Inflammation – a common pathogenic factor of arterial atherosclerotic and venous thromboembolic disease
Abstract
Inflammation is among the basic mechanisms of arterial atherosclerotc diseases and is most likely also involved in the onset of venous thromboembolic disease. Various risk factors for atherosclerosis cause damage to the vascular wall and trigger inflammatory changes, which may lead to the development of atherosclerosis. Therefore, people with advanced atherosclerosis, and particularly those with unstable atherosclerotic plaques as a result of intense inflammatory changes, are found to have elevated levels of inflammatory markers in the blood. The most frequent findings include elevated levels of highly specific C-reactive protein (hs-CRP), which is a non-specific systemic indicator of inflammation, and certain interleukins (interleukin–6, interleukin–8) that are considered to be more specific markers of vascular wall inflammation. Therefore, studies are underway to improve the prognostic value for cardiovascular events by the determination of inflammatory markers in the blood. However, due to the unspecifcity of individual inflammatory markers, different methods of their determination and close relation between marker levels and the established risk factors, these have failed to contribute significantly to the evaluation of the role of inflammation in the occurrence of cardiovascular events. Currently, the determination of hs-CRP as one of the most prominent risk factors is recommended only in persons at high risk for cardiovascular events, in those that do not
have classical risk factors and are at risk due to other causes, such as e.g. familial predisposition.
Recently, it has also been found that inflammation is implicated in the pathogenesis of venous thrombosis. In the case of a damaged venous wall inflammation occurs as a response to injury, while in idiopathic venous thrombosis without the presence of risk factors the vascular wall inflammation is probably a primary event that is followed by coagulation activation. Namely, there is a close association between inflammation and coagulation. Inflammation stimulates procoagulant activity and inhibits endogenous fibrinolysis, and therefore patients with the history of venous thrombosis present with elevated levels of systemic inflammatory markers, particularly of hs-CRP and interleukin. However, it has not been fully explained yet whether the elevated systemic inflammatory markers are a cause of a consequence of venous thrombosis. Te results of our study show that they are most probably a cause for prothrombotic characteristics of the blood and stimulate the occurrence of venous thrombosis, as patients with a history of venous thrombosis even in their stable period (3–5 years) present with elevated inflammatory markers.
The increased systemic inflammatory response in arterial atherosclerotic and venous thromboembolic disease is indicative of a close association between both diseases, which are similar as to their pathogenesis but have different clinical features.
The recognition of inflammatory basis of arterial and venous diseases is also important from the therapeutic point of view since until recently, in comparison with anticoagulants, medicines with anti-inflammatory activity were rather neglected. Not only has aspirin long been known for its antithrombocytic and also anti-inflammatory activity, it also appears to be effective in long-term prevention of recurrences and progressions of venous thromboses.
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