ABSTRACT
Advanced age is associated with a dramatic increase in the rates of venous and arterial
thrombotic events. Increases in fibrinogen, factors VIII and IX, and other coagulation
proteins, without a proportional increase in anticoagulant factors, likely contribute
to this risk. Recent studies have delineated a role for genomic elements in controlling
age-related expression of some coagulation proteins. Enhanced platelet activity as
well as molecular and anatomic changes in the vessel wall also contribute to the thrombotic
propensity. Advanced age is associated with elevated interleukin-6 (IL-6) and C-reactive
protein levels, indicating an inflammatory state that may be an important stimulus
for thrombus formation in the elderly. Despite evidence of a prothrombotic state,
many elderly people do not experience clinical thrombotic events. It is possible that
the increase in coagulation proteins and activation markers conveys a survival advantage,
such as inhibiting tumor angiogenesis. The recent epidemic in obesity may heighten
thrombotic risks in the elderly because adipose tissue is an important source of inflammatory
cytokines and plasminogen activator inhibitor-1 (PAI-1). As the population ages, further
studies will be warranted to define the mechanisms for thrombosis in the elderly.
KEYWORD
Aging - thrombosis - inflammation - fibrinolysis - angiogenesis
