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(Hypertension. 1995;26:355-362.)
© 1995 American Heart Association, Inc.

Articles

Arterial Wall Hypertrophy and Stiffness in Essential Hypertensive Patients

Stéphane Laurent

From the Department of Pharmacology, Broussais Hospital, and INSERM U337, Paris, France.

Correspondence to Stéphane Laurent, MD, PhD, Service de Pharmacologie, Hôpital Broussais, 96, Rue Didot, 75674 Paris Cédex 14, France.

	Abstract

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
Abstract The purpose of this article is to review some clinical and fundamental evidence that hypertension-induced arterial wall hypertrophy at the site of large and medium-sized arteries is not necessarily associated with a decreased arterial distensibility and increased elastic modulus, and to demonstrate the opposing effects of aging and hypertension-induced hypertrophy on the arterial mechanics in vivo. In the studies reported here, the elastic properties of large and medium-sized arteries were noninvasively assessed from the simultaneous measurement of internal diameter and blood pressure inside the systolic-diastolic range. The distensibility of a medium-sized artery, the radial artery, in untreated essential hypertensive patients was not significantly different from that of normotensive control subjects when the two groups were compared at their respective mean arterial pressures. Despite increased wall thickness, the stiffness of the radial artery wall material, assessed by the incremental modulus of elasticity (Young's modulus), was not increased in hypertensive patients. At the site of a larger, more elastic artery, such as the common carotid artery, distensibility of hypertensive patients was significantly lower than that of normotensive subjects when the two groups were compared at their respective mean arterial pressures, but distensibility at 100 mm Hg was not significantly different between the two groups. Aging may alter distensibility independently of blood pressure, because carotid distensibility at 100 mm Hg was negatively correlated with age. In spontaneously hypertensive rats the elastic modulus of the common carotid artery wall material was not significantly different from that of Wistar-Kyoto rats at a given circumferential stress. Therefore, the hypertension-induced wall thickening is not necessarily associated with a reduced arterial distensibility and increased elastic modulus.

Key Words: arteries • compliance • hypertension, essential • hypertrophy

	Introduction

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
During sustained hypertension the chronic increase in BP has been extensively reported to induce an increased arterial wall thickness and media-to-lumen ratio. The data on small arteries and arterioles^{1 2} have been confirmed by clinical studies performed on isolated subcutaneous arterioles³ and intramyocardial coronary arterioles.⁴ The observed morphological changes have been distinguished either as "remodeling" or "hypertrophy," depending on the decrease or increase of the external diameter, respectively.^{5 6} The functional consequences of the increased media-lumen ratio of small arteries and arterioles are still a matter of debate, and whether these changes are simply adaptive or play a primary role in the pathogenesis of the disease is not clear.⁶ From a theoretical point of view the increased wall thickness and media-lumen ratio can contribute to the increased resistance to flow, amplify the vascular response to pressor agents, reduce the ischemic-dependent maximal vasodilation, and impair the autoregulation of blood flow.^{1 2} In animals, Baumbach et al⁷ and Mulvany⁸ reported that the elastic properties of the arterial wall material, determined at a given wall stress, were improved in the small arteries from SHR compared with normotensive controls.

If the increased arterial wall thickness is the hallmark of hypertension, the relationships between large artery wall hypertrophy and compliance have rarely been the subject of in vivo specific studies.^{9 10} During hypertension the decrease in large artery compliance is considered one of the major determinants of the increase in pulse pressure^{11 12} and may contribute to the development of left ventricular hypertrophy.¹⁰ These consequences are all the more important to consider because pulse pressure and left ventricular hypertrophy recently have been shown to be cardiovascular risk factors independent of MAP.^{12 13}

The purpose of this article is to review some clinical and fundamental evidence that hypertension-induced arterial wall hypertrophy at the site of large and medium-sized arteries is not necessarily associated with a decreased arterial distensibility and an increased elastic modulus, to demonstrate the opposing effects of aging and hypertension-induced hypertrophy on the arterial mechanics in vivo, and to advance the concept of an "autoregulation" of arterial compliance during chronic hypertension.

