Published: 14 October 2021
Author(s): Fabio Cacciapaglia, Francesca Romana Spinelli, Matteo Piga, Gian Luca Erre, Garifallia Sakellariou, Andreina Manfredi, Ombretta Viapiana, Marco Fornaro, Sergio Colella, Alberto Floris, Arduino Aleksander Mangoni, Floriana Castagna, Caterina Vacchi, Giovanni Orsolini, Serena Bugatti, Giacomo Cafaro, Alberto Cauli, Elisa Gremese, Fabiola Atzeni, Elena Bartoloni
Section: Original article

Rheumatoid Arthritis (RA) is a chronic, systemic inflammatory disease characterized by a relatively high risk of atherosclerotic cardiovascular (CV) events. Notably, such risk has been reported to be similar to that of diabetes mellitus (DM) [1]. Large epidemiological studies suggest that a total of 70% of CV events are attributable to both traditional CV risk factors, mainly hypertension and smoking, combined with disease features [2]. In this setting, besides a genetic component, chronic inflammation may explain at least in part this CV burden by playing a dual role: a direct effect - by promoting endothelial and vessel damage and atherosclerosis progression; and an indirect effect - by modifying traditional CV risk factors such as lipid metabolism [3–5].


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