Hemodynamics induced after acute reduction of proximal thoracic aorta compliance

Ioannou, Christos V.; Stergiopulos, Nikolaos; Katsamouris, Asterios; Startchik, Irena; Kalangos, Afksendiyos; Licker, Marc; Westerhof, Nico; Morel, Denis R.

doi:10.1053/ejvs.2002.1917

Cited by 74 publications

(73 citation statements)

References 27 publications

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“…These results agree well, at least in a qualitative sense, with the in vivo experiments by Ioannou et al 4,5 Ioannou et al placed a non-compliant Dacron sleeve around the aortic arch of swines, thereby decreasing substantially the local aortic compliance. Two days after the operation, they reported an increase in PP by 86% and a decrease in total arterial compliance by 50% while the characteristic impedance of the proximal aorta increased to 2.5 times its control value.…”

Section: Discussionsupporting

confidence: 87%

“…This was proven by a large number of studies in animals 5,12 and in the human. 1 The increase in PP, when compliance decreases, can be attributed to loss in Windkessel function.…”

Section: Introductionmentioning

confidence: 93%

“…This was done in accordance to the results of in vivo studies, where acute decrease in compliance was always accompanied by increase in peripheral resistance as to preserve diastolic pressure and, in consequence, coronary perfusion. 4,5 Global Stiffening of the Arterial Tree Global stiffening was achieved by decreasing distensibility of all arterial segments by 40%. The level of decrease in distensibility was found by trial and error, the criterion being the same proximal aorta pulse pressure as the one obtained with local stiffening.…”

Section: Local Proximal Aorta Stiffeningmentioning

confidence: 99%

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Systolic Hypertension Mechanisms: Effect of Global and Local Proximal Aorta Stiffening on Pulse Pressure

2011

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Abstract-Decrease in arterial compliance leads to an increased pulse pressure, as explained by the Windkessel effect. Pressure waveform is the sum of a forward running and a backward running or reflected pressure wave. When the arterial system stiffens, as a result of aging or disease, both the forward and reflected waves are altered and contribute to a greater or lesser degree to the increase in aortic pulse pressure. Two mechanisms have been proposed in the literature to explain systolic hypertension upon arterial stiffening. The most popular one is based on the augmentation and earlier arrival of reflected waves. The second mechanism is based on the augmentation of the forward wave, as a result of an increase of the characteristic impedance of the proximal aorta. The aim of this study is to analyze the two aforementioned mechanisms using a 1-D model of the entire systemic arterial tree. A validated 1-D model of the systemic circulation, representative of a young healthy adult was used to simulate arterial pressure and flow under control conditions and in presence of arterial stiffening. To help elucidate the differences in the two mechanisms contributing to systolic hypertension, the arterial tree was stiffened either locally with compliance being reduced only in the region of the aortic arch, or globally, with a uniform decrease in compliance in all arterial segments. The pulse pressure increased by 58% when proximal aorta was stiffened and the compliance decreased by 43%. Same pulse pressure increase was achieved when compliance of the globally stiffened arterial tree decreased by 47%. In presence of local stiffening in the aortic arch, characteristic impedance increased to 0.10 mmHg s/mL vs. 0.034 mmHg s/mL in control and this led to a substantial increase (91%) in the amplitude of the forward wave, which attained 42 mmHg vs. 22 mmHg in control. Under global stiffening, the pulse pressure of the forward wave increased by 41% and the amplitude of the reflected wave by 83%. Reflected waves arrived earlier in systole, enhancing their contribution to systolic pressure. The effects of local vs.global loss of compliance of the arterial tree have been studied with the use of a 1-D model. Local stiffening in the proximal aorta increases systolic pressure mainly through the augmentation of the forward pressure wave, whereas global stiffening augments systolic pressure principally though the increase in wave reflections. The relative contribution of the two mechanisms depends on the topology of arterial stiffening and geometrical alterations taking place in aging or in disease.

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Section: Discussionsupporting

confidence: 87%

“…This was proven by a large number of studies in animals 5,12 and in the human. 1 The increase in PP, when compliance decreases, can be attributed to loss in Windkessel function.…”

Section: Introductionmentioning

confidence: 93%

Section: Local Proximal Aorta Stiffeningmentioning

confidence: 99%

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Systolic Hypertension Mechanisms: Effect of Global and Local Proximal Aorta Stiffening on Pulse Pressure

2011

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“…17,25 This hemodynamic consequence has been demonstrated in animal studies whereby application of noncompliant grafts around (or in replacement of) the proximal aorta acutely yields more pathological central BP waveforms (augmented BP) and increased myocardial load resulting in LV hypertrophy. [27][28][29] It is, therefore, not surprising that as the large arteries become stiff with age, 30 the altered aortic reservoir function largely accounts for the augmentation of the central BP waveform. 6 Once the reservoir function of the aorta is considered, the remaining contribution to the central BP waveform (the excess pressure) has been proposed to correspond to the excess LV work beyond the minimum needed for flow ejection into the proximal aorta.…”