	Noninvasive Assessment of Hypertension-Induced Large and Medium-Sized Artery Wall Hypertrophy

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
IMT of the CCA Wall
Partly because of the known association between carotid and coronary atherosclerosis,¹⁴ most of the noninvasive clinical studies on hypertension-induced arterial wall hypertrophy have focused on the CCA. BP has been reported as one of the main determinants of carotid IMT, together with other independent factors including aging and body mass index.^{9 10 14} Specifically, Roman et al¹⁰ have reported an increased IMT in hypertensive patients compared with normotensive subjects matched for age and cardiovascular risk factors using a classic B-mode vascular echograph validated for IMT measurements.

Determination of the Radial Artery Wall IMT
In contrast to the CCA, no previous IMT measurement has been performed at the site of smaller, more distal muscular arteries, which represent a large part of the arterial tree. Much of the present work focuses on the radial artery, which was chosen for several reasons. First, ultrasound examination is easy to perform because of its superficial rectilinear course. Second, in essential hypertension structural changes of the large artery wall involve increased amounts of vascular smooth muscle, which is more susceptible to being detected in a muscular rather than elastic artery. As the radial artery is a muscular artery devoid of atherosclerotic lesions even in patients with severe coronary disease, intima-media thickening should reflect morphological changes independent of atherosclerotic lesions. This is of particular relevance for any pathophysiological study carried out in individuals with essential hypertension. Third, we had the unique opportunity of comparing in vivo and in vitro measurements in patients who were scheduled for coronary bypass graft using the radial artery.^{15 16} Fourth, it is possible to determine its functional properties by simultaneously measuring the pulsatile changes in radial artery internal diameter with a high-resolution ultrasonic echotracking device (NIUS 02, SMH; marketed by Capital Medical Services)¹⁷ and the pulsatile changes in finger BP by a Finapres system (Ohmeda, BOC Group). By taking into account the time delay between the radial BP signal and the finger BP signal, it is possible to determine noninvasively the diameter-pressure curve over the systolic-diastolic range and to compare hypertensive patients with normotensive subjects at a common BP level.

Validation of the Radial Artery Wall IMT Measurements
Because the radial artery intima-media is thinner than the CCA, it cannot be measured with standard B-mode echocardiographic systems having a 5- or 7.5-MHz probe and requires a 10-MHz probe and specific analysis of the radio frequency signal with the NIUS 02 high-resolution pulse echotracking system.¹⁷ The "double peak" radio frequency signal is very similar to the "double-line pattern" observed on the typical B-mode image of a longitudinally scanned normal artery wall¹⁸ and has been related to the distinct acoustic interfaces between intima, media, and adventitia. In a previous study Tardy et al¹⁹ showed, using fixed bovine carotid arteries, that the radio frequency lines obtained by the NIUS echotracking system correlated well with the anatomic structure of the vessel wall.

To validate the ability of the high-resolution echotracking system to measure IMT, we determined the correlation between histological and ultrasonic measurements of IMT in 15 radial artery segments obtained from the distal end of the wrist-elbow harvest for coronary bypass grafting in patients with coronary heart disease.¹⁶ For arterial IMT the difference between ultrasound and histological measurements was 41±66 µm, with the higher measurements found by the ultrasonic device. In a subgroup of 11 patients we found a significant correlation between in vivo ultrasonic measurements of wall cross-sectional area at the preoperative stage and in vitro ultrasonic measurements of wall cross-sectional area obtained postoperatively in the same arterial segments at the same distending pressure (r=.929, P<.0001). Not unexpectedly, internal diameter was larger in vivo than in vitro, and IMT was smaller in vivo than in vitro.

Hypertrophy of the Radial Artery Wall in Hypertensive Patients
The IMT of the radial artery was measured in 60 hypertensive patients and 40 age-matched control subjects.²⁰ Of the 60 hypertensive patients, 33 were never treated and 27 were well controlled on antihypertensive medication. As far as can be determined from the patients' files, the mean hypertensive disease duration in these patients was 3.7±4.5 years (mean±1 SD; range, 1 to 13 years), and the mean antihypertensive treatment duration was 3.4±4.0 years (range, 1 to 12 years). Radial artery IMT and thickness-radius ratio were used to describe the radial artery structure. Diastolic internal diameter did not differ among the three groups, but radial artery IMT and thickness-radius ratio were significantly higher in the untreated hypertensive group than in the control group. In treated well-controlled hypertensive patients, radial artery IMT and thickness-radius ratio were not different from those of control subjects. For instance, when the 95th percentile of normal values (0.244 mm) was used as a partition value, 30 never-treated hypertensive patients (91%) and only 6 treated hypertensive patients (22%) had abnormal increases in radial artery wall thickness. Among the population of untreated patients, significant univariate relations existed between radial artery IMT and BP and radial artery IMT and age. In multivariate analysis, radial artery IMT was independently predicted by mean BP, age, and sex. Circumferential wall stress, calculated from diastolic internal diameter, wall thickness, and diastolic BP, was not different in the three groups. These results suggest that the increase in radial artery IMT is a reaction to the high BP according to the classic Laplace law to keep the wall stress constant during high BP and that long-term control of BP can normalize radial artery wall thickness.

