Simultaneous Measurement of Beat-to-Beat Carotid Diameter and Pressure Changes to Assess Arterial Mechanical Properties

Giannattasio, Cristina; Salvi, Paolo; Valbusa, Filippo; Kearney‐Schwartz, Anna; Capra, Anna; Amigoni, Maria; Failla, Monica; Boffi, L; Madotto, Fabiana; Benetos, A.; Mancia, Giuseppe

doi:10.1161/hypertensionaha.108.116509

Cited by 50 publications

(43 citation statements)

References 32 publications

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“…Thus it is difficult to evaluate in humans or in animal models the changes in arterial stiffness due to pressure recovery and/or to vascular wall protection (6,21). To clarify this point, a method has been developed to measure compliance and stiffness indexes at isobaric pressure, using an echotracking technique, with the limitation that only radial, brachial, or carotid artery parameters may be recorded in humans (11,18,24). In animal models, aortic parameters are directly analyzed with PWV and have also been measured with the echo-tracking devices NIUS2 (13) and Walltrack (29).…”

Section: Discussionmentioning

confidence: 99%

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Aortic stiffness in vivo in hypertensive rat via echo-tracking: analysis of the pulsatile distension waveform

Vayssettes-Courchay

Ragonnet

Isabelle

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Vayssettes-Courchay C, Ragonnet C, Isabelle M, Verbeuren TJ. Aortic stiffness in vivo in hypertensive rat via echo-tracking: analysis of the pulsatile distension waveform. Am J Physiol Heart Circ Physiol 301: H382-H390, 2011. First published May 20, 2011 doi:10.1152/ajpheart.00094.2011.-Large-artery stiffening is a major risk factor in aging and hypertension. Elevated blood pressure (BP) and vascular wall properties participate in arterial stiffening; we aimed to evaluate their respective role by combining echo-tracking and the spontaneously hypertensive rats (SHR) treated with low doses of a nitric oxide synthase inhibitor, shown to have arterial stiffening. Normotensive [Wistar-Kyoto (WKY)], SHR, and SHR treated for 2 wk with N G -nitro-L-arginine methyl ester (SHRLN) were anesthetized; BP and distension (pulsatile displacement) of the aortic walls with the ArtLab echo-tracking device were measured. Stiffness index increased in SHRLN vs. SHR; compliance, distensibility, and the slopes and area of the distension-pressure loop curve decreased. The pulsatile distension and pressure waveforms were strongly altered in SHRLN. Maximal values were decreased and increased, respectively, and the waveform kinetics also differed. Thus the area under the curve adjusted to heart rate (AUC/ms) was calculated. Acute BP reductions were induced by diltiazem in SHR and SHRLN, to levels similar to those of WKY. In SHR, compliance, distensibility, stiffness index, and the ascending slope of the distension-pressure loop reached the values of WKY, whereas they were only partially improved in SHRLN. Aortic distension (maximal value and AUC/ms) and the area of the distension-pressure loop were improved in SHR, but not in SHRLN. These data confirm the aortic stiffening induced by nitric oxide reduction in SHR. They show that the ArtLab system analyzes aortic stiffness in rats, and that the aortic pulsatile distension waveform is a parameter strongly dependent on the vascular wall properties.hypertension; compliance; distensibility; pulse-wave velocity; nitric oxide; spontaneously hypertensive rats ARTERIAL STIFFENING IS A MAJOR cardiovascular risk factor (6,17,26,27) in hypertension, end-stage renal disease, hypercholesterolemia, obesity, and diabetes (9,12,21,28). It is also an age-dependent alteration of the vascular wall (21) that has been defined as an early vascular aging factor (22). Elevated blood pressure, inflammation, endothelial dysfunction, remodeling, and hypertrophy are closely related factors that lead to organ damage and vascular stiffening. In hypertension, the long-term elevation of blood pressure leads to endothelial damage and vascular wall remodeling. It has also been proposed that remodeling may precede the hypertensive state (30). In hypertensive patients, major therapeutic targets to avoid cardiovascular events are decreases in blood pressure and improvement of the vascular wall protection (6, 21). Up until now, it remains difficult in humans and in animals to separate the causal effects of blood pressure eleva...

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Section: Discussionmentioning

confidence: 99%

“…2. This approach was already performed for the distension-pressure loop in humans (11,18) and rats (1).…”

Section: Discussionmentioning

confidence: 99%

Aortic stiffness in vivo in hypertensive rat via echo-tracking: analysis of the pulsatile distension waveform

Vayssettes-Courchay

Ragonnet

Isabelle

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…They have been developed to measure internal diameter, stroke change in diameter, and IMT with a high precision. [43][44][45][46][73][74][75] For the calculation of wall properties, it is assumed that the cross section of an artery is circular and the arterial wall is homogeneous and uniformly load-bearing. The elastic properties of the artery as a hollow structure (its capacity to accommodate a certain volume of blood) are assessed through arterial distensibility, determined from the systolic-diastolic variations in arterial cross-sectional area and local PP (Figure 4).…”

