Abstract
Objective: Increased cardiovascular morbidity and mortality have been observed in several immune mediated rheumatic diseases, including psoriatic arthritis (PsA). We evaluated subclinical atherosclerosis in PsA patients according with hypertensive status by studying non invasively structural and functional properties of arteries. Design and Method: We studied 41 consecutive patients with PsA (of whom, 23 hypertensives) attending hospital outpatient clinics. 40 normotensives healthy subjects (NC) and 19 hypertensives (HT-C) served as controls. We evaluated by B-mode ultrasound the carotid intima media thickness (IMT). Measurements were expressed as mean-IMT (cumulative mean of mean IMT measured in each carotid segment, common, bulb, and internal carotid artery, bilaterally) and as M-MAX (cumulative mean of maximum IMT). Endothelial function was evaluated by post-occlusion flow mediated dilation (FMD) of the brachial artery using high-sensitivity brachial ultrasonography. NO-independent vasodilation was evaluated by the response to sublingual glyceril trinitrate (GTN). Results: PsA had a higher mean-IMT compared to NC. Hypertensive PsA displayed higher M-MAX versus both HT-C (p = 0.007) and normotensive PsA (p = 0.026). FMD was significantly lower in PsA than in NC (8.9%), whereas there was no difference between hypertensive PsA (6.1%), normotensive PsA (5.7%), and HT-C (6.3%). GTN response was similar in all groups. The TNFα level was much higher in PsA patients than in the other groups. In the entire cohort, the IMT parameters were significantly related to TNFα as well as classical risk factors, including blood pressure and lipid profile, whereas FMD was inversely related to TNFα levels and blood pressure but not lipid parameters. Conclusions: Subclinical atherosclerosis is enhanced in PsA compared to NC. In PsA, the hypertensive status proved to exert an additional effect on M-MAX, a parameter of advanced pro-atherogenic remodelling. FMD was reduced in PsA irrespective of hypertensives status. Thus, PsA per se implies a pro-atherogenic remodelling which is enhanced by the hypertensive status. In addition, TNFα seems to play a role in the hampering the functional properties of vascular wall probably through endothelial dysfunction.
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