Background: Arterial stiffness is a precursor of hypertension and hallmark of vascular aging. Chronological age (CA), a robust determinant of arterial stiffness, is considered an insufficient indicator of aging and disparities associated with disease risk. Biological age (BA), the true age based on physiological decline, is recognized as a better indicator of disease risk however the interplay among BA, CA, and arterial stiffness remains inconclusive. We investigated the associations between BA, CA, and arterial stiffness as a potential pathway for higher cardiovascular risk among Black women and whether race modified these associations. Methods: In 230 women (n=150 White, n=80 Black) enrolled in the Predictive Health Institute cohorts (age range 25-49), arterial stiffness was assessed using carotid-femoral pulse wave velocity (cfPWV), measured by applanation tonometry (SphygmoCor®). BA was estimated using the Klemera-Doubal method from 11 different clinical biomarkers and CA. Accelerated age (AccA) was calculated as the difference between BA and CA. Overall and race-specific associations between BA and arterial stiffness adjusting for sociodemographics, health behaviors, and clinical factors were estimated using multiple linear regression. Results: Overall mean (SD) for CA and BA was 40 (6.1), and 38 (12.1) years, respectively. Mean (SD) for BA, AccA, and cfPWV were 43 (13.1), 1.6 (12.9), and 7.3 (1.1) in Black women and 36 (10.8), -3.2 (10.6), and 6.3 (0.8) in White women (Black-White difference in BA: 6.4 years, P=<0.001). Overall, BA (β=0.02 m/s per year, 95%CI: 0.00, 0.03) predicted cfPWV even after adjustment for CA, without a significant interaction by race (P=0.65). Conclusions: BA is a predictor of arterial stiffness after accounting for CA and additional relevant factors. Although there were no racial differences in this association, both BA and arterial stiffness were higher among Black compared to White women. Longitudinal studies are needed to identify BA patterns and CVD risk in Black women.

The authors have declared no competing interest.

This work was supported by funding in whole or in part by the National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), under Contract nos. [1 U01 HL079156-01 (Quyyumi)] and [1 U01 HL79214-01 (Gibbons)]; NIH, National Center for Research Resources (NCRR) [Grant M01- RR00039] for the Emory Clinical Interaction Unit (ACTSI); and NIH/NCRR [5P20RR11104] for the Morehouse CRC; NIH [K24HL077506-06 (Vaccarino)]; NIH/NCRR [5U54RR022814 (Din)]; and the Woodruff Fund (Emory Predictive Health Initiative). Research reported in this publication was also supported by the National Institute of Nursing Research, NHLBI, and National Institute on Minority Health and Health Disparities of the National Institutes of Health under Award Numbers [K23NR020631 (Spikes)]; [K24HL148521]; [T32HL130025]; and NIMHD [U54MD000214 (Thorpe)]. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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