Section: Aortic Reservoir and Excess Pressure: A Physiological Paradigmmentioning

confidence: 99%

Aortic Reservoir Pressure Corresponds to Cyclic Changes in Aortic Volume

Schultz

Davies

Hardikar

et al. 2014

ATVB

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C entral (aortic) blood pressure (BP) waveform indices independently predict cardiovascular events and all-cause mortality, 1 but the physiological mechanisms to explain the waveform morphology remain disputed. The well-established wave reflection theory ascribes transmission of discrete forward and backward (incident and reflected) waves as the principal contributory factor underlying the shape of the central BP waveform.2 However, while providing a plausible description of central BP morphology, recent studies have concluded that the influence of discrete reflected waves on central BP may be less than originally conceived, and this is probably because of wave dispersion along the aorta and entrapment of reflected waves in the periphery. 3,4 Indeed, augmentation of central BP may be largely attributable to forward wave propagation (as a result of left ventricular [LV] ejection) and proximal aortic reservoir function. [5][6][7][8][9] Importantly, wave separation theory obscures the pressure buffering role of the highly elastic proximal aorta (ie, the aortic reservoir), and a failure to consider this function may lead to incorrect interpretations of the physiology underlying central BP waveform morphology.The reservoir-excess pressure concept is an alternate method proposed to explain the underlying physiology of the aortic BP waveform. This method has been used invasively to study changes in aortic BP associated with both aging and exercise. 6,8 Moreover, indices derived from this model were recently shown to predict cardiovascular events (fatal and nonfatal) and procedures independent from brachial BP and other conventional cardiovascular risk parameters (eg, age, sex, cholesterol, smoking, diabetes mellitus), including Framingham risk score, in an analysis of the Conduit Artery Function Evaluation study. 10 In accounting for the reservoir function of the aorta, 7,11 the reservoir-excess pressure model is founded on the basis that aortic BP can be separated into © 2014 American Heart Association, Inc.

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“…Aortic reconstruction with a prosthetic noncompliant graft reduces this compliance and may have an adverse effect on cardiovascular hemodynamics, which in turn may lead to hypertension, cardiac hypertrophy and ischemia, the development of vessel wall disease and thrombosis formation [2,3,4,5,6,7,8]. Furthermore, the different radial dilation of the prosthesis and the host vessel leads to stress concentration in the sutures of the anastomoses, which may lead to fatigue failure of the suture line and tearing of the host artery resulting in anastomotic aneurysm formation [7].…”

Section: Introductionmentioning

confidence: 99%

Left Ventricular Hypertrophy Induced by Reduced Aortic Compliance

et al. 2009

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Aim: It was the aim of this study to investigate the long- term effects of reduced aortic compliance on cardiovascular hemodynamics and cardiac remodeling. Method: Sixteen swine, divided into 2 groups, a control and a banding group, were instrumented for pressure and flow measurement in the ascending aorta. Teflon prosthesis was wrapped around the aortic arch in order to limit wall compliance in the banding group. Hemodynamic parameters were recorded throughout a 60-day period. After sacrifice, the mean cell surface of the left ventricle was documented. Results: Banding decreased aortic compliance by 49 ± 9, 44 ± 16 and 42 ± 7% on the 2nd, 30th and 60th postoperative day, respectively (p < 0.05), while systolic pressure increased by 41 ± 11, 30 ± 11 and 35 ± 12% (p < 0.05), and pulse pressure by 86 ± 27, 76 ± 21 and 88 ± 23%, respectively (p < 0.01). Aortic characteristic impedance increased significantly in the banding group. Diastolic pressure, cardiac output and peripheral resistance remained unaltered. The mean left ventricular cell surface area increased significantly in the banding group. Conclusions: Acute reduction in aortic compliance results in a significant increase in characteristic and input impedance, a significant decrease in systemic arterial compliance and a subsequent increase in systolic and pulse pressures leading to left ventricular hypertrophy.

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Hemodynamics induced after acute reduction of proximal thoracic aorta compliance

Cited by 74 publications

References 27 publications

Systolic Hypertension Mechanisms: Effect of Global and Local Proximal Aorta Stiffening on Pulse Pressure

Systolic Hypertension Mechanisms: Effect of Global and Local Proximal Aorta Stiffening on Pulse Pressure

Aortic Reservoir Pressure Corresponds to Cyclic Changes in Aortic Volume

Left Ventricular Hypertrophy Induced by Reduced Aortic Compliance

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