Michelle J Ormseth1, Joseph F Solus2, Annette M Oeser2, Aihua Bian2, Tebeb Gebretsadik2, Ayumi Shintani2, Paolo Raggi2, C Michael Stein2. 1. From the departments of Medicine and Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee; the departments of Medicine and Radiology, Emory University, Atlanta, Georgia, USA; and the departments of Medicine and Radiology, University of Alberta, Edmonton, Alberta, Canada.M.J. Ormseth, MD, MSCI, Department of Medicine, Vanderbilt University Medical Center; J.F. Solus, PhD, Department of Medicine, Vanderbilt University Medical Center; A.M. Oeser, BS, MLAS, CCRP, Department of Medicine, Vanderbilt University Medical Center; A. Bian, MPH, Department of Biostatistics, Vanderbilt University Medical Center; T. Gebretsadik, MPH, Department of Biostatistics, Vanderbilt University Medical Center; A. Shintani, PhD, MPH, Department of Biostatistics, Vanderbilt University Medical Center; P. Raggi, MD, departments of Medicine and Radiology, University of Alberta; C.M. Stein, MD, Department of Medicine, Vanderbilt University Medical Center. michelle.ormseth@vanderbilt.edu. 2. From the departments of Medicine and Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee; the departments of Medicine and Radiology, Emory University, Atlanta, Georgia, USA; and the departments of Medicine and Radiology, University of Alberta, Edmonton, Alberta, Canada.M.J. Ormseth, MD, MSCI, Department of Medicine, Vanderbilt University Medical Center; J.F. Solus, PhD, Department of Medicine, Vanderbilt University Medical Center; A.M. Oeser, BS, MLAS, CCRP, Department of Medicine, Vanderbilt University Medical Center; A. Bian, MPH, Department of Biostatistics, Vanderbilt University Medical Center; T. Gebretsadik, MPH, Department of Biostatistics, Vanderbilt University Medical Center; A. Shintani, PhD, MPH, Department of Biostatistics, Vanderbilt University Medical Center; P. Raggi, MD, departments of Medicine and Radiology, University of Alberta; C.M. Stein, MD, Department of Medicine, Vanderbilt University Medical Center.
Abstract
OBJECTIVE: Telomeres protect against chromosomal end damage and shorten with each cell division; their length may be a marker of cardiovascular and overall biological aging. We examined the hypothesis that reduced telomere length is associated with increased coronary atherosclerosis in rheumatoid arthritis (RA). METHODS: We performed a cross-sectional study in 145 patients with RA and 87 control subjects frequency-matched for age, race, and sex. Coronary artery calcium score was determined by noncontrast cardiac computed tomography. Telomere length was measured from whole blood DNA, using real-time quantitative polymerase chain reaction and expressed as telomeric product to a single-copy gene product ratio (T/S ratio). Associations between telomere length, coronary artery calcium score, and 28-joint Disease Activity Score (DAS28) were assessed with Spearman correlation, proportional odds logistic regression, and linear regression, adjusting for age, race, and sex. RESULTS: Telomere length was significantly inversely correlated with age in patients with RA (ρ = -0.37, p < 0.001) and control subjects (ρ = -0.39, p = 0.001). Among patients with RA, for every interquartile range (IQR) decrease in telomere length (T/S ratio), the odds of higher coronary artery calcium score increased by 38% (95% CI: 4-60) after adjusting for age, race, and sex (p adjusted = 0.03). Telomere length was not associated with DAS28 (p adjusted = 0.17). Telomere length was not significantly different in patients with RA [median (IQR): 1.02 units (0.9-1.11)] compared to control subjects [1.05 units (0.95-1.17); p = 0.10]. CONCLUSION: Telomere length is inversely associated with coronary artery calcium score, independent of age, race, and sex in patients with RA.
OBJECTIVE: Telomeres protect against chromosomal end damage and shorten with each cell division; their length may be a marker of cardiovascular and overall biological aging. We examined the hypothesis that reduced telomere length is associated with increased coronary atherosclerosis in rheumatoid arthritis (RA). METHODS: We performed a cross-sectional study in 145 patients with RA and 87 control subjects frequency-matched for age, race, and sex. Coronary artery calcium score was determined by noncontrast cardiac computed tomography. Telomere length was measured from whole blood DNA, using real-time quantitative polymerase chain reaction and expressed as telomeric product to a single-copy gene product ratio (T/S ratio). Associations between telomere length, coronary artery calcium score, and 28-joint Disease Activity Score (DAS28) were assessed with Spearman correlation, proportional odds logistic regression, and linear regression, adjusting for age, race, and sex. RESULTS: Telomere length was significantly inversely correlated with age in patients with RA (ρ = -0.37, p < 0.001) and control subjects (ρ = -0.39, p = 0.001). Among patients with RA, for every interquartile range (IQR) decrease in telomere length (T/S ratio), the odds of higher coronary artery calcium score increased by 38% (95% CI: 4-60) after adjusting for age, race, and sex (p adjusted = 0.03). Telomere length was not associated with DAS28 (p adjusted = 0.17). Telomere length was not significantly different in patients with RA [median (IQR): 1.02 units (0.9-1.11)] compared to control subjects [1.05 units (0.95-1.17); p = 0.10]. CONCLUSION: Telomere length is inversely associated with coronary artery calcium score, independent of age, race, and sex in patients with RA.
Authors: Zhengwei Xie; Kyle A Jay; Dana L Smith; Yi Zhang; Zairan Liu; Jiashun Zheng; Ruilin Tian; Hao Li; Elizabeth H Blackburn Journal: Cell Date: 2015-02-26 Impact factor: 41.582
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Authors: H Vaziri; W Dragowska; R C Allsopp; T E Thomas; C B Harley; P M Lansdorp Journal: Proc Natl Acad Sci U S A Date: 1994-10-11 Impact factor: 11.205