A Genetic, Lipid-Independent Contribution to Coronary Artery Disease?

A specific LDLR gene polymorphism was associated with increased factor VIII coagulant activity, possibly leading to atherogenesis.

The low-density lipoprotein receptor (LDLR) regulates plasma levels of LDL cholesterol. Genetic mutations at the LDLR locus are associated with familial hypercholesterolemia and coronary artery disease (CAD). The LDLR also mediates the cellular uptake and degradation of coagulation factor VIII (FVIII). To determine whether three specific LDLR polymorphisms (rs688, rs2228671, and rs1122608) are associated with increased FVIII coagulant activity and CAD, investigators in Italy analyzed data from 692 patients with angiographically confirmed CAD and from 291 controls without CAD.

FVIII levels were higher in CAD patients than in controls (mean, 172 IU/dL vs. 149 IU/dL; P<0.001); this difference persisted after adjustment for traditional CAD risk …

Reviewing Author

David Green, MD, PhD

Disclosures

EquityNovartis

David Green, MD, PhD

Disclosures

EquityNovartis