The Hemostatic System as a Modulator of Atherosclerosis

Experimental data suggest that the hemostatic system can accelerate plaque vulnerability to thrombosis in vivo. However, clinical support for these findings remains weak. This comprehensive summary reviews the evidence. Cardiovascular disease is one of the leading causes of death and complications worldwide. The classic concept of atherosclerosis assigns a pivotal role to inflammation in the onset and progression of this disease. 1 , 2 Various inflammatory cell types (e.g., macrophages, neutrophils, and lymphocytes) play crucial roles in the destabilization and subsequent rupture or erosion of an atherosclerotic plaque, ultimately resulting in atherothrombosis. 3 Inflammation is closely linked to coagulation in several pathologic conditions. 4 Intriguingly, extensive bidirectional cross-talk between the two systems has been established in many complex diseases, 5 , 6 including atherosclerosis. Although there is no clinical evidence of a role for the . . .