	Relationship Between Arterial Wall Hypertrophy and Compliance at the Site of the Radial Artery

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
Arterial Compliance and Elastic Modulus
The decrease in arterial compliance observed in hypertensive patients has often been attributed to both the elevated distending pressure and the hypertension-induced structural changes (mainly an increased IMT) that occur with the sustained rise in BP to maintain the circumferential stress unchanged.¹ However, in a previous study²¹ we observed that distensibility and compliance of the radial artery of hypertensive patients were not significantly different from those of normotensive control subjects when the two groups were studied at their respective MAP values. At the site of the radial artery an increase in IMT²⁰ was not associated with a decrease in compliance,^{21 22} leading us to reconsider the issue of the relationship between arterial wall hypertrophy and compliance.

The radial artery parameters of 22 normotensive control subjects were compared with those from 25 age- and sex-matched never-treated essential hypertensive patients²³ ; the methodology used was that described above for the determination of radial artery wall hypertrophy. Circumferential wall stress, calculated from mean BP, internal diameter, and wall thickness (see Appendix), was not significantly different between the two groups (Table 1). Compliance calculated for a given BP, ie, 100 mm Hg (C₁₀₀), was greater in hypertensive patients than in normotensive subjects. In both groups C₁₀₀ was positively correlated with arterial wall cross-sectional area (P<.05) but not with age or MAP. If arterial compliance evaluates the elastic properties of the artery as a hollow structure, E_inc evaluates the elastic properties of the wall material and is calculated from IMT and pulsatile changes in diameter and BP according to Hooke's law (see Appendix). E_inc in hypertensive patients was not significantly different from that in normotensive subjects at their respective MAP values or for a given level of circumferential stress. For a given BP level (100 mm Hg) E_inc was significantly reduced in hypertensive patients compared with normotensive subjects. Thus, the main finding was that the stiffness of the radial artery wall material was not increased in hypertensive patients, despite wall hypertrophy.

View this table: [in this window] [in a new window]   Table 1. Radial Artery Parameters of Normotensive Subjects and Hypertensive Patients

To determine E_inc, we applied Hooke's law for thick-wall tubes. Indeed, the general case of a thick-wall tube was more appropriate for a vessel such as the radial artery, whose wall-lumen ratio is close to 0.3. Previous studies with the use of Young's modulus^{24 25} have generally been performed in larger, more proximal and more elastic arteries, such as the carotid artery or thoracic aorta, which are characterized by a smaller wall-lumen ratio (close to 0.1). A second advantage of Hooke's law is that it does not require knowledge of the unloaded (unstretched) state, ie, the diameter at zero transmural pressure (see Appendix). However, the application of Hooke's law to arterial wall mechanics has some limitations. Hooke's law, which states that strain is proportional to stress (within certain limits), assumes that the arterial wall material is homogeneous and isotropic. Obviously, the arterial wall is not homogeneous and is composed of various elements, including smooth muscle cells, collagen, elastin, and components of the extracellular matrix. Each of these elements has its own elastic modulus, and their relative contributions to arterial wall mechanics is not fully understood. In addition, it is generally accepted that the arterial wall is not isotropic, and several investigators describing the biaxial elastic properties of arteries^{24 25} have reported that arteries are stiffer in the longitudinal versus the circumferential direction. Despite these limitations, using Hooke's law for the study of in vitro arterial elastic properties (unpublished data, 1993), we found results similar to those obtained with the classic formula.^{24 25} Therefore, our conclusion that E_inc was significantly reduced in hypertensive patients compared with normotensive subjects for a given level of BP seems to be well founded.

