case-Control Studies
  • Cohort Studies
  • Dyslipidemias / drug therapy
  • Dyslipidemias / physiopathology*
  • Endarterectomy
  • Female
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
  • Immunohistochemistry
  • Lipoproteins / metabolism*
  • Male
  • Thromboplastin / drug effects
  • Thromboplastin / metabolism*
  • Thrombosis / physiopathology*

Substances

  • Apolipoprotein A-I
  • Apolipoproteins B
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Lipoproteins
  • lipoprotein-associated coagulation inhibitor
  • Thromboplastin