Does arterial stiffness mediate or suppress the associations of blood pressure with cardiac structure and function in adolescents?

There is limited understanding of the role of arterial stiffness in cardiovascular disease risk in the pediatric population, lagging behind strong evidence in the adult population. Arterial stiffness progression among adolescents with hypertension has been considered hypertension-mediated vascular damage. However, emerging pediatric reports suggest that arterial stiffness may precede increased blood pressure and hypertension, whereas increased blood pressure from childhood has been associated with signs of cardiac damage in mid-adulthood. Thus, this study used a third variable analytical approach to examine whether arterial stiffness mediates or suppresses the effects of increasing blood pressure on cardiac structure and function in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort of 1,778 adolescents. After an adjustment for cardiometabolic and lifestyle factors, arterial stiffness measured as carotid-femoral pulse wave velocity partly suppressed the association of higher systolic blood pressure with higher left ventricular mass (standardized regression coefficient, β = -0.012; = 0.017; suppression effect = 4%), partly mediated the associations of higher systolic and diastolic blood pressure with higher relative ventricular wall thickness, and partly suppressed the association of higher diastolic blood pressure with lower left ventricular diastolic function (β = -0.021; = 0.003; suppression effect = 14.5%). In conclusion, increasing arterial stiffness could attenuate some of the adverse effects of increased blood pressure on cardiac structure and function in adolescents possibly by modifying the Windkessel effects. The present study demonstrates that the associations of blood pressure with cardiac function and structure in adolescents may be mediated or suppressed by arterial stiffness depending on the blood pressure phenotype: systolic or diastolic. Arterial stiffness may be considered as an intermediate pathway to attenuate the effect of increased blood pressure on altered cardiac structure and function in youth.