Abstract

Objective: Altered central artery haemodynamics could have an unfavourable influence on the vasculature. A previous study has suggested that elevated excess pressure integral (INTXSP), derived from reservoir-excess pressure analysis, could reflect circulatory dysfunction and predispose to developing atherosclerosis. In this study, we aimed to determine whether an alteration in parameters derived from the reservoir-excess pressure analysis would be associated with vascular biomarkers of subclinical atherosclerosis in older adults. Design and method: The data from 958 older adults (69.0 ± 8.2yrs, 351 female, 456 with known cardiovascular disease) were analysed. Using radial artery tonometry, the parameters derived from the reservoir-excess pressure analysis including reservoir pressure integral, INTXSP, systolic rate constant (SRC) and diastolic rate constant were obtained. Common carotid artery intima-media thickness (CA-IMT), carotid bulb intima-media thickness (BL-IMT), common carotid artery wall-to-lumen ratio (CA-WLR) were also obtained using an ultrasound system. Results: Multivariate regression analysis revealed that INTXSP was directly associated with CA-IMT [B = 0.081 (95%CI: 0.029, 0.133)] and CA-WLR [B = 0.010 (95%CI: 0.002, 0.017)] after accounting for conventional cardiovascular risk factors and renal function. SRC was also inversely associated with CA-IMT [B = -0.056 (95%CI: -0.099, -0.012)] and CA-WLR [B = -0.009 (95%CI: -0.017, 0.000)] after accounting for conventional cardiovascular risk factors and renal function. When both INTXSP and SRC were entered into the same regression model together, only INTXSP was associated with those parameters. The observed association was independent of carotid-femoral pulse wave velocity and aortic systolic pressure. BL-IMT did not show any association with reservoir-excess pressure parameters. Conclusions: INTXSP was significantly associated with vascular biomarkers of subclinical atherosclerosis in older adults, suggesting that an elevated INTXSP is linked to the development of atherosclerosis.

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