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  • The influence of inflammation in the development of subclinical atherosclerosis in psoriatic arthritis: comment on ‘Cardiovascular comorbidities in patients with psoriatic arthritis: a systematic review’ by Jamnistki et al

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Correspondence
The influence of inflammation in the development of subclinical atherosclerosis in psoriatic arthritis: comment on ‘Cardiovascular comorbidities in patients with psoriatic arthritis: a systematic review’ by Jamnistki et al
  1. Miguel A González-Gay1,
  2. Carlos González-Juanatey2,
  3. Javier Llorca3,
  4. Santos Castañeda4
  1. 1Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marqués de Valdecilla, IFIMAV, Santander, Cantabria, Spain
  2. 2Cardiology Division, Hospital Universitario Lucus Augusti, Lugo, Spain
  3. 3Department of Computational Biology, School of Medicine, University of Cantabria, IFIMAV, and CIBER Epidemiología y Salud Pública (CIBERESP), Santander, Cantabria, Spain
  4. 4Department of Rheumatology, Hospital de La Princesa, IIS-Princesa, Universidad Autónoma de Madrid (UAM), Madrid, Spain
  1. Correspondence to Dr Miguel A Gonzalez-Gay, Hospital Universitario Marqués de Valdecilla, IFIMAV, Avenida de Valdecilla, s/n, Santander, Cantabria 39008, Spain; miguelaggay{at}hotmail.com

https://doi.org/10.1136/annrheumdis-2013-205154

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    We read with great interest the elegant systematic review on cardiovascular (CV) comorbidities by Jamnitski et al, in patients with psoriatic arthritis (PsA) published in the February 2013 issue of ARD.1 Overall, we agree that there is an increased CV risk in patients with PsA similar to that observed in patients with rheumatoid arthritis (RA).2 Therefore, adequate CV risk stratification is also required in PsA patients.

    The authors confirmed that subclinical atherosclerosis and CV risk factors are increased in patients with PsA when compared with controls.1 It is well known that inflammation promotes endothelial cell activation in patients with chronic inflammatory rheumatic diseases like RA.3 The presence of a chronic inflammatory state is responsible for the development of subclinical atherosclerosis and increased incidence of CV events …

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    Footnotes

    • Contributors MAG-G, CG-J, JL, and SC performed the interpretation of data, and all of them were responsible for the final drafting and elaboration of the manuscript.

    • Funding The studies conducted by the authors on atherosclerosis in rheumatic diseases have been supported by grants from ‘Fondo de Investigaciones Sanitarias’ PI06/0024, PS09/00748 and PI12/00060, and by RETICS Program RD12/0009/0013 (RIER) from ‘Instituto de Salud Carlos III’ (ISCIII) (Spain).

    • Competing interests None.

    • Patient consent Obtained.

    • Ethics approval This is a letter to the editor. However, the studies discussed in this letter that were performed by our group were approved by Spanish Ethics Committees of Galicia and Cantabria.

    • Provenance and peer review Not commissioned; internally peer reviewed.

    • Data sharing statement Our letter to the editor constitutes an original research. It was not previously sent for publication to any other journal.

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