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Original article
Association between anti-human heat shock protein-60 and interleukin-2 with coronary artery calcium score
  1. Abdulla A Damluji1,
  2. Archana Ramireddy1,
  3. Mohammed S Al-Damluji2,
  4. George R Marzouka1,
  5. Lynda Otalvaro1,
  6. Juan F Viles-Gonzalez1,
  7. Chunming Dong1,
  8. Carlos E Alfonso1,
  9. Robert C Hendel1,
  10. Mauricio G Cohen1,
  11. Mauro Moscucci1,
  12. Nanette H Bishopric1,
  13. Robert J Myerburg1
  1. 1Cardiovascular Division, University of Miami Miller School of Medicine, Miami, Florida, USA
  2. 2Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA
  1. Correspondence to Dr Robert J Myerburg, University of Miami, Miller School of Medicine, 1611 NW 12th Street, Room # Central 401, Miami, FL 33136, USA rmyerbur{at}med.miami.edu

Abstract

Introduction Based upon evidence suggesting that concentrations of anti-heat shock protein-60 (anti-HSP60) and interleukin-2 (IL-2) are associated with atherogenesis, we tested the hypothesis that anti-HSP60 and IL-2 are associated with coronary artery calcium (CAC) score, a marker of subclinical atherosclerosis.

Methods We evaluated 998 asymptomatic adults, age 45–84 years, without known coronary disease from the Multi-Ethnic Study of Atherosclerosis (MESA), who had anti-HSP60 measured at baseline. Tertiles of serum anti-HSP60 were evaluated. The associations of IL-2 and anti-HSP60 with CAC were assessed using multivariate analyses, with adjustments for coronary risk factors and Framingham risk score.

Results Patients’ demographics, diabetes, hypertension, obesity, or dyslipidaemia did not show differences in levels of anti-HSP60. The median (IQR) Framingham risk score was 11 (5–22), 8 (5–16), and 9 (5–18) for the first, second, and third tertiles, respectively (p=0.043). IL-2 and tumour necrosis factor α (TNF-α) were associated with increased CAC (IL-2: OR 3.70, p<0.001; TNF-α: OR 4.63, p<0.001). In multivariate regression, the highest tertiles of anti-HSP60 and IL-2 were associated with increased risk of CAC (HSP60 T3: OR 1.49, p=0.022; IL-2: OR 2.49, p<0.001). After adjustment, significant progression of CAC was observed in patients with higher baseline levels of anti-HSP60 (estimate 31.73, p=0.016) and IL-2 (estimate 34.39, p=0.024).

Conclusions Increased concentrations of inflammatory markers (IL-2 and anti-HSP60) are associated with an increased CAC at baseline and follow-up in healthy asymptomatic adults. Future studies should be carried out to assess its association with early development of atherosclerosis.

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