Central Pulse Pressure Is a Major Determinant of Ascending Aorta Dilation in Marfan Syndrome

Jondeau, Guillaume; Boutouyrie, Pierre; Lacolley, Patrick; Laloux, Brigitte; Dubourg, Olivier; Bourdarias, Jean-Pierre; Laurent, Stéphane

doi:10.1161/01.cir.99.20.2677

Cited by 165 publications

(130 citation statements)

References 19 publications

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“…40 Central PP, which is influenced by aortic stiffness, is a powerful determinant of ascending aorta diameter in MFS patients, regardless of age and body surface area, whereas mean BP is not. 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 Syndromesupporting

confidence: 74%

“…40 In MFS patients, the increase in arterial stiffness is confined to the aorta, with no change in stiffness observed for the carotid, femoral, and radial arteries. 41 A clinical hallmark of MFS and the major cause of morbidity and premature death from this syndrome is aortic root dilatation and associated aortic regurgitation, dissection, and rupture. 40 The exact mechanisms leading to dilatation are not fully understood, but steady and pulsatile stresses are probably important, leading to the mechanical fatigue of abnormal elastic fibers and microdissections.…”

Section: Marfan Syndromementioning

confidence: 99%

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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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Section: Marfan Syndromesupporting

confidence: 74%

Section: Marfan Syndromementioning

confidence: 99%

Structural and Genetic Bases of Arterial Stiffness

2005

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“…Previous studies have shown that aortic dilation in patients affected by Marfan's syndrome was related to cPP, but not bPP. 8 In hypertensive subjects, collagen and elastin abnormalities are usually more pronounced than in age matched normotensive subjects, 25 but this process is magnified in Marfan's syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…[3][4][5][6][7] Moreover, in Marfan's disease, it has been previously shown that central blood pressure (cBP) has a key role in the pathogenesis of aortic aneurysms. 8 In hypertensive patients, the ARD, and in particular dilatation of the sinus of Valsalva, is associated with more pronounced alterations in cardiac structure and geometry than in normotensive subjects; 2 however, the relationship between aortic root size and both the central and the peripheral BP levels has not yet been fully investigated in patients with hypertension and aortic dilatation.…”

Section: Introductionmentioning

confidence: 99%

Aortic size index enlargement is associated with central hemodynamics in essential hypertension

et al. 2010

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The aim of this study was to evaluate the association between brachial and central blood pressure (bBP and cBP) levels and aortic root dilatation (ARD) in essential hypertensive patients. A total of 190 untreated and treated essential hypertensive patients (mean age, 55±11 years) were considered for this analysis. We measured pulsatile hemodynamics and the proximal aortic diameter directly using tonometry, ultrasound imaging (echocardiography) and Doppler. Ninety-one hypertensive patients had an ARD (defined as aortic size index (ASi)42 cm/m 2 ). Central hemodynamic variables were significantly associated with ASi. Patients with increased ASi were significantly older (60 ± 10 vs. 50 ± 11 years, Po0.0001) and had higher levels of the augmentation index (AIx; 28±10 vs. 21±10 Po0.0001), augmentation pressure (AP; 13±6 vs. 8±5 mm Hg, Po0.0001), and central pulse pressure (cPP; 44 ± 10 vs. 39 ± 8 mm Hg, Po0.0001) compared with patients with normal ASi. In a logistic regression analysis, the AIx was the only significant predictor of ASi. In hypertensive patients, the AIx and cBP were associated with ARD, whereas the bBP was not. Patients with an increased ASi may lose part of the elastic properties of the aorta, demonstrating a strict correlation between ASi and central hemodynamic indexes, in particular, the cPP and AIx.

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“…The resultant aortic stiffness increase predominates much more in the central elastic arteries than in the distal arteries, and thus generates an increase in central pressure pulse. 29) Because of these physiological and pathological PP amplifications between central and peripheral arteries, [30][31][32] brachial PP, used in the aortic stiffness index formula, may not reflect aortic PP. Additionally, it is an important limitation that the times of the measurements of blood pressure and echocardiography are not simultaneous.…”

Section: Discussionmentioning

confidence: 99%

<b>Color Doppler Tissue Imaging in Assessing the Elastic Properties of the Aorta and in Predicting Coronary Artery Disease</b>

et al. 2002

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SUMMARYWe hypothesized that the change in aortic elastic properties could directly be shown with color Doppler tissue imaging (CDTI), that these findings could be related to aortic stiffness and distensibility and that, through these, coronary artery disease (CAD) could be predicted.One hundred and twenty six patients (group I: 83 with CAD, mean age 54±10 years, 18 female, 65 male; group II: 43 without CAD, mean age 53±10 years, 27 female, 16 male) having been evaluated for coronary artery disease by angiography were examined by echocardiography. Arterial pressure was measured immediately before echocardiographic evaluation. Internal aortic systolic and diastolic diameters by M-mode echocardiography and aortic upper wall tissue velocities (Aortic S, E, A, m/sec) by CDTI were measured 3 cm above the aortic valve. Lateral mitral annulus tissue velocities (Annulus S, E, A, m/sec) were also recorded. Aortic distensibility (cm 2 •dynes -1 ) and aortic stiffness index were calculated using formulas. In the statistical analyses, CAD risk factors and left ventricular ejection fraction were used for adjustment.Aortic stiffness (2.79±3.49 vs 1.62±1.31, P=0.03), distensibility (1.55±1.46 vs 2.37±3.08, P=0.04), and aortic S velocity (0.057±0.016 vs 0.064±0.015, P=0.02) differed significantly between groups I and II. After adjustment, while aortic stiffness and S velocity were still statistically different (P=0.04; P=0.03 respectively), the significance of the difference in aortic distensibility disappeared (P=0.051). Aortic stiffness and aortic S velocity (0.06 m/sec<) were important CAD determinants (Odds ratio=1.4 P=0.03; Odds ratio=3.6 P=0.01, respectively), but aortic distensibility was not. Aortic stiffness was correlated only with aortic S velocity (r=-0.28, P=0.01), and aortic distensibility had a significantly positive correlation with aortic S velocity (r= 0.20, P=0.02). The interobserver and intraobserver correlation coefficients for aortic S velocities were 0.65 and 0.71, respectively (P<0.05).Elastic properties of the aorta can directly be assessed by reproducibly measuring the movements in the upper wall of the aorta by CDTI. Reduced aortic S velocity is associFrom the

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Central Pulse Pressure Is a Major Determinant of Ascending Aorta Dilation in Marfan Syndrome

Abstract: In patients with MFS, local PP, estimated from carotid PP, was a major determinant of ascending aorta diameter, whereas brachial PP was not. Increased arterial stiffness was confined to the aorta.

Cited by 165 publications

References 19 publications

Structural and Genetic Bases of Arterial Stiffness

Structural and Genetic Bases of Arterial Stiffness

Aortic size index enlargement is associated with central hemodynamics in essential hypertension

<b>Color Doppler Tissue Imaging in Assessing the Elastic Properties of the Aorta and in Predicting Coronary Artery Disease</b>

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