are increased in ageing individuals. Memory T-cell clones also increase and are directed toward a few epitopes of common viruses, such as cytomegalovirus and Epstein-Barr virus.41,42
a quantitative gradient in inflammation: high levels of IL-6 (a pro-inflammatory cytokine often used as a measure of inflammation), for example, are associated with an increased risk of frailty in the elderly.43 In healthy centenerians this low-grade inflammatory response is associated with anti-inflamm-ageing, i.e. with biological mechanisms that control inflammation.39,40
Comments and Perspectives There seems to be
Anti-inflammatory agents have traditionally been commonly used in antithrombotic therapy: both aspirin and heparins possess anti-inflammatory activity.45,46
However, aspirin, is often used at
antiplatelet dosages that do not elicit an anti-inflammatory effect (i.e. do not inhibit cyclo-oxygenase-2 [COX-2]).47
Added to this, the The natural conclusion from these
experimental observations is that excess inflammation is a noxious impediment to healthy ageing. It is not currently known whether this low-grade chronic inflammation and coagulation activation is directly linked to the increasing incidence of thrombosis, both arterial and venous, with age (the risk doubles for every decade after 40 years of age).44
It is likely, however, that in ageing – as in the chronic
diseases mentioned – persistent inflammation is a predisposing factor for thrombosis. It is also plausible that other intervening precipitating factors common in the elderly population, such as cardiovascular disease, cancer and metabolic derangement, trigger the thrombotic events.
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