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Physiological and clinical insights from reservoir-excess pressure analysis.

ABSTRACT: There is a growing body of evidence indicating that reservoir-excess pressure model parameters provide physiological and clinical insights above and beyond standard blood pressure (BP) and pulse waveform analysis. This information has never been collectively examined and was the aim of this review. Cardiovascular disease is the leading cause of mortality worldwide, with BP as the greatest cardiovascular disease risk factor. However, brachial systolic and diastolic BP provide limited information on the underlying BP waveform, missing important BP-related cardiovascular risk. A comprehensive analysis of the BP waveform is provided by parameters derived via the reservoir-excess pressure model, which include reservoir pressure, excess pressure, and systolic and diastolic rate constants and Pinfinity. These parameters, derived from the arterial BP waveform, provide information on the underlying arterial physiology and ventricular-arterial interactions otherwise missed by conventional BP and waveform indices. Application of the reservoir-excess pressure model in the clinical setting may facilitate a better understanding and earlier identification of cardiovascular dysfunction associated with disease. Indeed, reservoir-excess pressure parameters have been associated with sub-clinical markers of end-organ damage, cardiac and vascular dysfunction, and future cardiovascular events and mortality beyond conventional risk factors. In the future, greater understanding is needed on how the underlying physiology of the reservoir-excess pressure parameters informs cardiovascular disease risk prediction over conventional BP and waveform indices. Additional consideration should be given to the application of the reservoir-excess pressure model in clinical practice using new technologies embedded into conventional BP assessment methods.

SUBMITTER: Armstrong MK

PROVIDER: S-EPMC7611663 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundAbnormal blood pressure (BP) responses to exercise can predict adverse cardiovascular outcomes, but their optimal measurement and definitions are poorly understood. We combined frequently sampled BP during cardiopulmonary exercise testing with vascular stiffness assessment to parse cardiac and vascular components of exercise BP.MethodsCardiopulmonary exercise testing with BP measured every two minutes and resting vascular tonometry were performed in 2858 Framingham Heart Study participants. Linear regression was used to analyze sex-specific exercise BP patterns as a function of arterial stiffness (carotid-femoral pulse wave velocity) and cardiac-peripheral performance (defined by peak O2 pulse).ResultsOur sample was balanced by sex (52% women) with mean age 54±9 years and 47% with hypertension. We observed variability in carotid-femoral pulse wave velocity and peak O2 pulse across individuals with clinically defined exercise hypertension (peak systolic BP [SBP] in men ≥210 mm Hg; in women ≥190 mm Hg). Despite similar resting SBP and cardiometabolic profiles, individuals with higher peak O2 pulse displayed higher peak SBP (P≤0.017) alongside higher fitness levels (P<0.001), suggesting that high peak exercise SBP in the context of high peak O2 pulse may in fact be favorable. Although both higher (favorable) O2 pulse and higher (adverse) arterial stiffness were associated with greater peak SBP (P<0.0001 for both), the magnitude of association of carotid-femoral pulse wave velocity with peak SBP was higher in women (sex-carotid-femoral pulse wave velocity interaction P<0.0001). In sex-specific models, exercise SBP measures accounting for workload (eg, SBP during unloaded exercise, SBP at 75 watts, and SBP/workload slope) were directly associated with the adverse features of greater arterial stiffness and lower peak O2 pulse.ConclusionsHigher peak exercise SBP reflects a complex trade-off between arterial stiffness and cardiac-peripheral performance that differs by sex. Studies of BP responses to exercise accounting for vascular and cardiac physiology may illuminate mechanisms of hypertension and clarify clinical interpretation of exercise BP.

Project description:INTRODUCTION:The development and propagation of the aortic blood pressure wave remains poorly understood, despite its clear relevance to major organ blood flow and potential association with cardiovascular outcomes. The reservoir pressure model provides a unified description of the dual conduit and reservoir functions of the aorta. Reservoir waveform analysis resolves the aortic pressure waveform into an excess (wave related) and reservoir (compliance related) pressure. The applicability of this model to the pressure waveform as it propagates along the aorta has not been investigated in humans. METHODS:We analysed invasively acquired high-fidelity aortic pressure waveforms from 40 patients undergoing clinically indicated coronary catheterization. Aortic waveforms were measured using a solid-state pressure catheter at five anatomical sites: the ascending aorta, the transverse aortic arch, the diaphragm, the level of the renal arteries, and at the aortic bifurcation. Ensemble average pressure waveforms were obtained for these sites for each patient and analysed to obtain the reservoir pressure [Pr(t)] and the excess pressure [Px(t)] at each aortic position. RESULTS:Systolic blood pressure increased at a rate of 2.1?mmHg per site along the aorta, whereas diastolic blood pressure was effectively constant. Maximum Pr decreased only slightly along the aorta (changing by -0.7?mmHg per site), whereas the maximum of Px increased from the proximal to distal aorta (+4.1?mmHg per site; P?<?0.001). The time, relative to the start of systolic upstroke, of the occurrence of the maximum excess pressure did not vary along the aorta. Of the parameters used to derive the reservoir pressure waveform the systolic and diastolic rate constants showed divergent changes with the systolic rate constant (ks) decreasing and the diastolic rate constant (kd) increasing along the aorta. CONCLUSIONS:This analysis confirms the proposition that the magnitude of the calculated reservoir pressure waveform, despite known changes in aortic structure, is effectively constant throughout the aorta. A progressive increase of excess pressure accounts for the increase in pulse pressure from the proximal to distal aorta. The reservoir pressure rate constants seem to behave as arterial functional parameters. The accompanying decrease in ks and increase in kd are consistent with a progressive decrease in aortic compliance and increase in impedance. The reservoir pressure waveform therefore provides a model that might have utility in understanding the generation of central blood pressure and in specific cases might have clinical utility.

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Physiological and clinical insights from reservoir-excess pressure analysis.

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