Carotid Plaque, Arterial Stiffness Gradient, and Remodeling in Hypertension

Beaussier, Hélène; Masson, Ingrid; Collin, C.; Bozec, Erwan; Laloux, Brigitte; Calvet, D.; Zidi, M.; Boutouyrie, Pierre; Laurent, Stéphane

doi:10.1161/hypertensionaha.108.115972

Cited by 58 publications

(62 citation statements)

References 43 publications

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“…15;Isabelle et al,unpublished observations). The purpose of the present study was to take this model as a tool to improve the analysis of arterial stiffening using a recently developed echotracking device, the ArtLab, which is presently only investigated in human studies (2,28).…”

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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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%

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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“…This has been used to show that established risk factors, including hypertension, are associated with inward bending strain. 32 Most other approaches to evaluating arterial mechanics examine disease-free vessels. It remains to be seen whether these differences in stress are associated with increased risk of plaque rupture and subsequent adverse clinical events.…”

Section: Methodologiesmentioning

confidence: 99%

Arterial Stiffness and Hypertension

2010

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A rterial stiffness is increasingly recognized as an important prognostic index and potential therapeutic target in patients with hypertension. It is closely linked to, but by no means synonymous with, raised blood pressure, and its physiopathology is still not fully understood. Aortic stiffness and arterial pulse wave reflections are key determinants of elevated central systolic pressure and are associated with adverse cardiovascular outcomes, independent of blood pressure. Indeed, the 2003 European Society of Hypertension guidelines on the management of hypertension acknowledge the potential role of arterial stiffness measurement in clinical management 1 and have prompted the publication of a consensus document on the measurement of central blood pressure and hemodynamics. 2 A detailed expert consensus document has also been published on the methodologic and clinical issues around arterial stiffness. 3 Broader implementation of these techniques into routine care seems inevitable. In this review, we have examined recent research in this field published in Hypertension, focusing on mechanistic work, methods for measuring stiffness, important clinical associations, and effects of treatment. Mechanisms and Causes of Arterial StiffnessHypertension and arterial stiffness are closely associated with age. 4 Degeneration of compliant elastin fibers, and deposition of stiffer collagen, is considered a key cause of age-related arterial stiffening. Moreover, blood pressure plays a significant role in determining vessel wall structure, with remodeling occurring to compensate for changes in wall stress. One potential mechanism is through matrix metalloproteinases, which modulate extracellular matrix proteins. When angiotensin II is given to mice, matrix metalloproteinase 9 activity is induced, resulting in enhanced collagen degradation. This improves the intrinsic distensibility of elastic arteries and, thus, blunts any blood pressure rise. 5 Impairment of this compensatory mechanism may, therefore, contribute to increased stiffness. The organization of elastic fibers is also important. Inhibition of the vascular adhesion protein semicarbazide-sensitive amine oxidase in a rat model results in reduced elastin fiber cross-linking, leading to morphological changes. This, in turn, increases vascular fragility and arterial stiffness. 6 In humans, aortic calcification has also been shown to be positively associated with both aortic stiffness and isolated systolic hypertension. 7 Previous work has demonstrated that pharmacological agents targeted at vascular wall structure (eg, "AGE" breakers targeted at age-related advanced glycation end-product cross-links 8 ) can improve arterial compliance. Understanding the mechanisms underlying aortic calcification and defining the roles of semicarbazide-sensitive amine oxidase, matrix metalloproteinases, and similar molecules in the pathogenesis of human hypertension may lead to other novel therapeutic approaches.In addition to having structural determinants, arterial stiffness is influence...

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“…The percades is thought to contribute to the initiation/progression of atherosclerosis 67) . In addition, local arterial stiffness may affect the arterial vulnerability to plaque formation 68) .…”

Section: B: Impaired Coronary Blood Flowmentioning

confidence: 99%

Brachial-Ankle PWV: Current Status and Future Directions as a Useful Marker in the Management of Cardiovascular Disease and/or Cardiovascular Risk Factors

Tomiyama

Matsumoto

Shiina

et al. 2016

J Atheroscler Thromb

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Since 2001, brachial-ankle pulse wave velocity (brachial-ankle PWV) measurement has been applied for risk stratification of patients with atherosclerotic cardiovascular disease and/or its risk factors in Japan. Measurement of the brachial-ankle PWV is simple and well standardized, and its reproducibility and accuracy are acceptable. Several cross-sectional studies have demonstrated a significant correlation between the brachial-ankle PWV and known risk factors for cardiovascular disease; the correlation is stronger in subjects with cardiovascular disease than in those without cardiovascular disease. We conducted a meta-analysis, which demonstrated that the brachial-ankle PWV is an independent predictor of future cardiovascular events. Furthermore, the treatment of cardiovascular risk factors and lifestyle modifications have been shown to improve the brachial-ankle PWV. Thus, at present, brachial-ankle PWV is close to being considered as a useful marker in the management of atherosclerotic cardiovascular disease and/or its risk factors.

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Carotid Plaque, Arterial Stiffness Gradient, and Remodeling in Hypertension

Cited by 58 publications

References 43 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

Arterial Stiffness and Hypertension

Brachial-Ankle PWV: Current Status and Future Directions as a Useful Marker in the Management of Cardiovascular Disease and/or Cardiovascular Risk Factors

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