Jump to comment:

• Response to Gonzalez-Gay's eLetter on Cardiovascular comorbidities in patients with psoriatic arthritis: a systematic review
  Michael T Nurmohamed
  Published on: 13 April 2016
• The influence of inflammation in the development of subclinical atherosclerosis in psoriatic arthritis. Comment on the article by Jamnistki et al.
  Miguel A González-Gay
  Published on: 13 April 2016

• Published on: 13 April 2016

  Response to Gonzalez-Gay's eLetter on Cardiovascular comorbidities in patients with psoriatic arthritis: a systematic review

  • Michael T Nurmohamed, MD
  • Other Contributors:
    • Anna Jamnitski, Deborah Symmons, Mike Peters, Naveed Sattar, Iain McInnes

  Dear Editor,

  In their comments about our systematic review on cardiovascular (CV) comorbidities in patients with psoriatic arthritis, (1) dr Gonzalez-Gay and colleagues, point out that in their studies, (2,3) in contrast to our Table 4, they did demonstrate a correlation between inflammatory parameters and flow-mediated dilatation (FMD) or intima media thickness (IMT). This is indeed correct when these tests are c...

  Show More

  Dear Editor,

  In their comments about our systematic review on cardiovascular (CV) comorbidities in patients with psoriatic arthritis, (1) dr Gonzalez-Gay and colleagues, point out that in their studies, (2,3) in contrast to our Table 4, they did demonstrate a correlation between inflammatory parameters and flow-mediated dilatation (FMD) or intima media thickness (IMT). This is indeed correct when these tests are correlated with inflammatory parameters at the time of diagnosis. However, we felt that it is more appropriate to correlate the inflammatory parameters with the time when the (functional) vascular testing was done. Then the correlations of FMD and inflammatory parameters were not statistically significant (Table 3). (2)
  Similarly, univariate analysis revealed no significant correlation between DAS28, ESR/CRP (at time diagnosis or at time of testing) with IMT (Table 2), (3) as also indicated in our Table 4, albeit that one may argue that some sort of AUC measure should have been used as IMT is more a reflection of a cumulative atherosclerotic burden. Finally, we fully agree with dr. Gonzalez-Gay and colleagues that further studies are needed that investigate if and to what extent anti- inflammatory treatment and/or modification of CV decreases the CV risk in patients with PsA.

  References

  1. Jamnitski A, Symmons D, Peters MJL, et al. Cardiovascular comorbidities in patients with psoriatic arthritis: a systematic review. Ann Rheum Dis 2013;72:211-6.

  2. Gonzalez-Juanatey C, Llorca J, Miranda-Filloy JA, et al. Endothelial dysfunction in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum 2007;57:287-93.

  3. Gonzalez-Juanatey C, Llorca J, Amigo-Diaz E, et al. High prevalence of subclinical atherosclerosis in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum 2007;57:1074-80.

  Conflict of Interest:

  None declared

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top
• Published on: 13 April 2016

  The influence of inflammation in the development of subclinical atherosclerosis in psoriatic arthritis. Comment on the article by Jamnistki et al.

  • Miguel A González-Gay, Dr
  • Other Contributors:
    • Carlos González-Juanatey, Javier Llorca, Santos Castaneda

  Dear Editor,

  We read with great interest the elegant systematic review on cardiovascular (CV) comorbidities in patients with psoriatic arthritis (PsA) published in the February 2013 issue of ARD by Jamnitski et al.[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 re...

