Association Between Local Pulse Pressure, Mean Blood Pressure, and Large-Artery Remodeling

Boutouyrie, Pierre; Bussy, Caroline; Lacolley, Patrick; Girerd, Xavier; Laloux, Brigitte; Laurent, Stéphane

doi:10.1161/01.cir.100.13.1387

Cited by 394 publications

(307 citation statements)

References 17 publications

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“…First, as reported in a previous study (27), brachial artery blood pressure measurements may not always accurately reflect blood pressure in the common carotid artery. Although comparisons of intra-arterial pressure in the large vessels with brachial artery pressures determined by noninvasive oscillometric methods are in generally good agreement (28), pulse pressure measured by pressure waveforms in the carotid artery is greater than that observed in the brachial artery (29). Second, in addition to mechanical factors, neurohumoral and genetic factors should be considered in any analysis of carotid artery remodeling, because they can directly influence the remodeling not only of conduit arteries but also of arterioles.…”

Section: Discussionmentioning

confidence: 98%

Vascular Remodeling of the Carotid Artery in Patients with Untreated Essential Hypertension Increases with Age.

et al. 2002

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We examined whether hypertrophy of the carotid artery in patients with untreated essential hypertension is associated with compensatory carotid artery enlargement as these patients age. Carotid ultrasonography was evaluated in 163 patients with untreated essential hypertension (74 males and 89 females) and in 76 normotensive subjects. Intima-media end-diastolic thickness (IMT) and outer vessel diameter (VD) were measured, and relative wall thickness (IMT/R, R VD/2) and vascular mass (VM) were calculated. Determinants of vascular hypertrophy in patients with untreated essential hypertension were also investigated. VD, VM, and IMT were significantly correlated with age in both the normotensive and hypertensive groups. Additionally, IMT was significantly correlated with VD in both groups. There was no correlation between increasing age and IMT/R in either group. IMT, VD and VM were significantly higher in the hypertensive group 50 years than in age-matched normotensive controls. However, IMT/R was significantly higher in the 50-59 years hypertensive group than in normotensive controls of the same age group. In addition to age, VM was ing process of compensatory enlargement that preserves the luminal diameter despite the increase in the size of the plaque (2, 3). Glagov et al. (2) and Zarins et al. (3) found a highly significant association of artery size and plaque area in left human coronary arteries, which delayed the decrease in the vascular lumen until the lesion occupied about 40% of the internal elastic lamina. Similar investigations have been made in pathoanatomic studies of postmortem specimens (4), epicardial ultrasound imaging (5), and intravascular ultrasound of the coronary arteries (6). These studies examined arterial sites with moderate and large atherosclerotic plaques.

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Section: Discussionmentioning

confidence: 98%

Vascular Remodeling of the Carotid Artery in Patients with Untreated Essential Hypertension Increases with Age.

et al. 2002

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“…PWV is included amongst the risk factors for cardiovascular disease (21) and is strongly predictive for cardiovascular events in hypertensive individuals (22). An increase in aortic stiffness may increase the risk of stroke through several mechanisms such as an increase in central pulse pressure or an increase in carotid intimamedia thickness, promoting the development of atherosclerotic lesions and thus the likelihood of plaque rupture (3)(4)(5). The present study proposed an exciting, alternative physiopathological approach.…”

Section: Pwvmentioning

confidence: 91%

Arterial Stiffness is Associated with Tissue Doppler Atrial Conduction Times and P Wave Dispersion in Hypertensive Patients

Elsherbiny

2012

Intern. Med.

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Background Arterial stiffness is strongly predictive for cardiovascular events in hypertensive individuals and it may increase the risk of stroke. This study was designed to evaluate the possible relationship between arterial stiffness and atrial electromechanical delay and P wave dispersion (PWD), as determinants of AF risk. Materials and MethodsThe study included 75 hypertensive patients and 45 healthy control subjects. Atrial electromechanical coupling (time interval from the onset of P wave on ECG to the beginning of A wave with tissue Doppler echocardiography [PA]), intraatrial and interatrial electromechanical delay (EMD) and PWD were measured. Stiffness index β & PWV was measured to assess the arterial stiffness. Results The interatrial EMD and PWD were prolonged in hypertensive patients compared to controls (p< 0.01 for both), There was increased arterial stiffness (PWV and stiffness index β) in hypertensive patients compared to controls (6.43 ± 1.73 vs. 4.8 ± 1.6 m/sec & 4.9 ± 2.8 vs. 2.63 ± 1.2, p<0.01 for both). By multivariate analysis; PWV and Stiffness index β were independently correlated with interatrial EMD (B ± SE= 0.42 ± 1.87, B ± SE=0.39 ± 0.21 p<0.01 for both) and PWD (B ± SE=0.37 ± 1.93, p<0.01, B ± SE=0.25 ± 0.18, p<0.05 respectively). Conclusion In hypertensive patients arterial stiffness indexes increased and showed a significant correlation with interatrial EMD and PWD independent of other variables. Further research is needed to determine whether interventions that reduce arterial stiffness will limit the growing incidence of AF.

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“…41 Similar findings have been reported in hypertensive subjects: carotid PP is a major independent determinant of carotid internal diameter, whereas mean BP is not. 42 Thus, aortic dilatation probably results from the failure of abnormal elastic fibers to sustain physiological pulsatile stress by analogy with aging.…”

Section: Marfan Syndromementioning

confidence: 99%

Structural and Genetic Bases of Arterial Stiffness

2005

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Abstract-Arterial stiffness has independent predictive value for cardiovascular events. We review data concerning the heritability of arterial stiffness, and propose an integrated view of the structural and genetic determinants of arterial stiffness, based on a candidate gene approach and recent studies on gene expression profile. Arterial stiffness seems to have a genetic component, which is largely independent of the influence of blood pressure and other cardiovascular risk factors. In animal models of essential hypertension (SHR and SHR-SP), structural modifications of the arterial wall include an increase in the number of elastin/smooth muscle cell (SMC) connections, and smaller fenestrations of the internal elastic lamina, possibly leading to redistribution of the mechanical load toward elastic materials. These modifications may give rise to mechanisms that explain why changes in arterial wall material accompanying wall hypertrophy in these animals are not associated with an increase in arterial stiffness. In monogenic connective tissue diseases (Marfan, Williams, and Ehlers-Danlos syndromes) and the corresponding animal models, precise characterization of the arterial phenotype makes it possible to determine the influence of abnormal genetically determined wall components on arterial stiffness. Such studies have highlighted the role of extracellular matrix signaling in the vascular wall and have shown that elastin and collagen not only display elasticity or rigidity but also are involved in the control of SMC function. These data provide strong evidence that arterial stiffness is affected by the amount and density of stiff wall material and the spatial organization of that material.

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Association Between Local Pulse Pressure, Mean Blood Pressure, and Large-Artery Remodeling

Cited by 394 publications

References 17 publications

Vascular Remodeling of the Carotid Artery in Patients with Untreated Essential Hypertension Increases with Age.

Vascular Remodeling of the Carotid Artery in Patients with Untreated Essential Hypertension Increases with Age.

Arterial Stiffness is Associated with Tissue Doppler Atrial Conduction Times and P Wave Dispersion in Hypertensive Patients

Structural and Genetic Bases of Arterial Stiffness

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