Previously Published Data
The fact that isobaric compliance and distensibility of the radial artery were either unchanged or increased in hypertensive patients^{21 22} may appear surprising because several studies have demonstrated that sustained hypertension decreases large artery distensibility and compliance. This has been reported for pressure-dimension experiments as well as ring and strip studies of human and animal large arteries both in vivo and in vitro.^{11 12 24 25 26} Thus, in contrast to large arteries our findings suggest a normal distensibility at the site of medium-sized arteries during sustained hypertension, despite hypertrophy of the arterial wall. A likely explanation for the difference in our findings and those of previous studies is that the arteries examined in these studies were of different sizes. Composition of the arterial wall varies with vessel size,²⁷ and the effect of hypertension on conduit arteries may vary with vessel caliber. For instance, previous studies on forearm arterial distensibility have not documented a decrease. Using determination of pulse-wave velocity measured on the human forearm enclosed in an airtight box, Gribbin et al²⁸ showed that for the same mean transmural pressure, normotensive and hypertensive individuals had the same pulse-wave velocity and therefore the same distensibility. Whereas distensibility of the basilar artery and branches of the posterior cerebral artery has been reported to be reduced in SHR compared with normotensive WKY,²⁹ the incremental distensibility of cerebral arterioles was significantly greater in older SHR than in WKY.⁷ Possible mechanisms that might explain the increase in distensibility for a given BP level are unknown. However, the fact that we observed a significant relationship between compliance calculated at 100 mm Hg and wall cross-sectional area suggests that arterial wall hypertrophy may be associated with these mechanisms.

We have shown that at MAP, the elastic modulus in hypertensive patients was not significantly increased compared with that in normotensive subjects. Moreover, the elastic modulus was significantly reduced in hypertensive patients when both populations were compared at the same level of BP (ie, 100 mm Hg). The E_inc-pressure curve depends not only on the properties of the wall material but also on the way in which the material is arranged. Therefore, to provide information that is dependent on the properties of the material only, we calculated elastic modulus for a given circumferential stress. Under these conditions no significant increase in E_inc was observed in hypertensive patients. The fact that E_inc of the radial artery wall material was not increased in hypertensive patients compared with that obtained in normotensive subjects at the same level of BP or circumferential stress is apparently contrary to the in vitro observations that the stiffness of arterial wall material is increased in hypertension.^{11 24} It should be emphasized, however, that several studies have shown that arterial wall stiffness is heterogeneous and that alterations at peripheral sites may not invariably reflect those that occur centrally. For example, using autopsy samples, Learoyd and Taylor³⁰ observed that in the case of the thoracic aorta the values of Young's modulus calculated for a given BP were increased in old compared with young individuals. For peripheral arteries this relationship was reversed, the younger vessels having the greater E_inc. However, such a comparison may not be an appropriate means of comparing changes in arterial wall mechanics because of the stress dependence of arterial wall mechanics. In animals, Baumbach et al⁷ and Mulvany⁸ showed that the elastic modulus of the wall materials for a given wall stress was decreased in the small arteries from SHR compared with normotensive controls.

Our results suggest that the elastic response of the radial artery is maintained despite hypertrophy of the arterial wall. An advantage of hypertrophy is that an increase in wall thickness presumably attenuates increases in wall stress that accompany increases in intravascular pressure. We suggest that at the site of distal, muscular, medium-sized arteries, a second advantage of arterial wall hypertrophy could be the maintenance of a "normal" compliance despite the increased intravascular pressure through the adaptation of E_inc.

	Relationship Between Arterial Wall Hypertrophy and Compliance at the Site of the CCA

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
Clinical Studies
Despite numerous investigations analyzing the influence of risk factors on the IMT of the CCA,^{9 10 14} the relationships between arterial wall hypertrophy and compliance have rarely been the subject of specific studies in hypertensive individuals. Riley et al⁹ have reported increased carotid artery Young's elastic modulus (ie, an increased stiffness of the wall material) and IMT with aging, but the independent role of BP has not been analyzed. Roman et al¹⁰ have reported a decreased carotid distensibility associated with an increased IMT in hypertensive patients compared with age-matched normotensive subjects. When differences in wall thickness were taken into account using Young's modulus, the stiffness of the carotid wall material was not different in hypertensive patients compared with normotensive subjects.³¹ However, the two groups were compared at their respective mean BP values, and the confounding effect of the elevated distending pressure in hypertensive patients could not be ruled out.

