Inflammation and thrombosis in cardiovascular disease

Abstract

Purpose of review: This article will summarize recent observations that provide mechanistic insight into the molecular and cellular links between inflammation and thrombosis in the context of cardiovascular and other thromboinflammatory disease states.

Recent findings: Several disease conditions are characterized by a thromboinflammatory state in which interactions of blood cells and components with the vascular wall perpetuate both thrombotic and inflammatory pathways. Targeting these pathways may be of benefit in inflammatory conditions and cardiovascular disease.

Summary: Ongoing clinical trials should provide additional insight into the hypothesis that the thromboinflammatory state contributes to adverse clinical outcomes.

Figure 1. Contribution of platelet–leukocyte interactions to a thromboinflammatory state

Platelets are activated at the site of endothelial damage or in the microcirculation of infected/inflamed tissue. Activated platelets bind leukocytes to form heterotypic complexes, and communicate signals that result in a variety of specific responses. Platelets mediate the recruitment of leukocytes at the site of atherosclerosis or thrombus formation, as well as in inflamed tissue. In some cases, these interactions mediate platelet–leukocyte co-migration across the mucosal epithelium. In this way, platelets contribute to the promotion of inflammatory reactions, which, when not controlled, can exacerbate tissue damage. Platelets might support lymphocyte homing in peripheral lymph nodes, stimulate isotype switching and production of IgG by B lymphocytes, and might help lymphocyte responses to viruses and neutrophil response to bacteria. In this way, platelets contribute to host defense. Illustration by Matt Hazzard, University of Kentucky, Information Technology.