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Background/Objectives: Large artery stiffening is a novel risk factor for cognitive impairment including Alzheimer’s disease. Loss of impedance mismatch between central and cerebral arteries promotes cerebrovascular dysfunction via chronic transmission of excessive pulsatile pressure and flow to the brain. Cerebrovascular dysfunction uncouples cerebral blood flow supply from metabolic demand, contributing to hypoperfusion and acidosis. Conversely, greater impedance mismatch may protect against cerebrovasculature dysfunction, brain acidosis and cognitive impairment. Values for brain T1rho, a novel pH-sensitive MRI biomarker, are higher (more acidic) in patients with cognitive impairment compared with healthy controls. However, relations of T1rho with 1) large artery stiffness and central pulsatile hemodynamics and 2) memory performance are unknown. Methods/Results: Middle-aged/older adults (n = 31, 68 ± 2 years) underwent vascular, global T1rho MRI and memory testing. In a subset (n = 17), common carotid artery (CCA) intima-medial thickness (IMT) and pulsatile pressure/flow hemodynamics were measured (applanation tonometry, Doppler ultrasonography). In the entire cohort, higher T1rho was associated with greater aortic stiffness (cfPWV; r = 0.36, p = 0.054, covariate: MAP) and lower memory performance (r = −0.43, p = 0.03, education). In the subset, greater CCA IMT was correlated with higher cfPWV (r = 0.45, p = 0.08, MAP), suggesting that elevated aortic stiffness may promote concentric CCA remodeling. Higher CCA characteristic impedance was associated with lower T1rho (r = −0.57, p = 0.02) and higher memory performance (r = 0.46, p = 0.08). T1rho was not correlated with CCA reflection coefficient or pulsatile flow parameters (p > 0.05). Conclusion: These preliminary data suggest that compensatory remodeling of the CCA artery associated with elevated aortic stiffness may be protective against alterations in brain pH and cognitive performance.

Systolic blood pressure (SBP) differs between the brachial artery and aorta. Prospective data suggest that central pressure predicts future cardiovascular events, but it is unclear if it is superior to brachial pressure. Methods and Results: A systematic review and individual participant data meta-analysis from 15 studies was undertaken. Study-specific associations of central and brachial pressure with cardiovascular outcomes, with and without mutual adjustment, were determined using Cox proportional hazard models, and random effect models to estimate pooled estimates. Of 22,433 participants, 908 had a myocardial infarction (MI) and 641 a stroke. The pooled age, sex, height and heart rate adjusted hazard ratio (HR) [95% CI] per SD increase in brachial SBP was 1.17 [1.03, 1.32] for MI and 1.28 [1.13, 1.46] for stroke and 1.16 [1.02, 1.33] and 1.33 [1.15, 1.53] for central SBP, respectively. Mutual adjustment attenuated the HRs for MI: brachial SBP (1.16 [0.90, 1.48]), central SBP (1.09 [0.87, 1.38]) and stroke: brachial SBP (1.18 [0.97, 1.42]), central SBP (1.19 [0.99, 1.44]). However, associations between central SBP and stroke, after adjustment for brachial SBP, were higher in those aged

Background-—Accurate assessment of mechanical properties of the proximal aorta is a requisite first step for elucidating the pathophysiology of isolated systolic hypertension. During systole, substantial proximal aortic axial displacement produces longitudinal strain, which we hypothesize causes variable underestimation of ascending aortic circumferential strain compared to values in the longitudinally constrained descending aorta.

Relations between central versus brachial blood pressure and major cardiovascular disease (CVD) events remain controversial. Central measures derived using radial tonometry and a generalized transfer function as implemented using the SphygmoCor device may better predict CVD risk compared to central pressures from carotid tonometry. We used proportional hazards models to examine relations of augmentation index, central systolic and pulse pressure, and central-to-peripheral pulse pressure amplification obtained using the Sphygmocor algorithm to first-onset major CVD events in 2183 participants (mean age 62 years, 58% women) in the Framingham Heart Study. During median follow-up of 7.8 (range 0.2 to 8.9) years, 149 participants (6.8%) had an incident event. Augmentation index (P = 0.6), central systolic pressure (P = 0.20), central pulse pressure (P = 0.24) and pulse pressure amplification (P = 0.15) were not related to outcomes in models that adjusted for age, sex, clinic systolic blood pressure, use of antihypertensive therapy, total and high density lipoprotein cholesterol concentrations, smoking, and presence of diabetes. When models were repeated using supine oscillometric systolic pressure recorded at the time of tonometry and excluding cases with tonometry pulse height variations >5%, pulse diastolic variation >5%, pulse shape variation >4% or an operator index

Objectives: Left ventricular contraction produces longitudinal strain in the proximal aorta. As a result, aortic stiffening may impair optimal mechanical ventricular-vascular coupling and left ventricular (LV) systolic function, particularly in the long axis. LV global longitudinal strain (GLS) has recently emerged as a sensitive measure of early cardiac dysfunction. In this study, we investigated the relation between aortic stiffness and GLS in a large community-based sample. Methods: In 2516 participants (age 39–90 years, 57% women) of the Framingham Offspring and Omni cohorts, free of cardiovascular disease, we performed tonometry to measure aortic stiffness and echocardiography to assess cardiac function. Aortic stiffness was evaluated as carotid-femoral pulse wave velocity (CFPWV) and as characteristic impedance (Zc), and GLS was calculated using speckle tracking-based measurements. Results: In multivariable analyses adjusting for age, sex, height, systolic blood pressure, augmentation index, LV structure, and additional cardiovascular disease risk factors, increased CFPWV (β±SE: 0.122±0.030 SD strain per SD CFPWV, P