ReviewCardiovascular disease in patients with spondyloarthropathies
Introduction
Excess cardiovascular mortality was reported recently in patients with spondyloarthropathies [1]. The excess was not explained by the cardiac manifestations of spondyloarthropathies. Life-style factors, drugs used to treat spondyloarthropathies, genetic factors, and chronic inflammation may contribute to the increased cardiovascular risk [2], [3], [4].
Section snippets
Aortic root disease
The aortic root is the main cardiac target of spondyloarthropathies, which cause inflammatory sclerosis affecting all three layers of the aortic wall. Apart from aortic regurgitation, aortic root involvement is detectable by echocardiography in 61% of patients with ankylosing spondylitis (AS) [6], [7]. Echocardiography shows thickening of the posterior aortic wall with or without dilation at the level of the valve, whereas neither the sinotubular junction nor the Valsalva sinuses are dilated [8]
Spondyloarthropathies and conventional cardiovascular risk factors
Current smoking is associated with greater severity of clinical and radiographic abnormalities and with poorer functional outcomes, compared to non-smokers [26], [27]. A consequence of the greater functional impairment in smokers is a less active lifestyle, which increases the risk of cardiovascular disease. The main lipid-profile abnormality in patients with spondyloarthropathies may be a reduction in the HDL-cholesterol level. HDL-cholesterol levels lower than 0.35 g/L are associated with an
Spondyloarthropathy constitutes a cardiovascular risk factor per se
The excess cardiovascular mortality in patients with spondyloarthropathies is not fully explained by the cardiac manifestations of spondyloarthropathies and the increased prevalence of conventional cardiovascular risk factors. Both the HLA-B27 genotype and chronic inflammation contribute to the development of cardiovascular disease [5].
Role for treatments used to combat inflammation
NSAIDs constitute the mainstay of the treatment of spondyloarthropathies. NSAID therapy is known to affect blood pressure control [37]. A 1993 meta-analysis showed that NSAIDs decreased the efficacy of antihypertensive agents, most notably those targeting the rennin–angiotensin–aldosterone system [38]. The effects of celecoxib and rofecoxib were evaluated in a population of patients with hypertension and chronic inflammatory joint disease [39]. Rofecoxib induced greater systolic blood pressure
Conclusion
The excess cardiovascular mortality in patients with spondyloarthropathies requires careful follow-up and close collaboration between the rheumatologist and the cardiologist. In addition to the cardiac manifestations of spondyloarthropathies, evaluation and treatment of conventional cardiovascular risk factors (age, family history, hypertension, diabetes, active and passive smoking, inactive lifestyle, and dyslipidaemia) are in order to decrease the risk of premature atheroma. Most
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