Obviously, when BP increases during the cardiac cycle from diastole to systole, distensibility decreases (Fig 1). These short-term changes should not be confounded with long-term adaptive changes. Particularly, whether the decrease in large artery distensibility observed in hypertensive patients is due primarily to an increase in distending pressure or to hypertension-induced changes in structural properties has been much debated.²⁴ To address this issue we determined noninvasively the diameter-pressure curve of the CCA over the systolic-diastolic range by continuously recording both the pulsatile changes in internal diameter using a high-resolution echotracking system (Wall Track System, Pie Medical) and, simultaneously on the contralateral artery, the pressure waveform using high-fidelity applanation tonometry (Millar Instruments, Inc).³² The distensibility-pressure curve was then derived and arterial distensibility compared in 23 normotensive subjects and 15 hypertensive patients matched for age, sex, body surface area, serum cholesterol, and smoking at their respective MAP values or at a common distending pressure (100 mm Hg). As far as can be determined from the patients' files, the mean hypertensive disease duration in these patients was 2.4±3.5 years (mean±1 SD; range, 0.5 to 6 years). Distensibility decreased as BP increased (Fig 1), and distensibility at MAP was significantly lower in hypertensive patients than normotensive subjects (Table 2). In hypertensive patients the distensibility-pressure curve was shifted toward higher levels of BP, and a large part of the curve overlapped that of normotensive subjects. No significant downward shift of the distensibility-pressure curve was observed in hypertensive patients, and distensibility at 100 mm Hg was not significantly different from that of normotensive subjects. Similar conclusions were drawn for compliance. These results suggest that the increase in distending pressure per se could explain the decrease in arterial distensibility and compliance observed in hypertensive patients. As we discussed above, other studies on forearm arterial distensibility in hypertension reached the same conclusions.²⁸

View larger version (17K): [in this window] [in a new window]   Figure 1. Line graph shows cross-sectional distensibility-pressure curves in 23 normotensive subjects () and 15 age- and sex-matched untreated essential hypertensive patients (). Results are presented as mean±SEM.

View this table: [in this window] [in a new window]   Table 2. Arterial Pressure and Common Carotid Artery Parameters of Normotensive Subjects and Hypertensive Patients

The question then arises whether hypertension-induced arterial wall hypertrophy may lead at the site of the CCA to adaptive changes in Young's modulus similar to those observed at the site of the radial artery. Since carotid IMT was not measured in the above study, only an indirect approach can be used. By carefully selecting a majority of hypertensive patients who either had never-treated, sustained hypertension of long duration or had stopped treatment at least 6 months before the study, we increased the likelihood of carotid artery wall hypertrophy being present in our population. We must admit that we cannot rule out the possibility that the never-treated hypertensive patients may not have been hypertensive long enough for the wall to have undergone histological and mechanical changes such as those seen in experiments on SHR. However, since it is likely that structural changes of the carotid artery wall were present in our hypertensive patients, the present results suggest that hypertension-induced changes in CCA structural properties probably play only a minor role in the observed decrease in distensibility and compliance. In addition, from the present data and the values of CCA wall thickness observed in normotensive subjects and hypertensive patients by Roman et al,^{10 31} it can be estimated that E_inc was significantly higher in hypertensive than normotensive individuals when the two populations were compared at their respective MAP values (1.32±0.52 versus 0.96±0.41 kPa · 10³, respectively; mean±SD; P<.05). However, E_inc was not significantly different between hypertensive patients and normotensive subjects when the two groups were compared at the same level of distending pressure, eg, 100 mm Hg (0.98±0.43 versus 1.27±0.44 kPa · 10³, respectively). These data are estimations only, and further studies should be performed to simultaneously determine the pulsatile changes in carotid lumen diameter, wall thickness, and BP to compare E_inc at a given level of BP or circumferential stress.

Animal Studies
Some animal studies are consistent with these clinical findings. Hayoz et al²² determined the cross-sectional compliance of the carotid artery in WKY and SHR according to the methodology used in clinical studies and reported that the compliance-pressure curve of SHR, although shifted toward higher BP levels, was not significantly different from that of WKY. Similar results were found in our laboratory.³³ Moreover, when E_inc was determined from carotid IMT and the distensibility-pressure curve²³ in both strains, the E_inc-pressure curve was significantly shifted to the right in SHR, indicating that E_inc was not increased compared with WKY at a common BP level despite carotid wall hypertrophy (55±3 versus 42±1 µm in SHR and WKY, respectively; P<.001). In addition, E_inc was not significantly different between WKY and SHR when the two groups were compared at a given level of circumferential stress (Fig 2). These findings concerning "dynamic cross-sectional" compliance (since compliance was determined from the pulsatile changes in arterial cross section and pressure) are consistent with some studies of "static volumetric" carotid artery compliance, in which compliance was determined in situ from step increases in distending pressure and resulting volume. In these studies, Levy et al³⁴ and Benetos et al³⁵ reported that carotid compliance of SHR was not significantly different from that of control normotensive rats when they were compared within the same high BP range (150 to 200 mm Hg).

