Noninvasive Measurement of Medium-Sized Artery Intima-Media Thickness in Humans: In vitro Validation

Girerd, Xavier; Mourad, Jean‐Jacques; Acar, Christophe; Heudes, Didier; Chiche, S.; Bruneval, Patrick; Mignot, J; Billaud, E; Safar, Michel; Laurent, Stéphane

doi:10.1159/000159037

Cited by 88 publications

(54 citation statements)

References 22 publications

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“…Previous findings in genetic hypertensive rats indicate marked interactions between a HSD, increased wall thickness, and increase in Fn. [27][28][29][30] The increase in wall thickness and Fn may contribute to the increase in vascular wall elastic modulus in proportional to the level of circumferential wall stress through an increased number of cell matrix attachments sites. 22 Interestingly, the decrease in MAP in HSD rats treated with valsartan was not associated with a significant reduction in CA wall thickness.…”

Section: Discussionmentioning

confidence: 99%

Effects of Valsartan on Mechanical Properties of the Carotid Artery in Spontaneously Hypertensive Rats Under High-Salt Diet

et al. 2001

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Abstract-The aim of this investigation was to evaluate the influence of a high-salt diet (HSD) on the effects of valsartan, an angiotensin II type 1 (AT 1 ) receptor antagonist, on carotid arterial stiffness and structure in spontaneous hypertensive rats (SHR). Carotid arterial stiffness was studied in SHR receiving a HSD or a normal-salt diet (NSD) from the 10th to 20th week of age. Within each of the 2 groups, the animals received treatment with either placebo or valsartan (30 mg · kg Ϫ1 · d Ϫ1 ) administered on the 4th to 20th week of age. Arterial pressure, wall stress, incremental elastic modulus (Einc), medial cross-sectional area, and EIIIA fibronectin isoform were significantly increased in placebo-HSD rats compared with placebo-NSD rats with no change in the ratio of collagen to elastin. Valsartan reduced mean arterial pressure in both NSD and HSD rats but reduced pulse pressure only in NSD rats. In NSD rats, valsartan reduced Einc and medial cross-sectional area. In HSD, valsartan increased Einc and did not modify medial cross-sectional area and fibronectin. In valsartan-treated rats, the ratio of collagen to elastin was greater in HSD than in NSD rats. In conclusion, the effects of AT 1 blockade are greatly influenced by salt intake in SHR. Despite a reduction in mean arterial pressure in HSD rats, AT 1 blockade was not able to prevent the effects of a HSD on pulse pressure, carotid artery stiffness, and hypertrophy. Key Words: salt Ⅲ angiotensin II Ⅲ AT 1 blockade Ⅲ large artery stiffness Ⅲ carotid artery P revious reports have shown that plasma renin-angiotensin activity is reduced in rats receiving a high-salt diet (HSD). 1-4 However, a long-term HSD in salt-sensitive animals-Dahl salt-sensitive rats, 5 stroke-prone hypertensive rats, 6 -8 or ANP knockout mice 9 -is known to stimulate plasma renin activity. These observations suggest that the effects observed during perturbation of the renin-angiotensin aldosterone system by a high sodium intake may depend on the animal model used. Recently, Wang and Du 10 observed an increased expression of angiotensin II type 1 (AT 1 ) receptor mRNA in arterial preparations derived from Wistar and Sprague-Dawley rats maintained on a HSD. In contrast, when Dahl rats were treated with a HSD, decreases in aortic mRNA and AT 1 receptor density were observed. 5 Together, these results suggested that 1 modification associated with high sodium intake may be at the level of the AT 1 receptor. Interestingly, in spontaneously hypertensive rats (SHR) treated with a HSD, an enhanced functional response to angiotensin II and AT 1 receptor antagonists was demonstrated, suggesting that sodium modified AT 1 activity in SHR. 11,12 Although AT 1 receptor antagonists have been shown to reduce mortality in salt-sensitive animal models (Dahl rats or stroke-prone rats), 7,[13][14][15] there is little evidence available that AT 1 receptor antagonists continually block the elevated blood pressure and arterial abnormalities observed in SHR during high sodium intake.The aim of this inves...

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Section: Discussionmentioning

confidence: 99%

Effects of Valsartan on Mechanical Properties of the Carotid Artery in Spontaneously Hypertensive Rats Under High-Salt Diet

et al. 2001

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“…With the subject in a supine position and the arm immobile at heart level, the transducer was oriented perpendicularly to the longitudinal axis of the vessel using the acoustic Doppler signal. After switching to A-mode, the echo beams corresponding to the posterior lumen-intima and media-adventitia interfaces were made visible on a computer screen [15,16] and the wall thickness of the artery was measured [16] as the distance between the inner and outer wall echoes. The echoes scattered back from the inner posterior and anterior walls of the artery were also visualized on the computer screen and electronically digitized (using a fast transducer from analogue to digital) to allow internal diameter variations to be determined at 50 Hz with a spatial resolution of 0.0025 mm [15,16].…”

