| Summary: | Growing evidence shows that patients with rheumatoid arthritis (RA) have up to twice the risk of developing cardiovascular disease (CVD) compared to those without RA. Generally, these RA patients have higher levels of inflammation in their bodies, and this inflammation is thought to be the link between RA and CVD, but the mechanism is poorly understood. One possibility is through the overproduction of hyaluronan (HA) in the extracellular matrix, which is associated with stiffening of the arterial wall in animal models. Results of this study show that RA patients had higher serum HA (54.8±67.5 vs. 17.5±17.6 ng/mL, p<0.0001) and aortic pulse wave velocity (aPWV) compared to non-RA controls. In regression analysis HA was independently associated with aPWV. Eight weeks of anti-inflammatory anti-TNF-α therapy lead to a significant reduction of aPWV (8.99±1.83 vs 8.30±1.51m/s, p<0.0001), with a trend towards HA reduction (93.5±134.8 vs 78.6±82.1 ng/ml, p=0.3), but this trend did not reach statistical significance. However, rat aortas successfully treated with hyaluronidase (21.5±15.8 vs 0.00±0.00 ng/mL, p<0.0001) showed no reduction in mechanical stiffness (Em at 100mmHg: 2151±239 vs 2149±488 kPa, p=0.9) after HA removal. Together, these data suggest that while HA is associated with arterial stiffening in RA patients and may be reduced by anti-inflammatory treatment, HA itself may not have a direct influence on the mechanical properties of the arterial wall.
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