What is the clinical evidence from this study?

Study design: Cohort. Population: Cardiovascular risk (aortic stiffness) (n=3769). Intervention: Central obesity (10 cm increase in waist circumference) vs. Lower waist circumference. Primary outcome: Aortic pulse wave velocity (aPWV) at follow-up (MD 0.40 m/s, 95% CI 0.24;0.56, p=<0.0001).

May 22, 2012Open Access

Determinants of Aortic Stiffness: 16-Year Follow-Up of the Whitehall II Study

Q: What are the key findings of this study?

Central obesity was a strong predictor of aortic stiffness, with a 10 cm increase in waist circumference associated with a 0.40 m/s increase in aortic pulse wave velocity in men.

Key Result

Central obesity was a strong predictor of aortic stiffness, with a 10 cm increase in waist circumference associated with a 0.40 m/s increase in aortic pulse wave velocity in men.

Study Design

Type

Cohort (n=3,769)

Structured PICO

Population

3,769 British civil servants aged 35-55 years, free of baseline coronary heart disease and diabetes, followed for 16 years to assess determinants of aortic stiffness.

Outcome

Aortic pulse wave velocity at follow-up (2007-2009)surrogate

Central obesity is a strong long-term predictor of aortic stiffness, with heart rate in men and adiponectin in women also serving as key predictors, suggesting sex-specific pathways in vascular aging.

Main Result

Mean Difference: 0.4 (95% CI 0.24–0.56)

p-value: p=<0.0001

Limitations

Study population restricted to middle-aged British civil servants of White ethnicity, limiting generalizability
Lack of a baseline measure of aPWV prevents concluding causality
Use of a tape measure to determine carotid-femoral path length may have overestimated the distance in obese individuals
Potential healthy survivor effect due to loss to follow-up

Abstract

BACKGROUND: Aortic stiffness is a strong predictor of cardiovascular disease endpoints. Cross-sectional studies have shown associations of various cardiovascular risk factors with aortic pulse wave velocity, a measure of aortic stiffness, but the long-term impact of these factors on aortic stiffness is unknown. METHODS: In 3,769 men and women from the Whitehall II cohort, a wide range of traditional and novel cardiovascular risk factors were determined at baseline (1991-1993) and aortic pulse wave velocity was measured at follow-up (2007-2009). The prospective associations between each baseline risk factor and aortic pulse wave velocity at follow-up were assessed through sex stratified linear regression analysis adjusted for relevant confounders. Missing data on baseline determinants were imputed using the Multivariate Imputation by Chained Equations. RESULTS: Among men, the strongest predictors were waist circumference, waist-hip ratio, heart rate and interleukin 1 receptor antagonist, and among women, adiponectin, triglycerides, pulse pressure and waist-hip ratio. The impact of 10 centimeter increase in waist circumference on aortic pulse wave velocity was twice as large for men compared with women (men: 0.40 m/s (95%-CI: 0.24;0.56); women: 0.17 m/s (95%-CI: -0.01;0.35)), whereas the opposite was true for the impact of a two-fold increase in adiponectin (men: -0.30 m/s (95%-CI: -0.51;-0.10); women: 0.61 m/s (95%-CI: -0.86;-0.35)). CONCLUSION: In this large prospective study, central obesity was a strong predictor of aortic stiffness. Additionally, heart rate in men and adiponectin in women predicted aortic pulse wave velocity suggesting that strategies to prevent aortic stiffening should be focused differently by sex.

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