Decreased Coagulability Has No Clinically Relevant Effect on Atherogenesis

Author:

Šrámek A.1,Reiber J.H.C.1,Gerrits W.B.J.1,Rosendaal F.R.1

Affiliation:

1. From the Departments of Clinical Epidemiology (A.S., F.R.R.), and Radiology (J.H.C.R.) and the Hemostasis and Thrombosis Research Center (F.R.R.), Leiden University Medical Center, Leiden; and the Department of Hematology (W.B.J.G.), Leyenburg Hospital, The Hague, the Netherlands.

Abstract

Background Hemostasis affects ischemic cardiovascular disease through its role in formation of occluding arterial thrombi. Several studies suggest that hemostasis also might play a role in atherogenesis. We investigated whether individuals with an inherited bleeding tendency are protected against development of atherosclerosis. Methods and Results A total of 76 individuals with an inherited bleeding tendency (hemophilia and von Willebrand disease) and 142 healthy controls were included in the present study. Early atherosclerotic vessel-wall changes were quantified by measurement of intima-media thickness in the carotid and femoral arteries by B-mode ultrasonography. To validate intima-media thickness measurements, measurements also were performed in 77 individuals with clinically proven atherosclerosis and in 34 healthy, age-matched controls. A large difference in intima-media thickness was found between individuals with proven atherosclerosis and healthy controls, in particular for the femoral artery (difference for carotid artery, 0.16 mm; femoral artery, 0.53 mm). Comparison between patients with a bleeding tendency and healthy controls showed only minimally reduced intima-media in femoral artery in individuals with a bleeding tendency (adjusted difference, −0.078 mm; 95% CI, −0.17 to 0.018 mm). Subgroup analysis revealed that in subjects with moderate to severe hemophilia, vessel walls were thinnest (adjusted difference, −0.10 mm; 95% CI, −0.27 to 0.061 mm). Conclusions Hypocoagulability caused by hemophilia or von Willebrand disease has at most a limited effect on atherogenesis.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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