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Pulsatile arterial haemodynamics in heart failure.

ABSTRACT: Due to the cyclic function of the human heart, pressure and flow in the circulation are pulsatile rather than continuous. Addressing pulsatile haemodynamics starts with the most convenient measurement, brachial pulse pressure, which is widely available, related to development and treatment of heart failure (HF), but often confounded in patients with established HF. The next level of analysis consists of central (rather than brachial) pressures and, more importantly, of wave reflections. The latter are closely related to left ventricular late systolic afterload, ventricular remodelling, diastolic dysfunction, exercise capacity, and, in the long-term, the risk of new-onset HF. Wave reflection may also represent a suitable therapeutic target. Treatments for HF with preserved and reduced ejection fraction, based on a reduction of wave reflection, are emerging. A full understanding of ventricular-arterial coupling, however, requires dedicated analysis of time-resolved pressure and flow signals, which can be readily accomplished with contemporary non-invasive imaging and modelling techniques. This review provides a summary of our current understanding of pulsatile haemodynamics in HF.

SUBMITTER: Weber T

PROVIDER: S-EPMC6234849 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature

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Pulsatile arterial haemodynamics in heart failure.

Weber Thomas T Chirinos Julio A JA

European heart journal 20181101 43

Due to the cyclic function of the human heart, pressure and flow in the circulation are pulsatile rather than continuous. Addressing pulsatile haemodynamics starts with the most convenient measurement, brachial pulse pressure, which is widely available, related to development and treatment of heart failure (HF), but often confounded in patients with established HF. The next level of analysis consists of central (rather than brachial) pressures and, more importantly, of wave reflections. The latt ...[more]

PMID: 29947746

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Project description:New findingsWhat is the central question of this study? Does cerebrovascular pulsatility respond differently to acute increases in arterial stiffness in middle-aged compared with young adults? What is the main finding and its importance? Compared with young adults, middle-aged adults exhibited similar changes in cerebral pulsatile damping despite attenuated changes in carotid diameter and cerebrovascular pulsatility during blood pressure-dependent, but not blood pressure-independent, increases in large artery stiffness.AbstractAcute manipulation of arterial stiffness through interventions that increase sympathetic activity might provoke cerebral pulsatility and damping and reveal whether cerebrovascular haemodynamics respond differently to transient elevations in arterial stiffness in middle-aged compared with young adults. We compared cerebral pulsatility and damping in middle-aged versus young adults during two different sympathetic interventions [cold pressor test (CP) and lower-body negative pressure (LBNP)] that increase arterial stiffness acutely. Cerebrovascular haemodynamics were assessed in 15 middle-aged (54 ± 7 years old; 11 female) and 15 sex-matched young adults (25 ± 4 years old) at rest and during the CP test (4 min, 6.4 ± 0.8°C) and LBNP (6 min, -20 mmHg). Mean blood pressure was measured continuously via finger photoplethysmography. Carotid-femoral pulse wave velocity (cfPWV) and carotid stiffness were measured via tonometry and ultrasound. Blood velocity pulsatility index (PI) was measured at the middle cerebral (MCA) and common carotid artery (CCA) using Doppler, with pulsatile damping calculated as CCA PI divided by MCA PI. Increases in cfPWV were driven by changes in mean pressure during CP but not during LBNP in both groups (P < 0.05). Pulsatile damping decreased in both groups (P < 0.05) despite reductions in MCA PI and greater carotid dilatation during CP in young compared with middle-aged adults (P < 0.05). Pressure-independent increases in cfPWV during LBNP did not alter pulsatile damping but decreased MCA PI in both young and middle-aged adults (P < 0.05). These data suggest that changes in carotid diameter and cerebrovascular pulsatility differ between young and middle-aged adults despite similar changes in cerebral pulsatile damping during blood pressure-dependent, but not blood pressure-independent, increases in large artery stiffness.

Project description:AimsInteratrial shunting (IAS) reduces left atrial pressure in patients with heart failure. Several clinical trials reported that IAS improved the New York Heart Association score and exercise capacity. However, its effects on haemodynamics vary depending on shunt size, cardiovascular properties, and stressed blood volume. To maximize the benefit of IAS, quantitative prediction of haemodynamics under IAS in individual patients is essential. The generalized circulatory equilibrium framework determines circulatory equilibrium as the intersection of the cardiac output curve and the venous return surface. By incorporating IAS into the framework, we predict the impact of IAS on haemodynamics.Methods and resultsIn seven mongrel dogs, we ligated the left anterior descending artery and created impaired cardiac function with elevated left atrial pressure (baseline: 7.8 ± 1.0 vs. impaired: 11.9 ± 3.2 mmHg). We established extracorporeal left-to-right atrial shunting with a centrifugal pump. After recording pre-IAS haemodynamics, we changed IAS flow stepwise to various levels and measured haemodynamics under IAS. To predict the impact of IAS on haemodynamics, we modelled the fluid mechanics of IAS by Newton's second law and incorporated IAS into the generalized circulatory equilibrium framework. Using pre-IAS haemodynamic data obtained from the dogs, we predicted the impact of IAS flow on haemodynamics under IAS condition using a set of equations. We compared the predicted haemodynamic data with those measured. The predicted pulmonary flow [r2 = 0.88, root mean squared error (RMSE) 11.4 mL/min/kg, P < 0.001), systemic flow (r2 = 0.92, RMSE 11.2 mL/min/kg, P < 0.001), right atrial pressure (r2 = 0.92, RMSE 0.71 mmHg, P < 0.001), and left atrial pressure (r2 = 0.83, RMSE 0.95 mmHg, P < 0.001) matched well with those measured under normal and impaired cardiac function. Using this framework, we further performed a simulation study to examine the haemodynamic benefit of IAS in heart failure with preserved ejection fraction. We simulated the IAS haemodynamics under volume loading and exercise conditions. Volume loading and exercise markedly increased left atrial pressure. IAS size-dependently attenuated the increase in left atrial pressure in both volume loading and exercise. These results indicate that IAS improves volume and exercise intolerance.ConclusionsThe framework developed in this study quantitatively predicts the haemodynamic impact of IAS. Simulation study elucidates how IAS improve haemodynamics under volume loading and exercise conditions. Quantitative prediction of IAS haemodynamics would contribute to maximizing the benefit of IAS in patients with heart failure.

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Pulsatile arterial haemodynamics in heart failure.

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Pulsatile arterial haemodynamics in heart failure.

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