Association between anti-human heat shock protein-60 and interleukin-2 with coronary artery calcium score.

Pubmed ID: 25561686

Journal: Heart (British Cardiac Society)

Publication Date: March 1, 2015

MeSH Terms: Humans, Male, Female, Aged, Aged, 80 and over, Middle Aged, Prospective Studies, Calcium, Antibodies, Coronary Vessels, Chaperonin 60, Interleukin-2

Grants: R01 HL071094

Authors: Damluji AA, Ramireddy A, Al-Damluji MS, Marzouka GR, Otalvaro L, Viles-Gonzalez JF, Dong C, Alfonso CE, Hendel RC, Cohen MG, Moscucci M, Bishopric NH, Myerburg RJ

Cite As: Damluji AA, Ramireddy A, Al-Damluji MS, Marzouka GR, Otalvaro L, Viles-Gonzalez JF, Dong C, Alfonso CE, Hendel RC, Cohen MG, Moscucci M, Bishopric NH, Myerburg RJ. Association between anti-human heat shock protein-60 and interleukin-2 with coronary artery calcium score. Heart 2015 Mar;101(6):436-41. Epub 2015 Jan 5.

Studies:

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.