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      Static versus Dynamic Distensibility of the Carotid Artery in Humans

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          In clinical studies, the elastic behavior of central arteries is usually assessed by measuring dynamic distensibility. In this study, we aimed to investigate how dynamic and static distensibility of the common carotid artery (D<sub>dyn</sub> and D<sub>stat</sub>, respectively) are related in 28 healthy volunteers of 20–71 years. The carotid diameter and its change with the pressure pulse were measured using an ultrasound echo-tracking device. Arterial blood pressure was measured by Finapres and carotid pressure was determined by applanation tonometry. D<sub>dyn</sub> was determined at rest using the pressure pulse, while D<sub>stat</sub> was determined during pressor responses induced by handgrip or cold pressor test. Data are given as mean ± 1 SD. In younger subjects (<35 years), D<sub>stat</sub> did not differ from D<sub>dyn</sub> (7.0 ± 3.4 vs. 6.5 ± 2.1·10<sup>–3</sup>·mm Hg<sup>–1</sup>, respectively), whereas in older subjects (>35 years), D<sub>stat</sub> was significantly higher than D<sub>dyn</sub> (3.8 ± 1.4 vs. 2.1 ± 0.9· 10<sup>–3</sup>·mm Hg<sup>–1</sup>, p < 0.001). For all subjects, D<sub>stat</sub> and D<sub>dyn</sub> decreased with increasing age and mean arterial pressure (MAP). Using stepwise multiple regression analysis, the strongest predictor of D<sub>stat</sub> proved to be MAP, while that of D<sub>dyn</sub> was age. D<sub>stat</sub> was found to be linearly related to the hysteresis loop area of the pressure-diameter relation (r = 0.94), i.e. to vessel wall viscosity. It is concluded that, with increasing age, static distensibility overestimates the distension capacity of large arteries.

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          Association between high heart rate and high arterial rigidity in normotensive and hypertensive subjects.

          The dynamic elastic modulus of central arteries is very frequency-dependent Although resting heart rate is a potent independent risk factor for morbidity and mortality both from cardiovascular and from noncardiovascular disease, no link between tachycardia and arterial stiffness has ever been established. To relate arterial stiffness to heart rate in a population with relatively low cardiovascular risk. Pulse-wave velocity measurements and high-resolution echo-tracking techniques were used to determine the degree of arterial distension (of carotid and femoral arteries, and terminal aorta) and the velocity of the pulse wave (aorta and upper and lower limbs) at the same time as heart rate, in members of a large population of normotensive and hypertensive subjects in a multicenter study in Paris, Fleury-Merogis and Grenoble (France). A high heart rate was strongly associated with reduced distension and elevated pulse-wave velocity, even after adjustment for age and blood pressure. A high aortic pulse-wave velocity was also negatively associated with a low baroreflex sensitivity. The most significant associations between high heart rate and high arterial rigidity were found for the carotid artery, the thoracic aorta, and the lower limbs, but there was no significant result for the terminal aorta and the arm arteries. This study demonstrates that there is a statistically significant positive link between high heart rate and high arterial stiffness measured at the site of central and lower limb arteries. Since an elevated heart rate has been shown to be associated with cardiovascular risk, such findings may be relevant for future cardiovascular studies in epidemiology.
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            Wave reflections and the arterial pulse.

            Studies of aortic dynamics have provided new information about the peripheral pulse. This brief review provides a summary of these findings and relates them to a number of clinical conditions.
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              Distension capacity of the carotid artery and ambulatory blood pressure monitoring. Effects of age and hypertension.

              In hypertension, the principal components of the mechanical stress acting on the arterial wall may be evaluated not only from the level of peak systolic and end-diastolic blood pressure but also by the level of pulse pressure and variability of blood pressure measured by ambulatory monitoring. The purpose of the present study was, in a population of 51 subjects with essential hypertension, to determine the influence of these parameters and of heart rate on the distension capacity of the common carotid artery, measured noninvasively by high-resolution echo-tracking techniques. The pulsatile change in diameter of the carotid artery diameter, estimated either in absolute or relative values, was shown to be significantly and independently correlated with four mechanical parameters deduced from daytime ambulatory blood pressure measurements: baseline diastolic blood pressure (the lower the diastolic blood pressure, the higher the distension capacity; r = -0.44; P < .001); pulse pressure (the higher the pulse pressure, the higher the distension capacity; r = 0.32; P < .024); variability of diastolic blood pressure (the higher the variability, the higher the distension capacity; r = 0.37; P < .008); and mean heart rate (the higher the heart rate, the more reduced the distension capacity; r = -0.28; P < .05). Multiple regression analysis indicated that mean diastolic blood pressure and its variability, mean heart rate, and pulse pressure acted independently on carotid artery distension, even after adjustment for age. The present study suggests for the first time that, in humans, hypertension may act on the arterial wall not only through the amplitude of peak systolic and end-diastolic blood pressure but also through several other mechanical factors involving the level of pulse pressure and heart rate and also blood pressure variability. Thus, in addition to the level of blood pressure, carotid artery distension is specifically influenced by two factors independently implicated in the epidemiologic cardiovascular risk: pulse pressure and heart rate.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                April 2000
                31 March 2000
                : 37
                : 2
                : 103-111
                aClinical Research Department and Second Institute of Physiology, Semmelweis University of Medicine, Budapest, Hungary, and bDepartment of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands
                25721 J Vasc Res 2000;37:103–111
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 3, References: 36, Pages: 9
                Research Paper


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