View larger version (13K): [in this window] [in a new window]   Figure 2. Line graph shows mean elastic modulus–circumferential stress curves in seven WKY and seven SHR.

Clinical and Animal Studies
These results obtained in humans and rats at the site of the CCA together with those obtained at the site of the radial artery indicate that the hypertension-induced arterial wall hypertrophy may not necessarily be associated with a reduced compliance when hypertensive patients and normotensive subjects are compared for a given BP level. Moreover, despite arterial wall hypertrophy, the stiffness of the wall material is not increased in hypertensive patients, whether they are compared with normotensive subjects at a given level of BP or circumferential stress. The mechanism explaining the lack of increase in elastic modulus remains purely speculative. Mulvany³⁶ suggested that this could be an alteration either in the characteristics of the individual wall components or in the relative proportions of these components in the wall. As Baumbach et al⁷ suggested for cerebral arterioles, the structural and functional changes of arterial wall material that occur during sustained hypertension could be a means by which large and medium-sized arteries maintain their distensibility characteristics despite wall hypertrophy.

	Opposing Effects of Aging and Hypertension-Induced Arterial Wall Hypertrophy on Arterial Distensibility

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
In regard to the large artery, hypertension is often looked upon as an accelerated form of aging because pathological arterial wall changes similar to those of aging are seen at an earlier age.³⁷ As in aging, the major changes in impedance and in the contours of arterial pressure and flow waves are due to decreased arterial distensibility. We have previously shown that local CCA distensibility and compliance decreased more rapidly with aging in hypertensive patients than normotensive subjects.^{38 39 40} Two different mechanisms have been suggested to explain these earlier alterations in hypertensive subjects: structural changes caused by arterial degeneration or functional changes caused by the increased distending pressure.^{11 26 37} The determination of the distensibility-pressure curve in 23 normotensive and 15 hypertensive patients of various ages (range, 23 to 75 and 34 to 81 years, respectively) gave us the opportunity to analyze the respective role of aging and BP in the decreased distensibility. Aging may alter distensibility independently of BP, as we observed a negative correlation between distensibility calculated at 100 mm Hg (Dist₁₀₀) and age. In addition, in multivariate analysis of the 38 patients as a whole and according to gender, Dist₁₀₀ was independently correlated with aging and the presence or absence of hypertension. A striking finding was the positive correlation of Dist₁₀₀ with the presence of hypertension (r=.51, P<.01) and its negative correlation with aging (r=-.38, P<.01). In addition, according to gender Dist₁₀₀ was correlated positively with MAP (used here to reflect the degree of the hypertensive disease and likely that of carotid wall hypertrophy; r=-.45, P<.01) and negatively with aging (r=-.45, P<.01). Therefore, aging and increased distending pressure could reduce carotid distensibility, whereas hypertension-induced wall hypertrophy could have the opposing effect. Several authors^{11 26 37 38 39 40} have shown that hypertension accelerates the aging-induced alteration of arterial distensibility. In view of the present results, we suggest that the acceleration of this process may occur through an increase in distending pressure rather than through hypertension-induced changes in structural properties of the CCA.

	Hemodynamic Consequences of the Hypertension-Induced Arterial Wall Hypertrophy

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
From the above data it appears that the main hemodynamic consequences of the hypertension-induced arterial wall hypertrophy are (1) an attenuation of the age-induced decrease in arterial compliance at the site of large arteries and (2) the maintenance of a "normal" compliance at the site of distal medium-sized arteries. Maintenance of a "normal" medium-sized artery compliance despite the decrease in proximal compliance leads to reduction of the compliance gradient between proximal and distal arteries. Because the compliance gradient between different parts of the arterial tree has been reported to generate wave reflections,^{41 42} which increase pulse pressure and cardiac afterload, we suggest that this decrease in compliance gradient would be a means by which the vasculature could attenuate wave reflections and pulse pressure at central arterial sites. With regard to the smaller blood vessels downstream, the implications of a "normal" compliance of distal medium-sized arteries are not obvious. To our knowledge, this point has been analyzed only at the level of the cerebral circulation.^{5 7 43} For Baumbach and Heistad,⁴³ the increase in distensibility of cerebral arterioles when they are maximally dilated would tend to counteract encroachment on the lumen, thus minimizing impairment of maximal dilatation by hypertrophy. These authors suggested that the increase in arteriolar distensibility may also have detrimental effects by reducing the tensile strength of the arteriolar wall, therefore increasing the susceptibility of cerebral arterioles to rupture when the vessels dilate passively during short-term, severe increases in systemic arterial pressure.

