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Atherosclerotic disease in axial spondyloarthritis: increased frequency of carotid plaques

1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11

 

  1. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
  2. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
  3. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
  4. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
  5. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
  6. Division of Rheumatology, Hospital Comarcal, Laredo, Cantabria, Spain.
  7. Division of Rheumatology, Hospital Comarcal, Laredo, Cantabria, Spain.
  8. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
  9. Division of Cardiology, Hospital Lucus Augusti, Lugo, Spain.
  10. Division of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, Santander, and CIBER Epidemiología y Salud Pública (CIBERESP), Spain.
  11. Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain, and Cardiovascular Pathophysiology and Genomics Research Unit, University of the Witwatersrand, Johannesburg, South Africa.

CER7656
2015 Vol.33, N°3
PI 0315, PF 0320
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PMID: 26005760 [PubMed]

Received: 06/06/2014
Accepted : 16/09/2014
In Press: 25/05/2015
Published: 22/06/2015

Abstract

OBJECTIVES:
To establish whether subclinical atherosclerosis is increased in patients with axial spondyloarthritis (ax-SpA).
METHODS:
A set of 149 consecutive patients with no history of cardiovascular disease that fulfilled the Assessment of SpondyloArthritis International Society classification criteria for ax-SpA was studied by carotid ultrasonography. Carotid intima-media thickness (cIMT) and plaques were assessed. A series of 181 community-based controls with no cardiovascular disease were studied for comparison. To establish whether ax-SpA might have a direct effect on the risk of carotid plaques or an indirect effect via its putative influence on hypertension, dyslipidaemia or obesity, we obtained adjusted odds ratios (OR) for each clinical factor by the development of adjusted models.
RESULTS:
cIMT was increased in patients (0.621±0.123 mm) when compared to controls (0.607±0.117 mm) but the difference was not significant (p=0.30). Nevertheless, carotid plaques were more commonly observed in patients with ax-SpA than in controls (41.6% vs. 26.4%; p=0.003). Patients with plaques had longer duration of the disease than those without plaques (20.5±11.2 years vs. 12.0±8.6 years; p<0.001). Plaques were more frequent in patients with hip involvement (crude odds ratio 3.15, 95% confidence interval [CI] 1.02–9.75; p=0.05), syndesmophytes (crude OR 4.94, 95% CI 2.14–11.4; p<0.001), in patients with higher functional limitation and mobility index measured by BASFI (crude OR 1.16, 95% CI 1.02–1.33; p=0.03) and BASMI (crude OR 1.45, 95% CI 1.19–1.77; p<0.001), and in those with psoriasis (crude OR 3.94, 95% CI 1.31–11.84; p=0.02. However, except for psoriasis that continued being a strong risk factor for plaques after adjustment, the relationship between other clinical features of ax-SpA and carotid plaques disappeared in the adjusted models.
CONCLUSIONS:
Our results confirm the presence of subclinical atherosclerosis in patients with ax-SpA.

Rheumatology Article