Biological pathways in adolescent aortic stiffness

BACKGROUND: Aortic stiffening begins in youth and antedates future hypertension. In adults, excess weight, systemic inflamma-tion, dyslipidemia, insulin resistance, neurohormonal activation, and altered adipokines are implicated in the pathogenesis of increased aortic stiffness. In adolescents, we assessed the relations of comprehensive measures of aortic stiffness with body mass index (BMI) and related but distinct circulating biomarkers. METHODS AND RESULTS: A convenience sample of 246 adolescents (mean age, 16±2 years; 45% female, 24% Black, and 43% Hispanic) attending primary care or preventive cardiology clinics at 2 tertiary hospitals was grouped as normal weight (N=98) or excess weight (N=148, defined as BMI ≥age-and sex-referenced 85th percentile). After an overnight fast, participants underwent anthropometry, noninvasive arterial tonometry, and assays for serum lipids, CRP (C-reactive protein), glucose, insulin, renin, aldosterone, and leptin. We used multivariable linear regression to relate arterial stiffness markers (including carotid-femoral pulse wave velocity) to BMI z score and a biomarker panel. Carotid-femoral pulse wave velocity was higher in excess weight compared with normal weight group (5.0±0.7 versus 4.6±0.6 m/s; P<0.01). After multivariable adjustment, carotid-femoral pulse wave velocity was associated with BMI z score (0.09 [95% CI, 0.01–0.18]; P=0.04) and with low-density lipoprotein cholesterol (0.26 [95% CI, 0.03–0.50]; P=0.03). CONCLUSIONS: Higher BMI and low-density lipoprotein cholesterol were associated with greater aortic stiffness in adolescents. Maintaining optimal BMI and lipid levels may mitigate aortic stiffness.