Section: Measurement Of Arterial Stiffnessmentioning

confidence: 99%

The Structural Factor of Hypertension

Laurent

Boutouyrie

2015

Circulation Research

392

175

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P athophysiological studies have extensively investigated the structural factor in hypertension, including large and small artery remodeling and functional changes. Here, we review the recent literature on the alterations in small and large arteries in hypertension. We discuss the possible mechanisms underlying these abnormalities and we explain how they accompany and often precede hypertension. Finally, we propose an integrated pathophysiological approach to better understand how the cross-talk between large and small artery changes interacts in pressure wave transmission, exaggerates cardiac, brain, and kidney damage, and lead to cardiovascular and renal complications. We principally report on large and small artery in essential hypertension because this is the most dominant form. Other forms of hypertension, including renovascular hypertension, primary aldosteronism, and hypertension associated with diabetes mellitus, will be reported only for contrasting their characteristics with those of uncomplicated essential hypertension. For sake of clarity, we will oppose functional and structural changes, although both are interdependent and influence the global hemodynamic, and vice versa. Hypertension Compendium© 2015 American Heart Association, Inc. Abstract: Pathophysiological studies have extensively investigated the structural factor in hypertension, including large and small artery remodeling and functional changes. Here, we review the recent literature on the alterations in small and large arteries in hypertension. We discuss the possible mechanisms underlying these abnormalities and we explain how they accompany and often precede hypertension. Finally, we propose an integrated pathophysiological approach to better understand how the cross-talk between large and small artery changes interacts in pressure wave transmission, exaggerates cardiac, brain and kidney damage, and lead to cardiovascular and renal complications. We focus on patients with essential hypertension because this is the most prevalent form of hypertension, and describe other forms of hypertension only for contrasting their characteristics with those of uncomplicated essential hypertension. (Circ Res.

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“…19 Hysteresis is artificially created when a fixed time shift is applied to either one of the waveforms. 20 To obtain proper pressure-area curves, we aligned the waveforms on the dicrotic notch ( Figure 1). Timing of the dicrotic notch within the cardiac cycle can be determined accurately and reproducibly, if the signals have been acquired with an appropriate bandwidth (Ͼ20 Hz).…”

Section: Signal Processingmentioning

confidence: 99%

“…Invasive measurement of pressure-area curves in vivo permits such a comprehensive description of arterial stiffness as a function of pressure. 10,19,20 However, the challenge is to derive the pressure-dependent relationship for data obtained noninvasively.…”

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confidence: 99%

Noninvasive Assessment of Arterial Stiffness Should Discriminate Between Systolic and Diastolic Pressure Ranges

et al. 2010

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Abstract-Arterial stiffening plays an important role in the development of hypertension and cardiovascular diseases. The intrinsically nonlinear (ie, pressure-dependent) elastic behavior of arteries may have serious consequences for the accuracy and interpretation of arterial stiffness measurements and, ultimately, for individual patient management. We determined aortic pressure and common carotid artery diameter waveforms in 21 patients undergoing cardiac catheterization. The individual pressure-area curves were described using a dual exponential analytic model facilitating noise-free calculation of incremental pulse wave velocity. In addition, compliance coefficients were calculated separately in the diastolic and systolic pressure ranges, only using diastolic, dicrotic notch, and systolic data points, which can be determined noninvasively. Pulse wave velocity at systolic pressure exhibited a much stronger positive correlation with pulse pressure (PϽ0.001) and age (Pϭ0.012) than pulse wave velocity at diastolic pressure. Patients with an elevated systolic blood pressure (Ͼ140 mm Hg) had a 2.5-times lower compliance coefficient in the systolic pressure range than patients with systolic blood pressures Ͻ140 mm Hg (Pϭ0.002). Most importantly, some individuals, with comparable age or pulse pressure, had similar diastolic but discriminately different systolic pulse wave velocities and compliance coefficients. We conclude that noninvasive assessment of arterial stiffness could and should discriminate between systolic and diastolic pressure ranges to more precisely characterize arterial function in individual patients. Key Words: arterial structure and compliance Ⅲ pulse wave velocity Ⅲ blood pressure measurement Ⅲ systolic hypertension Ⅲ carotid arteries D ecreased elasticity of the arterial wall plays an important role in the development of hypertension and related cardiovascular complications, such as heart failure, stroke, and renal failure. 1-4 Therefore, noninvasive assessment of arterial stiffness has recently entered the European Society of Hypertension/European Society of Cardiology guidelines for the management of hypertension. 5 Basic studies have shown that the elastic behavior of the arterial system is nonlinear, that is, arterial stiffness is pressure dependent. 6 -11 This intrinsic property of the arterial system may have serious consequences for the quantitative assessment of arterial stiffness, and changes therein, in response to age, 12,13 physiological stress, 7 and possibly antihypertensive treatment. 14,15 Currently, arterial stiffness is assessed noninvasively either at the diastolic pressure level (aortic or carotid-femoral pulse wave velocity [PWV]) or estimated as an average over the diastolic-systolic pressure range. In the latter case, distensibility and compliance coefficients are calculated as, respectively, the relative and absolute changes in the cross-sectional area normalized to pulse pressure from diastolic minimum to systolic peak, 16 tacitly assuming a linear pressure-area relatio...

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Simultaneous Measurement of Beat-to-Beat Carotid Diameter and Pressure Changes to Assess Arterial Mechanical Properties

Cited by 50 publications

References 32 publications

Aortic stiffness in vivo in hypertensive rat via echo-tracking: analysis of the pulsatile distension waveform

Aortic stiffness in vivo in hypertensive rat via echo-tracking: analysis of the pulsatile distension waveform

The Structural Factor of Hypertension

Noninvasive Assessment of Arterial Stiffness Should Discriminate Between Systolic and Diastolic Pressure Ranges

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