  Show More

  Dear Editor,

  We read with great interest the elegant systematic review on cardiovascular (CV) comorbidities in patients with psoriatic arthritis (PsA) published in the February 2013 issue of ARD by Jamnitski et al.[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 in these patients.[4-6] Interestingly, several noninvasive imaging techniques offer a unique opportunity to study the relation of surrogate markers to the development of atherosclerosis. More specifically, brachial flow-mediated dilation (FMD) and carotid artery intima-media thickness (IMT) measurements have been used to assess endothelial function and establish subclinical atherosclerosis respectively. With respect to this, in table 4 of their review article, Jamnitski et al mentioned two studies by Gonzalez-Juanatey et al in which both parameters, FMD and IMT, were abnormal without being correlated with inflammatory markers.[7,8] This is in contradiction with the generalized concept supporting that persistent inflammatory burden causes endothelial dysfunction, subclinical atherosclerosis and increased risk of CV death. However, Gonzalez-Juanatey et al demonstrated that in patients with PsA without clinically evident CV disease or classic atherosclerosis risk factors, there was significant correlation between CRP and ESR levels at the time of disease diagnosis and the presence of endothelial dysfunction, manifested by FMD impairment.[7] This observation was in keeping with epidemiological data that highlighted the relevance of baseline level of CRP as a predictor of CV mortality in patients with inflammatory polyarthritis.[9] PsA patients from the studies by Gonzalez-Juanatey et al were being actively treated and had low disease activity at the time of the ultrasonography assessment. This may explain the lack of significant correlation between ESR and CRP and surrogate markers of subclinical atherosclerosis at that time.[7,8] Nevertheless, when data from carotid ultrasound were evaluated, it was seen that PsA patients exhibited greater carotid artery IMT than did matched controls, and it was correlated with age at diagnosis, disease duration, total cholesterol and LDL cholesterol.[8]
  In any case, correlation between FMD and carotid IMT does not always occur.
  In a former study on patients with RA we observed that carotid IMT was negatively associated with FMD when the time from disease diagnosis ranged from 7.5-20 years but not within the first 5 years after disease diagnosis. It is probably due to the fact that abnormal IMT and endothelial dysfunction reflect different stages of atherosclerosis disease.[10]
  Finally, in agreement with Jamnitski et al,[1] we support the claim that further studies are needed to confirm whether inflammatory suppression or modification of traditional CV risk factors, or both, will reduce CV risk en patients with PsA.

  References

  1. Jamnitski A, Symmons D, Peters MJL, et al. Cardiovascular comorbidities in patients with psoriatic arthritis: a systematic review. Ann Rheum Dis 2013;72:211-6.

  2. Del Rincon I, O'Leary DH, Freeman GL, et al. Acceleration of atherosclerosis during the course of rheumatoid arthritis. Atherosclerosis 2007;195:354-60.

  3. Gonzalez-Gay MA, Gonzalez-Juanatey C, Martin J. Rheumatoid arthritis: a disease associated with accelerated atherogenesis. Semin Arthritis Rheum 2005;35:8-17.

  4. Sattar N, McCarey DW, Capell H, et al. Explaining how "high-grade" systemic inflammation accelerates vascular risk in rheumatoid arthritis [review]. Circulation 2003;108:2957-63.

  5. Del Rincón I, Williams K, Stern MP, et al. Association between carotid atherosclerosis and markers of inflammation in rheumatoid arthritis patients and healthy subjects. Arthritis Rheum 2003;48:1833-40.

  6. Gonzalez-Gay MA, Gonzalez-Juanatey C, Lopez-Diaz MJ, et al. HLA-DRB1 and persistent chronic inflammation contribute to cardiovascular events and cardiovascular mortality in patients with rheumatoid arthritis. Arthritis Rheum 2007;57:125-32.

  7. Gonzalez-Juanatey C, Llorca J, Miranda-Filloy JA, et al. Endothelial dysfunction in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum 2007;57:287-93.

  8. Gonzalez-Juanatey C, Llorca J, Amigo-Diaz E, et al. High prevalence of subclinical atherosclerosis in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum 2007;57:1074-80.

  9. Goodson NJ, Symmons DP, Scott DG, et al. Baseline levels of C-reactive protein and prediction of death from cardiovascular disease in patients with inflammatory polyarthritis: a ten-year followup study of a primary care-based inception cohort. Arthritis Rheum 2005;52:2293-9.

  10. González-Juanatey C, Llorca J, González-Gay MA. Correlation between endothelial function and carotid atherosclerosis in rheumatoid arthritis patients with long-standing disease. Arthritis Res Ther 2011;13:R101.

  Conflict of Interest:

  None declared

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top