Abstract 3431: Pulse Pressure Is Inversely Related to Aortic Root Diameter: Implications for the Pathogenesis of Systolic Hypertension
Background: The age-associated increase in central arterial stiffness manifests as a rise in pulse pressure, which leads to a marked increase in the prevalence of systolic hypertension among older individuals. Aortic root diameter (AoD) also increases with advancing age. According to the prevailing views, hypertension contributes to a further increase in AoD. Conversely, it has been suggested that the age-associated increase in AoD may partially compensate for the increased arterial stiffness. We tested the hypothesis that AoD is inversely associated with pulse pressure.
Methods: The study population comprised 1256 individuals, aged 30 –79 years (48% women, 48% hypertensive), none of whom were on antihypertensive medications. Brachial pulse pressure (bPP) was calculated as the difference between sphygmomanometric systolic and diastolic blood pressures. Central pulse pressure (cPP) was derived from calibrated carotid artery pressure waveforms. AoD was measured by echocardiography at the level of the Sinuses of Valsalva. The relationships of AoD with bPP and cPP were evaluated with multiple regression analyses.
Results: bPP was 54 ± 18 mmHg in women and 50 ± 14 mmHg in men, and AoD was 28.9 ± 3.5 mm in women and 31.9 ± 3.5 mm in men. After adjusting for age, age2, height, weight, and mean arterial pressure, bPP was inversely associated with AoD in both sexes. This inverse association persisted even after adjusting for aortic pulse wave velocity, carotid intima-media thickness, reflected waves, and left ventricular end-diastolic diameter and wall thickness. In the fully adjusted models predicting bPP, the regression coefficients for AoD were −0.48 in men (p = 0.0003, model R2=0.51) and −0.40 in women (p = 0.01, model R2= 0.61). Similarly, cPP was inversely associated with AoD in both men (coefficient = −0.45, p = 0.0007, model R2=0.50) and women (coefficient = −0.40, p = 0.01 model R2= 0.61). Thus, each 1 mm increase in AoD was associated with a 0.4 – 0.5 mmHg decrease in bPP and cPP in both sexes.
Conclusions: Contrary to the prevailing views, AoD is independently and inversely associated with both bPP and cPP. These findings suggest that a small AoD may contribute to the pathogenesis of systolic hypertension. Longitudinal studies are needed to examine this possibility.