BACKGROUND: Increased aortic stiffness contributes to systolic hypertension and increased cardiovascular risk. The augmentation index (AI), ie, the percentage of central pulse pressure attributed to reflected wave overlap in systole, was proposed as a noninvasive indicator of increased arterial stiffness. We evaluated this hypothesis by investigating relations between AI and other direct measures of aortic stiffness. METHODS: Tonometric carotid- and femoral-pressure waveforms, Doppler aortic flow, and aortic-root diameter were assessed in 123 individuals with uncomplicated systolic hypertension and 29 controls of comparable age and sex. Carotid-femoral pulse-wave velocity (PWV) was assessed from the carotid-femoral time delay and body-surface measurements. Aortic PWV was assessed from the ratio of the upstroke of carotid pressure and aortic flow velocity and was used to calculate proximal aortic compliance as [aortic area]/[1.06 x (aortic PWV)(2)]. RESULTS: Partial correlations (adjusted for age, sex, presence of hypertension, height, weight, and systolic ejection period) showed no association between AI and carotid-femoral PWV (R = -0.05, P = .54). The AI was significantly though weakly related directly with aortic compliance (R = 0.21, P = .012) and inversely with aortic PWV (R = -0.198, P = .017). However, higher stiffness (lower compliance and higher PWV) was associated with lower AI. CONCLUSIONS: Increased AI is not a reliable surrogate for increased aortic stiffness. Decreasing AI with decreasing compliance (increasing aortic stiffness) may be attributable to impedance matching and reduced wave reflection at the interface between the aorta and the muscular arteries.
BACKGROUND: Increased aortic stiffness contributes to systolic hypertension and increased cardiovascular risk. The augmentation index (AI), ie, the percentage of central pulse pressure attributed to reflected wave overlap in systole, was proposed as a noninvasive indicator of increased arterial stiffness. We evaluated this hypothesis by investigating relations between AI and other direct measures of aortic stiffness. METHODS: Tonometric carotid- and femoral-pressure waveforms, Doppler aortic flow, and aortic-root diameter were assessed in 123 individuals with uncomplicated systolic hypertension and 29 controls of comparable age and sex. Carotid-femoral pulse-wave velocity (PWV) was assessed from the carotid-femoral time delay and body-surface measurements. Aortic PWV was assessed from the ratio of the upstroke of carotid pressure and aortic flow velocity and was used to calculate proximal aortic compliance as [aortic area]/[1.06 x (aortic PWV)(2)]. RESULTS: Partial correlations (adjusted for age, sex, presence of hypertension, height, weight, and systolic ejection period) showed no association between AI and carotid-femoral PWV (R = -0.05, P = .54). The AI was significantly though weakly related directly with aortic compliance (R = 0.21, P = .012) and inversely with aortic PWV (R = -0.198, P = .017). However, higher stiffness (lower compliance and higher PWV) was associated with lower AI. CONCLUSIONS: Increased AI is not a reliable surrogate for increased aortic stiffness. Decreasing AI with decreasing compliance (increasing aortic stiffness) may be attributable to impedance matching and reduced wave reflection at the interface between the aorta and the muscular arteries.
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