Elsevier

Joint Bone Spine

Volume 78, Issue 4, July 2011, Pages 378-382
Joint Bone Spine

Original article
Investigation of effects of different treatment modalities on structural and functional vessel wall properties in patients with ankylosing spondylitis

https://doi.org/10.1016/j.jbspin.2010.09.023Get rights and content

Abstract

Aim

Ankylosing spondylitis (AS) is a chronic systemic inflammatory disease that is associated with increased cardiovascular burden. The aim of this study was to investigate vascular structural and functional changes in patients with AS, with special emphasis on the effects of different treatment modalities, through evaluation of level of vascular stiffness (pulse wave velocity [PVW]) and carotid intima media thickness (IMT-C).

Methods

A total of 67 AS patients, and age, sex, body mass index (BMI) smoking status, lipid profiles and blood pressure-matched healthy control subjects (n = 34) were studied. Of these, 34 patients were on anti-TNF alpha and 33 on non steroid anti inflammatory drugs (NSAIDs). The IMT-C and PWV values of the right common carotid artery were measured by high-resolution ultrasound.

Results

The AS patients (n = 67) had significantly higher PWV values than the controls [9.0 ± 1.49 m/sec vs. 8.27 ± 0.90 m/sec, P = 0.004; 95% confidence interval (CI), −1.22 to −0.24]. Multiple stepwise linear regression analysis revealed that PWV could only be explained by systolic blood pressure (P < 0.05) and IMT (P < 0.05) in AS. Even though IMT-C in anti-TNF alpha treated group was higher compared to the NSAID treated group, it was not statistically significant (P = 0.5).

Conclusion

PWV was found to be higher in AS patients than in the control group, and there was no significant difference between the average PWV values of AS patients treated with anti -TNF alpha or NSAIDs.

Introduction

Ankylosing spondylitis (AS) is a chronic inflammatory disease involving mainly the sacroiliac joints and the spine. However, AS may show some extraarticular manifestations including cardiovascular involvement [1], [2]. Cardiovascular involvement in AS includes aortic involvement causing aortic regurgitation, myocardial involvement associated with conduction defects, arrhythmias and pericardial involvements, in the course of AS, is a very important extraarticular complication. The overall mortality of the patients with AS is 1.5 times higher than the normal population, and circulatory or cardiovascular involvement has been estimated to account for 20–40% of this excess mortality [1], [3], [4], [5]. The exact mechanism underlying the association between AS and the cardiovascular involvement has not been fully understood. However, inflammation plays an important role in the pathogenesis of atherosclerosis and it is likely that chronic systemic inflammation contributes to the increased cardiovascular mortality and morbidity. In a recent study, the presence of subclinical atherosclerosis was identified in AS 2. However, dyslipidemia, smoking, diabetes mellitus and hypertension also play important roles for development of atherosclerosis [6]. Another study indicated that patients with AS have higher BMI and are higher rate of cigar smokers compared to the controls. And those patients had more pronounced parameters showing systemic inflammation. It is also known that high BMI and smoking are among to atherosclerosis risk factors. However, the association between atherosclerosis and AS is still debated [7], [8].

Pulse wave velocity (PWV) is a marker for arterial stiffness and increased vascular stiffness recently being recognized as an independent risk factor for cardiovascular disease (CVD) [9]. Measurement of the intima-media thickness of the common or internal carotid artery (IMT-C) with a high-resolution ultrasonography is an important indicator for and indirect way of assessing the early stages of atherosclerosis [10].

Recent studies indicates an increased subclinical atherosclerosis in AS patients without clinically evident CVD and TNF-alpha blockade does not seem to improve arterial stiffness in AS patients, but those studies suffer from lack of statistical power and not clearly established the effects of TNF-alpha blockade therapy [2], [10], [11].

The aim of this study was to evaluate the level of subclinical atherosclerosis, and to evaluate effects of different treatment modalities on vascular structural and functional changes, assessed by PWV and IMT-C, in AS patients in comparison with controls.

Section snippets

Methods

This study was conducted between June and November 2008. Sixty-seven AS patients and 34 healthy controls were enrolled. Informed consent was obtained before the examination, and approval for the study was granted by the local Ethical Committee. All the patients met The New York diagnostic criteria for AS [12]. The patients with AS had long-standing disease duration (mean ± standard deviation, 7.7 ± 4.8 years).

We excluded patients with diabetes mellitus (fasting blood glucose > 7 mmol/l) and patients

Results

Clinical characteristics of patients with AS are given in Table 1. The mean disease duration was 7.7 ± 4.8 years (y). The AS patients also had a significantly higher mean CRP level than healthy controls, indicating systemic inflammation. The controls were consisted of 25 men and nine women. The mean age of controls was 37.7 ± 8.2 y. There were no significant differences between the patients and control groups with regard to mean age, gender distribution, number of smokers, blood pressure levels,

Discussion

In this study, by evaluating the presence and level of subclinical atherosclerosis in AS patients through IMT-C and PWV, markers of subclinical atherosclerosis, and vascular stiffness in patients on anti-TNF alpha, it was found that AS patients had higher PWV but there were no statistically significant difference between patients with AS and controls with respect to the IMT-C levels.

It has been shown that male AS patients have a 40% higher cardiovascular mortality risk than to the general

Conflict of interest statement

None of the authors has any conflicts of interest to declare.

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