Section: Methodsmentioning

confidence: 99%

Progression of large artery structural and functional alterations in Type I diabetes

et al. 2001

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We have previously shown that Type I (insulin-dependent) diabetes mellitus is accompanied by a reduced distensibility of the carotid artery, the radial artery and the aorta [1]. We have also shown that this reduction is associated with an increased thickness of the vessel walls and that both changes can be found even in relatively young subjects with no increase in blood pressure and no macrovascular or microvascular complications [1]. This provides evidence that in diabetes there is an alteration of mechanical function and structure which involves both large elastic and middle-size muscle arteries [2±9]. It also provides evidence that this is an early phenomenon of the disease, promoting (1) the remodelling of smaller arteries [10,11] which could facilitate a blood pressure increase, a condition commonly associated with diabe-Progression of large artery structural and functional alterations in Type I diabetes Abstract Aims/hypothesis. Type I (insulin-dependent) diabetes mellitus is accompanied by reduced arterial distensibility and increased arterial wall thickness even in normotensive subjects with no micro-macrovascular complications. It is not known whether, and how fast, these subclinical markers of vascular damage develop over time.Methods. We measured arterial wall distensibility in radial, common carotid artery and abdominal aorta in 60 normotensive patients (aged 35.0 1.2 years, means SE) with Type I diabetes with no microvascular or macrovascular complications and in 20 healthy control subjects matched for age. Arterial distensibility was determined by continuous measurements of arterial diameter through echotracking techniques and by using either the Langewouters (radial artery) or the Reneman formula (carotid artery and aorta). The same echotracking techniques allowed us to ascertain the radial and carotid artery wall thickness. Data were collected before and after 23 1 months.Results. In the first study, carotid artery distensibility was similar but radial artey and aortic distensibility was less (p < 0.01) in patients with diabetes than in control subjects (±39 % and 25 % respectively). This was accompanied by an increase (p < 0.01) in both radial (42 %) and carotid artery wall thickness (46 %). After 23 1 months diabetic subjects showed a further reduction in arterial distensibility (radial±12 %, p < 0.05; carotid±8 %, NS; aorta±20 % p < 0.05) and an increase in arterial wall thickness (radial + 15 %; carotid 14 %, p < 0,05). No change in distensibility and wall thickness values occurred in control subjects. Conclusion/interpretation. The early reduction in arterial distensibility and increase in arterial wall thickness characterizing uncomplicated normotensive Type I diabetes patients shows a measurable worsening over the short term. [Diabetologia (2001) 44: 203±208]

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“…With the subject supine and the arm immobile at heart level, the transducer was oriented perpendicularly to the longitudinal axis of the vessel based on the acoustic Doppler signal. After switching to A-mode the echo beams corresponding to the posterior lumen-intima and media-adventitia interfaces were made visible on a computer screen [29,30] and the wall thickness of the artery was measured [30] as the distance between the inner and outer wall echoes. The backscattered echoes from the inner posterior and anterior walls of the artery were also visualised on the computer screen and electronically digitised (via an analogic/digital fast transducer) to allow internal diameter variations to be derived at a 50 Hz with a spatial resolution of 0.0025 mm [29,30].…”

Section: Methodsmentioning

confidence: 99%

Early impairment of large artery structure and function in Type I diabetes mellitus

et al. 1999

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Diabetes mellitus is associated with an increased risk of atherosclerosis [1]. Atherosclerosis is responsible for the increased rate of coronary heart disease, cerebrovascular disease and peripheral artery disease typical of diabetes mellitus [2±13]. It is not, however, well established how early alterations in large artery function, that may preceed the appearance and favour the progression of atherosclerotic lesions, i. e. a reduced arterial distensibility, occur in diabetic patients [14±16]. This is because most studies on arterial distensibility have been done in Type II (non-insulindependent) diabetes mellitus, where it is difficult to separate the arterial stiffening due to abnormalities Diabetologia (1999) Abstract Aims/hypothesis. Diabetes mellitus is associated with an increased incidence of atherosclerosis. How early functional and structural alterations of large arteries that may preceed atherosclerosis occur in the course of this disease has, however, never been conclusively documented. Methods. We evaluated arterial wall distensibility in the radial artery, common carotid artery and abdominal aorta in 133 patients (aged 35.4 ± 0.9 years, means ± SEM) with Type I (insulin-dependent) diabetes mellitus and no macrovascular complications. Arterial distensibility was derived from continuous measurements of arterial diameter through echotracking techniques and use of either the Langewouters (radial artery) or the Reneman (carotid artery and aorta) formula. The same echotracking techniques enabled us to obtain radial artery and carotid artery wall thickness. Data were compared with those from 70 age-matched normotensive control subjects. Results. In diabetic patients arterial distensibility was consistently less (p < 0.01) than in control subjects, the reduction averaging 26 %, 14 % and 25 % for the radial artery, carotid artery and aorta, respectively. This was accompanied by an increase (p < 0.01) in both radial and carotid artery wall thickness. The changes were more pronounced in patients with microalbuminuria, retinopathy or neuropathy or both. They were evident also in those without microvascular complications. This was the case also when subjects in whom diabetes was associated with hypertension (n = 30) were excluded from data analysis. Carotid and aortic wall abnormalities showed a relation with the duration of disease and blood pressure whereas radial artery abnormalities showed a relation with glycated haemoglobin. Conclusion/interpretation. Type I diabetes is characterised by diffuse arterial wall stiffening and thickening which progress with the severity of the disease but can clearly be seen also in the absence of any diabetic-related complication. This suggests that in diabetes stiffening and thickening are an early marker of vascular damage. [Diabetologia (1999) 42: 987± 994]

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Noninvasive Measurement of Medium-Sized Artery Intima-Media Thickness in Humans: In vitro Validation

Cited by 88 publications

References 22 publications

Effects of Valsartan on Mechanical Properties of the Carotid Artery in Spontaneously Hypertensive Rats Under High-Salt Diet

Effects of Valsartan on Mechanical Properties of the Carotid Artery in Spontaneously Hypertensive Rats Under High-Salt Diet

Progression of large artery structural and functional alterations in Type I diabetes

Early impairment of large artery structure and function in Type I diabetes mellitus

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