Background/Purpose: Chronic inflammatory arthritis is associated with increased cardiovascular disease (CVD) risk. The mechanisms behind this link include chronic inflammation, comorbidities and disease-related drugs. CV risk management according to local guidelines with aggressive suppression of inflammation for patients with RA, AS and PsA has been recommended. However, in contrast to RA where the bulk of supporting evidence exists, fewer studies have addressed CVD risk in AS. Moreover, the beneficial impact of anti-TNF agents, which are increasingly used in AS, has been extensively reported biasing somehow the link between AS per se and CVD risk. We aimed to compare subclinical atherosclerosis burden between AS patients to healthy controls and patients with RA.

Methods:   We examined 81 consecutive non-diabetic AS patients free of clinical CVD (age 46.8±13.3, 85% men, disease duration 10 years (2-24), BASDAI 1.4 (0.4-3.2), BASFI 2.0 (0.95-2.85)). Current smokers were 62% of patients, 16% had dyslipidemia and 31% had hypertension, whereas 62% were receiving anti-TNF treatment.  A subgroup of 68 AS patients could be exactly matched 1:1 with healthy controls for age, gender, smoking, dyslipidemia and hypertension. We also matched 14 AS patients with more than 10 years of disease duration 1:1 to non-diabetic RA patients, for age, gender and disease duration. Finally, we identified 24 of the 31 anti-TNF treatment-naïve patients whom we were able to match 1:1 for age and gender, smoking dyslipidemia and hypertension with 24 healthy controls. We evaluated subclinical atheromatosis in aortic and femoral arterial beds (presence of plaques), arterial hypertrophy (intimal-medial thickness adjacent to plaques when present; cross sectional area), and arterial carotid/aortic stiffness (by ultrasound and pulse wave velocity).

Results: Fewer patients with AS than controls had plaques (n=24 vs n=32, respectively, p=0.163). This observation was extended to the subgroup of 35 AS patients with more than 10 years of disease duration (n=14 vs n=22, respectively, p=0.056). Even when taking into consideration anti-TNF-naïve patients, there were no differences compared to controls. Neither BASDAI nor BASFI scores were found to be associated with the presence of plaques. Finally, and despite the small number of matched patients, presence and multiple localization of plaques were more prevalent in RA than in AS patients with more than 10 years disease duration (p=0.053 and 0.045, respectively). Notably, all indices of arterial hypertrophy and arterial carotid/aortic stiffness were comparable between AS patients and their matched controls.

Conclusion: In this group of relatively young Greek patients, AS (even long-standing disease) – in contrast to RA – does not associate with accelerated atheromatosis compared with very closely matched healthy controls.  The differential CVD risk between AS and RA requires further investigation as it may have significant clinical implications in terms of prevention strategies.