Therefore, during chronic hypertension arterial compliance appears to be "autoregulated" through arterial wall hypertrophy in order to remain unchanged at the site of medium-sized arteries despite the increased distending pressure and to compensate for the age-induced decrease in arterial compliance at the site of large arteries.

	Conclusion

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
We have summarized and discussed several clinical and animal studies showing that arterial wall hypertrophy does not increase the elastic modulus of the arterial wall material during sustained hypertension. Aging and hypertension-induced hypertrophy appear to have opposing effects on the elastic properties of the carotid artery, the former reducing distensibility and the latter increasing it. The structural and functional changes of the arterial wall material that are associated with the hypertension-induced hypertrophy could be a means by which medium-sized arteries maintain their distensibility characteristics, despite increased distending pressure, and large arteries compensate for the age-induced decrease in arterial compliance. These findings led us to advance the concept of an "autoregulation" of arterial compliance during chronic hypertension through arterial wall hypertrophy.

	Selected Abbreviations and Acronyms

 

BP = blood pressure CCA = common carotid artery Einc = incremental modulus of elasticity IMT = intima-media thickness MAP = mean arterial pressure SHR = spontaneously hypertensive rat(s) WKY = Wistar-Kyoto rat(s)

	Acknowledgments

 
This study was performed with grants from Institut National de la Santé et de la Recherche Médicale (INSERM) and Fondation pour la Recherche Médicale as well as from a grant (BIOMED) of the European Community. I gratefully thank Drs Michel Safar, Xavier Girerd, Patrick Lacolley, and Pierre Boutouyrie for critical review of the manuscript.

	Appendix 1

Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
The relationship between pressure, P, and lumen cross-sectional area, LCSA, was fitted with the use of an arctangent function and three optimal fit parameters¹⁷ :

(1)

where D is the internal diameter assuming a cylindrical vessel. The three parameters , ß, and fully characterize the diameter-pressure curve.

Local arterial cross-sectional compliance, C, in the case of a cylindrical vessel is defined by the change in lumen cross-sectional area (LCSA) for a given change in intravascular pressure (P).^{24 25}

(2)

Because of the nonlinearity of the cross section–pressure curve, compliance decreases as BP increases. To determine compliance for a given level of BP, we established the compliance-pressure curve over the systolic-diastolic range. This was done by deriving the equation of the pressure-LCSA curve.¹⁷ Using Equation 1, we obtained the following analytic form for the local arterial compliance:

(3)

Arterial cross-sectional distensibility is the compliance value normalized for the lumen cross-sectional area and is defined by

(4)

Circumferential wall stress () was calculated as =MPBxD/2h, where MBP is the mean blood pressure, D the mean lumen diameter, and h the combined thickness of the media and intima.^{24 25 27 30}

In contrast to compliance, which provides information about the elasticity of the vessel as a whole, E_inc provides direct information on the elastic properties of the wall material independently of the vessel geometry. By definition, for a cylindrical vessel with wall stiffnesses that are equal in all directions, E_inc is the slope of the stress-strain curve and can be defined by

(5)

where =(d-d_o)/d_o is the strain and d_o the diameter at zero transmural pressure. For in vivo measurements, d_o is in general unknown, which prevents the calculation of the strain and consequently the estimation of the modulus of elasticity. The application of Hooke's law does not require knowledge of the unloaded (unstretched) state. The incremental elastic modulus is calculated as

(6)

where LCSA is the lumen cross-sectional area calculated as a function of BP as described above, WCSA is the mean wall cross-sectional area, and distensibility is a function of BP calculated as described above.²³

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Top Abstract Introduction Noninvasive Assessment of... Relationship Between Arterial... Relationship Between Arterial... Opposing Effects of Aging... Hemodynamic Consequences of the... Conclusion Appendix 1 References

 
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