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Biomedical subjects

M E Safar

Publications and source records attributed to M E Safar.

At least 55 records · Page 3Linked to original sources
PubMed2000

Assessment of vascular aging and atherosclerosis in hypertensive subjects: second derivative of photoplethysmogram versus pulse wave velocity.

The pulse wave velocity (PWV) and the photoplethysmogram (PTG) are noninvasive methods for evaluating the pulse wave. The PWV has been associated with age and arterial hypertension, and an index of the second derivative of PTG (SDPTG) is correlated with age and other risk factors for atherosclerosis. The aim of this study was to compare SDPTG and PWV concerning the influencing factors of vascular compliance, including age and atherosclerosis, in a large hypertensive population. We studied consecutively 524 essential hypertensives, 140 with atherosclerotic alterations (AA), defined on the basis of clinical events including coronary heart disease, peripheral vascular disease, stroke, and abdominal aorta aneurysm. The PWV carotid-femoral was measured by a Complior device and the SDPTG was recorded by Fukuda FCP-3166. The augmentation index (AUI) of PTG was defined as the ratio of the late systolic peak to that of the early systolic peak in the pulse. The SDPTG consists of an a,b,c, and d wave in systole and an e wave in diastole; an SDPTG aging index (AI) was calculated as (b-c-d-e)/a. The patients with AA presented a higher PWV (14.9 +/- 4 m/sec v 12.4 +/- 2 m/sec, P < .001), PTG AUI (0.322 +/- 0.16 v 0.252 +/-0.09, P < .001), and SDPTG AI (-0.093 +/- 0.03 v -0.271 +/- 0.018, P < .001). However, in patients 60 years of age, only PWV remained higher in those with AA, whereas in patients >60 yr, both PWV and SDPTG AI remained higher in those with AA. The PWV was independently influenced by age, systolic blood pressure, glucose, AA, and plasma creatinine, whereas the PTG AUI was influenced by age and systolic pressure and the SDPTG AI by age and AA. In a logistic regression model for the presence of AA, including age, plasma creatinine, smoking, and diastolic BP, PWV was a significant independent determinant of AA, whereas SDPTG-AI weakly entered into the model. This study provides evidence that the aortic PWV reflects better than the SDPTG the modifications of the arterial compliance related to age, blood pressure, and atherosclerosis. However, the SDPTG AI may be useful for evaluation of vascular aging in hypertensives.

Aged↗
PubMed2000

Long-term cardiovascular effects of high "osteoprotective" dose levels of 17 beta-estradiol in spontaneously hypertensive rats.

The effects of estrogen replacement therapy in menopausal women are more obvious on bones than on the cardiovascular system. The optimal estrogen dosage may differ in these different parts of the body. In hypertensive rats, low doses have been shown to reduce arterial collagen and stiffness, whereas higher dosages are required for osteoprotection. From 4 to 20 weeks of age, female spontaneously hypertensive rats (SHRs) were divided into four groups: without ovariectomy, under placebo or 17 beta-estradiol (10 micrograms/kg/day), and with ovariectomy under either placebo or 17 beta-estradiol (same dosage). Serial tail systolic blood pressure measurements were performed, and histomorphometry of the thoracic aorta was determined at the end of the study. Under estrogen, blood pressure was unchanged, whereas the aortic wall-to-lumen ratio was increased, particularly in the presence of ovariectomy. The elastin to collagen ratio was significantly decreased, due both to a decrease in elastin and an increase in collagen density, with no change in media thickness. The latter findings were not observed when ovariectomy was performed. Independent of changes in wall stress, high-dose estrogen increases the aortic extracellular matrix in female SHRs. This increase may be reversed in the presence of ovariectomy, suggesting that estrogen was not the only gonadal factor responsible for altered vascular structure and function.

Animals↗
PubMed2000

Acute and chronic sympathoinhibition on carotid artery diameter of spontaneously hypertensive rats: effects of clonidine and flesinoxan.

1. Hypertensive conduit arteries are thicker and stiffer than those of normotensive controls. Whether they are specifically sensitive to central sympathoinhibition has never been investigated. 2. The effects of acute (24 h infusion) and chronic (4 week infusion) treatments with clonidine (0.01 and 0.1 mg/kg per day) and flesinoxan (1 and 3 mg/kg per day) on carotid artery diameter were investigated in spontaneously hypertensive rats. At the end of treatment, blood pressure (BP) was recorded in the rats while they were conscious. Rats were then anaesthetized for carotid artery diameter measurements using an ultrasonic echotracking device. 3. In conscious rats, clonidine significantly decreased BP and heart rate (HR) following acute but not chronic treatment. In contrast, flesinoxan significantly decreased BP following both the acute and chronic treatment. In anaesthetized animals, the two agents have opposite effects on isobaric carotid artery diameter, with a decrease under clonidine and an increase under flesinoxan. After 4 weeks infusion, the reactivity of aortic rings was studied in organ chambers. Flesinoxan, but not clonidine, caused the relaxation of potassium chloride precontracted aortic segments. 4. The results indicate that although clonidine and flesinoxan are centrally acting antihypertensive agents, the drug-induced changes in isobaric carotid diameter may be influenced by local factors independent of the central action of the two drugs.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2000

Postischemic vasodilation, endothelial activation, and cardiovascular remodeling in end-stage renal disease.

