In the last decades a large amount of evidences linked rheumatoid arthritis (RA) to atherosclerosis. In particular, it is well established that RA patients have an increased risk of cardiovascular events that is not fully explained by smoke and other classic cardiovascular risk factors. In fact, RA and atherosclerosis may share several common pathomechanisms; inflammation undoubtedly plays a primary role in these settings, being involved in the appearance and progression of both diseases. In fact, proinflammatory cytokines such as tumor necrosis factor alpha and interleukin-6, involved in the pathogenesis of RA, are also independently predictive of subsequent cardiovascular disease (CVD) events in these patients. In RA inflammation may alter HDL constituents and the concentration of LDL and HDL, thus facilitating atherosclerosis and CVD events. On the other hand, also the increase of oxidative processes, frequently observed in RA, may induce atherosclerosis. Interestingly some genetic polymorphisms associated with RA occurrence may enhance atherosclerosis, thus confirming the link between these diseases; however there are some polymorphisms associated with RA susceptibility which do not increase CVD risk; this behavior is a further confirmation that several mechanisms may influence atherosclerotic processes in RA. Moreover, atherosclerosis may be directly mediated also by underlying autoimmune processes, and indirectly by the occurrence of metabolic syndrome and impaired physical activity. Finally, the effects of RA therapies on cardiovascular system in general and on atherosclerosis in particular, are really wide and different. Therefore, RA treatment comprehends drugs that may either increase or reduce CVD. However, the starting point of every RA treatment is that disease control, or better remission, is the best way we have for the reduction of cardiovascular morbidity and mortality in these patients.

Atherosclerosis and rheumatoid arthritis: more than a simple association

CAVAGNA, LORENZO;CAPORALI, ROBERTO
2012-01-01

Abstract

In the last decades a large amount of evidences linked rheumatoid arthritis (RA) to atherosclerosis. In particular, it is well established that RA patients have an increased risk of cardiovascular events that is not fully explained by smoke and other classic cardiovascular risk factors. In fact, RA and atherosclerosis may share several common pathomechanisms; inflammation undoubtedly plays a primary role in these settings, being involved in the appearance and progression of both diseases. In fact, proinflammatory cytokines such as tumor necrosis factor alpha and interleukin-6, involved in the pathogenesis of RA, are also independently predictive of subsequent cardiovascular disease (CVD) events in these patients. In RA inflammation may alter HDL constituents and the concentration of LDL and HDL, thus facilitating atherosclerosis and CVD events. On the other hand, also the increase of oxidative processes, frequently observed in RA, may induce atherosclerosis. Interestingly some genetic polymorphisms associated with RA occurrence may enhance atherosclerosis, thus confirming the link between these diseases; however there are some polymorphisms associated with RA susceptibility which do not increase CVD risk; this behavior is a further confirmation that several mechanisms may influence atherosclerotic processes in RA. Moreover, atherosclerosis may be directly mediated also by underlying autoimmune processes, and indirectly by the occurrence of metabolic syndrome and impaired physical activity. Finally, the effects of RA therapies on cardiovascular system in general and on atherosclerosis in particular, are really wide and different. Therefore, RA treatment comprehends drugs that may either increase or reduce CVD. However, the starting point of every RA treatment is that disease control, or better remission, is the best way we have for the reduction of cardiovascular morbidity and mortality in these patients.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/461468
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