Association of shorter mean telomere length with large artery stiffness in patients with coronary heart disease
Background. Accumulating evidence implicates leukocyte telomere length (LTL) shortening as a potential risk predictor for cardiovascular disease. Arterial stiffness chronicles the cumulative burden of cardiovascular disease risk factors. Therefore, the capacity of LTL to predict arterial stiffness w...
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Veröffentlicht in: | The aging male 2011-03, Vol.14 (1), p.27-32 |
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Sprache: | eng |
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Zusammenfassung: | Background. Accumulating evidence implicates leukocyte telomere length (LTL) shortening as a potential risk predictor for cardiovascular disease. Arterial stiffness chronicles the cumulative burden of cardiovascular disease risk factors. Therefore, the capacity of LTL to predict arterial stiffness was examined.
Methods. A total of 275 unrelated Chinese males: 163 patients with coronary artery disease (CAD) and 112 healthy controls, 40-73 years of age were included in this study. The relative telomere length of leukocytes was determined by a real-time fluorescence quantitative polymerase chain reaction (PCR). Large artery stiffness was measured with carotid-femoral pulse wave velocity (PWV).
Results. The relative telomere length (T/S) ratio was significantly shorter in patients with CAD (0.79 ± 0.26) than in control subjects (1.08 ± 0.22) (p < 0.001). The correlation between LTL and PWV in patients with CAD was stronger than that in the controls (r = −0.467, r2 = 0.227, p < 0.001 for patients with CAD versus r = −0.223; r 2 = 0.050; p = 0.018 for controls). The loge-transformed T/S ratio was inversely correlated with age (r = −0.345; p < 0.001), PWV (r = −0.326; p < 0.001) and C-reactive protein ( r = −0.133; p = 0.027).
Conclusions. The data show an association of leukocyte telomere length shortening with increased arterial stiffness and cardiovascular burden, suggesting that telomere length is a biomarker of large artery elasticity and CAD. Further studies are warranted to study the role of LTL dynamics in the pathogenesis of atherosclerosis. |
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ISSN: | 1368-5538 1473-0790 |
DOI: | 10.3109/13685538.2010.529196 |