| Summary: | Many inflammatory conditions are associated with an increased risk of cardiovascular disease (CVD) and mortality. As well as accelerated atherosclerosis, increased plaque instability and endothelial dysfunction; arterial stiffness has been proposed as one of the potential mechanisms underlying the increased CVD in these patients. Indeed, patients with chronic inflammatory conditions such as rheumatoid arthritis (RA), lupus erythematosus, human immunodeficiency virus, chronic obstructive pulmonary disease (COPD), and inflammatory bowel disease have been shown to have increased arterial stiffness. This appears to correlate with the level of inflammation, suggesting that arterial stiffness may be reversible with anti-inflammatory treatment. Numerous small-scale interventional studies have demonstrated that anti-inflammatory and cholesterol-reduction therapies with pleiotropic effects can reduce arterial stiffness in certain inflammatory conditions.
The association between increased arterial stiffness and inflammation appears obvious, yet the mechanism is poorly understood. One of the proposed mechanisms is arterial inflammation. In FDG PET/CT studies, patients with psoriasis, COPD and RA have been shown to have sub-clinical aortic inflammation. Arterial inflammation can subsequently lead to changes in the hydration state of the arterial wall and the composition of extracellular matrix, such as changes in glycosaminoglycan (GAG) synthesis. Indeed, animal studies have shown that overproduction of GAGs in the aorta resulted in thinning of the elastic lamellae and therefore aortic stiffening. Also, inflammatory cytokines can cause vascular smooth muscle cell proliferation, and phenotypic transformation resulting in an increased bioapatite formation, which can lead to calcification and stiffening. Furthermore, the release of matrix metalloproteinases from leukocytes can degrade elastin fibres within the arterial media.
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