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Background: Elastic arteries stiffen via 2 main mechanisms: (1) load-dependent stiffening from higher blood pressure and (2) structural stiffening due to changes in the vessel wall. It is unknown how these different mechanisms contribute to incident cardiovascular disease (CVD) events. Methods: The MESA (Multi-Ethnic Study of Atherosclerosis) is a longitudinal study of 6814 men and women without CVD at enrollment, from 6 communities in the United States. MESA participants with B-mode carotid ultrasound and brachial blood pressure at baseline Exam in (2000–2002) and CVD surveillance (mean follow-up 14.3 years through 2018) were included (n=5873). Peterson’s elastic modulus was calculated to represent total arterial stiffness. Structural stiffness was calculated by adjusting Peterson’s elastic modulus to a standard blood pressure of 120/80 mm Hg with participant-specific models. Load-dependent stiffness was the difference between total and structural stiffness. Results: In Cox models adjusted for traditional risk factors, load-dependent stiffness was significantly associated with higher incidence of CVD events (hazard ratio/100 mm Hg, 1.21 [95% CI, 1.09–1.34] P P =0.10). Analysis of participants who were normotensive (blood pressure P P =0.16). Conclusions: These results provide valuable new insights into mechanisms underlying the association between arterial stiffness and CVD. Load-dependent stiffness was significantly associated with CVD events but structural stiffness was not.

Introduction: Arterial stiffness can be separated into two main mechanisms: 1) load-dependent (LD) stiffening from higher blood pressure (BP) and (2) structural stiffening due to changes in the vessel wall. Structural stiffening is strongly associated with advancing age. LD stiffening is highly variable and is more strongly associated with CVD. Hypothesis: Optimal Life’s Simple 7 factors will be associated with a slower rate of increase in LD stiffness. Methods: MESA participants with carotid ultrasound at Exam 1 and Exam 5 (year 10) were included (n=2557). Peterson’s elastic modulus (PEM) was calculated to represent total stiffness. Structural stiffness was PEM adjusted to a standard BP of 120/80 mmHg using participant-specific models. LD stiffness was the difference between total and structural stiffness. Changes in stiffness mechanisms over 10 years for poor versus optimal Life’s Simple 7 (LSF) factors were compared with linear models adjusted for age, sex, race/ethnicity, study site, education, BP and lipid medication, C-reactive protein, Interleukin-6, and baseline stiffness. Results: No LS7 factors was associated with increased LD stiffening for the whole cohort. For the bottom quartile of baseline LD stiffness, smoking (2.55±1.23 kPa, p=0.039) was associated with increased LD stiffening. For the highest quartile of baseline LD stiffness, no LS7 factors were significantly associated with stiffening. Conclusion: Smoking was associated with increased LD stiffening in those with low baseline stiffness. Smoking cessation and prevention may be especially important in these individuals to promote healthy vascular aging.