Hemostasis and thrombosis in older adults

Abstract

The frequency of atherothrombotic events with increasing age may represent the cumulative end-result of upregulation of coagulation proteins, diminished fibrinolytic capacity, endothelial dysfunction with impaired regenerative capacity, and gene-environment interactions. There remains, however, an absence of clarity surrounding the mechanistic relationship between aging and the observed clinical phenotypes of coronary and cerebrovascular thrombosis causing myocardial infarction and stroke, respectively, among older adults. The complexity of atherothrombosis is heightened further by a concomitant bleeding tendency-conceivably an age-related vasculopathy involving small, hemostasis-maintaining vessels, that is characterized by impaired vascular healing, loss of anatomic integrity and vasoreactivity; and, immune incompetence, highlighting the integrated relationship between two teleological life-sustaining processes-an ability to stem blood loss following vascular injury and the capacity to localize and eradicate infection. An advanced understanding of hemostatic factors, vascular biology, immunology and vulnerability to both thrombosis and hemorrhage in aging will likely translate to improved risk prediction models, tailored pharmacotherapies and optimized outcomes. In direct response to a topic of global relevance and unmet need, the Journal of Thrombosis and Thrombolysis will publish a focused series devoted to hemostasis and thrombosis in older adults. Each contribution will appear within the Editors Page over the next six issues.