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Impact of gender and menopausal status on relationships between biological aging, as indexed by telomere length, and aortic stiffness.

Authors: Andrew R AR. Raymond, Gavin R GR. Norton, Angela J AJ. Woodiwiss, Richard L RL. Brooksbank
Published: 11/19/2014, American journal of hypertension

Background

Telomere length predicts cardiovascular disease (CVD) possibly through an impact of telomere attrition on aortic stiffness. Whether reduced biological aging and a lack of telomere length-aortic stiffness relationships in women contribute to the lower prevalence of CVD in women, prior to menopause, is uncertain.

Methods

We evaluated the relationship between telomere length and carotid-femoral (aortic) pulse wave velocity (PWV) in 580 randomly recruited participants of Black African descent (age = 44 ± 19 years; women: n = 361; premenopausal: n = 195). PWV was determined using carotid and femoral applanation tonometry (SphygmoCor). Relative leukocyte telomere length (T/S) was measured using quantitative real-time polymerase chain reaction assays.

Results

Men and women had similar T/S. T/S was inversely correlated with age (r = -0.14, P < 0.001) and this association was similar in all (r = -0.14, P < 0.01) and premenopausal (r = -0.17, P < 0.05) women as in men (r = -0.14, P < 0.05). An inverse relationship between T/S and PWV was noted both before (r = -0.20, P < 0.0001) and after (partial r = -0.14, P < 0.001) adjustments for confounders. No interaction between T/S and either sex or menopausal status was independently associated with PWV, and T/S was independently correlated with PWV in all (partial r = -0.14, P < 0.01) and premenopausal (partial r = -0.18, P < 0.05) women and in men (partial r = -0.15, P < 0.05).

Conclusions

Gender and premenopausal status do not affect age-related decreases in T/S and associations between T/S and PWV. In participants of African descent in whom telomere length did not differ by gender, the impact of gender prior to menopause on CVD is unlikely to be attributed to differences in the effect of biological aging on aortic stiffness.

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