Atherosclerosis and rheumatoid arthritis : More than a simple association
Cavagna, Lorenzo ; Boffini, Nicola ; Cagnotto, Giovanni LU
; Inverardi, Flora
; Grosso, Vittorio
and Caporali, Roberto
(2012)
In Mediators of Inflammation
2012.
p.1-9
- Abstract
In the last decades a large amount of evidence linked rheumatoid arthritis (RA) to atherosclerosis. In fact, RA patients have an increased risk of cardiovascular events that is not fully explained by other classic cardiovascular risk factors. RA and atherosclerosis may share several common pathomechanisms and inflammation undoubtedly plays a primary role. The 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). In RA, inflammation alters HDL constituents and the concentration of LDL and HDL, thus facilitating atherosclerosis and CVD events. On the other hand, also the increase of oxidative... (More)
In the last decades a large amount of evidence linked rheumatoid arthritis (RA) to atherosclerosis. In fact, RA patients have an increased risk of cardiovascular events that is not fully explained by other classic cardiovascular risk factors. RA and atherosclerosis may share several common pathomechanisms and inflammation undoubtedly plays a primary role. The 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). In RA, inflammation alters 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, induces atherosclerosis. Interestingly, some genetic polymorphisms associated with RA occurrence enhance atherosclerosis, however, other polymorphisms associated with RA susceptibility do not increase CVD risk. Several other 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. 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 CVD occurrence.
(Less)
- author
- Cavagna, Lorenzo
; Boffini, Nicola
; Cagnotto, Giovanni
LU
; Inverardi, Flora
; Grosso, Vittorio
and Caporali, Roberto
- publishing date
- 2012-10-29
- type
- Contribution to journal
- publication status
- published
- in
- Mediators of Inflammation
- volume
- 2012
- article number
- 147354
- pages
- 1 - 9
- publisher
- Hindawi Limited
- external identifiers
-
- pmid:23024462
- scopus:84867790335
- ISSN
- 0962-9351
- DOI
- 10.1155/2012/147354
- language
- English
- LU publication?
- no
- id
- bd60aac5-75d7-41f2-be87-e65296623114
- date added to LUP
- 2019-07-01 22:08:50
- date last changed
- 2024-06-27 01:12:18
@article{bd60aac5-75d7-41f2-be87-e65296623114,
abstract = {{<p>In the last decades a large amount of evidence linked rheumatoid arthritis (RA) to atherosclerosis. In fact, RA patients have an increased risk of cardiovascular events that is not fully explained by other classic cardiovascular risk factors. RA and atherosclerosis may share several common pathomechanisms and inflammation undoubtedly plays a primary role. The 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). In RA, inflammation alters 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, induces atherosclerosis. Interestingly, some genetic polymorphisms associated with RA occurrence enhance atherosclerosis, however, other polymorphisms associated with RA susceptibility do not increase CVD risk. Several other 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. 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 CVD occurrence.</p>}},
author = {{Cavagna, Lorenzo and Boffini, Nicola and Cagnotto, Giovanni and Inverardi, Flora and Grosso, Vittorio and Caporali, Roberto}},
issn = {{0962-9351}},
language = {{eng}},
month = {{10}},
pages = {{1--9}},
publisher = {{Hindawi Limited}},
series = {{Mediators of Inflammation}},
title = {{Atherosclerosis and rheumatoid arthritis : More than a simple association}},
url = {{http://dx.doi.org/10.1155/2012/147354}},
doi = {{10.1155/2012/147354}},
volume = {{2012}},
year = {{2012}},
}