Background: Pulse pressure (PP), a marker of arterial stiffening, is closely related to adverse outcomes in hypertensive patients. Correspondingly, less attention has been paid to the value of PP in the population with normal blood pressure. Methods: The study included normotensive elders aged over 60 years from the 1999–2014 National Health and Nutrition Examination Survey (NHANES). All included participants were followed up until the date of death or 31 December 2015. Restricted cubic spline analyses were used to explore the associations of PP with cardiovascular mortality and all-cause mortality. The population was categorized into two groups according to the optimal cut-off of PP for all-cause mortality by X-tile software. Propensity matching score analysis was further performed to reduce confounding bias. The Kaplan–Meier curves and Cox proportional hazard models were applied to estimate the associations of widening PP cardiovascular mortality and all-cause mortality. Subgroup analyses were also conducted. Results: A total of 6309 participants were included (52.9% men and median age 69 (63, 75) years). The median follow-up duration was 74 (42, 114) months. The restricted cubic spline analyses revealed that continuous PP was linearly related to cardiovascular mortality (p for linearity < 0.001; p for nonlinearity = 0.284) and nonlinearly related to all-cause mortality (p for nonlinearity = 0.001). After propensity score matching, 1855 subjects with widening PP and 1855 matched counterparts were included (50.2% men and average age 72 (66, 78) years, 50.9% men and average age 72 (66, 78) years, respectively), of which 966 (26.0%) died during a median follow-up duration of 71 (39, 105) months. In the Cox proportional hazards model, widening PP was associated with increased cardiovascular mortality Hazard Ratio (HR) 1.47; 95% Confidence Interval (CI) 1.07–2.00, p < 0.05] and all-cause mortality (HR 1.15; 95% CI 1.01–1.31, p < 0.05). After adjusting for other traditional risk factors, the association of widening PP with cardiovascular mortality (HR 1.44; 95%CI 1.05–1.98, p < 0.05) remained, and the association of widening PP with all-cause mortality was not statistically significant (p > 0.05). Conclusion: In the normotensive elder population, a low-risk population without traditional coronary risk factors, PP is an independent risk factor for cardiovascular mortality.

OBJECTIVETo determine the role of ascending aorta dilatation in the relationship between pulse pressure (PP) and left ventricular (LV) hypertrophy.METHODS A total of 1556 Chinese elderly hypertensive patients were retrospectively studied. Transthoracic echocardiography was used to obtain the aortic and cardiac structure measurements. In addition, brachial blood pressure was measured, and total arterial compliance, systemic vascular resistance, arterial elastance, and end-systolic LV elastance were calculated. The participants were divided into four groups according to the status of ascending aortic diameter and PP. RESULTSLV mass index increased in succession in the four groups, i.e., the group with the normal aorta and lower PP, with the normal aorta and higher PP, with aortic dilatation and lower PP, and with aortic dilatation and higher PP (P trend < 0.001). Total arterial compliance −1 , arterial elastance, and end-systolic LV elastance were slightly higher in the individuals with normal aorta compared to those with aortic dilatation, regardless of PP being lower or higher (P < 0.01). Compared to the group with the normal aorta and lower PP, individuals with aortic dilatation had a significantly increased multivariable adjusted risk of LV hypertrophy, and higher PP further exacerbated this risk [aortic dilatation with lower PP (OR = 1.75, 95% CI: 1.01-3.04) and aortic dilatation with higher PP (OR = 3.42, 95% CI: 2.03-5.77)]. In the relation between PP and LV mass index (β = 0.095, P < 0.001), -41.3% of the total effect was attributable to mediation by ascending aortic diameter (P < 0.0001). CONCLUSIONSIn Chinese elderly patients with hypertension, ascending aorta dilatation could reduce the influence of elevated PP on LV hypertrophy.