BACKGROUND: Cardiovascular complications are the major cause of death in end-stage renal disease (ESRD) patients. These complications are associated with concomitant cardiac and vascular remodeling, including left ventricular (LV) hypertrophy and hypertrophy of arterial walls. The endothelium influences the process of arterial remodeling. ESRD patients are characterized by the development of both cardiovascular remodeling and endothelial dysfunction. METHODS: Common carotid artery (CCA) intima-media thickness (IMT), CCA diameter, CCA distensibility, LV mass, and function were determined in 60 stable ESRD patients on hemodialysis and 34 age-, sex-, and blood pressure (BP)-matched controls, and their relationships with endothelial alterations were estimated by forearm postischemic vasodilation [flow debt repayment (FDR)] measured by venous plethysmography. We also evaluated the relationships between FDR and several cardiovascular risk factors or markers of inflammatory response or endothelial activation, for example, duration of dialysis, BP, smoking habits, cholesterol, parathormone (PTH), serum albumin, plasma fibrinogen, C-reactive protein (CRP), plasma homocysteine, plasminogen activator inhibitor (PAI-1), and von Willebrand factor (vWF). RESULTS: ESRD patients had increased LV mass, CCA diameter and CCA IMT, and had decreased CCA distensibility (P < 0.05). While the postischemic peak flow was comparable in controls and ESRD patients (29.2 +/- 9.1 vs. 27.9 +/- 0.2 mL/100 mL/min), FDR was lower in ESRD patients (116 +/- 31 vs. 88 +/- 32%, P < 0.001) because of the shorter duration of vasodilation (127 +/- 36 vs. 96 +/- 32 s, P < 0.001). The time to complete FDR was longer in ESRD patients (110 +/- 54 vs. 162 +/- 72 s, P < 0.001). ESRD patients had lower high-density lipoprotein cholesterol and serum albumin (P < 0.01) and higher triglycerides, fibrinogen, plasma homocysteine, vWF (P < 0.01), and PAI-1 (P < 0.05). For ESRD patients, significant negative age- and pressure-independent correlations were established between FDR and CCA diameter, duration of dialysis, and PAI-1. FDR was positively correlated with serum albumin. FDR and time to FDR were negatively correlated with CCA IMT and LV mass. CCA distensibility was positively associated with FDR (P < 0.001) and negatively with time to FDR (P < 0.001). The PAI-1 concentration was positively correlated with CCA IMT (P < 0.01) and negatively with CCA distensibility (P < 0.001). CONCLUSIONS: Our data provide the first evidence that cardiac and arterial remodeling in ESRD patients are inversely related to forearm reactive hyperemia. The diminished hyperemic response is due to the shorter duration of hyperemia and is associated with higher concentrations of serum markers of endothelial activation, suggesting that, in ESRD patients, endothelial dysfunction may be a factor influencing cardiovascular changes.

Adult↗
PubMed2000

Pulse pressure, arterial stiffness, and cardiovascular risk.

Systolic and diastolic blood pressures are the exclusive mechanical factors usually considered as predictors of cardiovascular risk in populations of normotensive and hypertensive subjects at large. However, if hypertension is considered as a mechanical factor acting on the arterial wall with substantial deleterious consequences, the totality of the blood pressure curve should be considered in order to investigate the cardiovascular risk. The purpose of this review is to show that in addition to systolic and diastolic blood pressures, other hemodynamic indices that have particular relevance for cardiac complications and that originate from pulsatile pressure should be taken into account, with important consequences in cardiovascular epidemiology and in the pathophysiology of hypertensive end-organ damage.

Arteries↗
PubMed2000

Association between the apolipoprotein E polymorphism and arterial wall thickness in asymptomatic adults.

OBJECTIVES: The polymorphism of the apolipoprotein E gene (epsilon2, epsilon3, epsilon4) affects plasma cholesterol but the relationship with artery wall thickness has indicated contradictory results. This study investigated the relationship between apolipoprotein E polymorphism and vascular phenotypes of the carotid and radial arteries, two arterial sites differently affected by atherosclerosis. METHODS: We studied a cohort of 320 Caucasian subjects (age 49 +/- 12 years) without evidence of cardiovascular disease. Structural (internal diameter and wall thickness) and functional phenotypes (compliance, distensibility) were evaluated for the common carotid and the radial arteries using high resolution echo-tracking devices. Genotypes of apolipoprotein E were determined by allele-specific oligonucleotides hybridization. Because of the relative low frequency of some apolipoprotein E genotypes, they were designated as E2 (epsilon2/epsilon2, epsilon2/epsilon3), E3 (epsilon3/epsilon3), and E4 (epsilon4/epsilon4, epsilon3/epsilon4). RESULTS: Apolipoprotein E allele frequencies were epsilon2 = 0.08, epsilon3 = 0.79, epsilon4 = 0.13. Subjects with epsilon4 allele had the highest levels of total serum cholesterol and low density lipoprotein cholesterol; subjects with epsilon2 allele had the lowest levels (P < 0.001). Considering carotid hypertrophy as intima-media thickness > 660 microm, and radial hypertrophy as intima-media thickness > 260 microm, a logistic regression model testing determinants of arterial hypertrophy (age, gender, weight, systolic blood pressure, smoking habits, and total serum cholesterol) observed a significant and positive association between carotid hypertrophy and epsilon2 allele carriers (P= 0.03). In contrast, no association was found between hypertrophy and apolipoprotein E genotypes for the radial artery. No association was observed between the apolipoprotein E genotypes and functional artery parameters. CONCLUSIONS: In subjects without any evidence of cardiovascular disease, the presence of the epsilon2 allele is related to wall hypertrophy in carotid artery despite favourable effect on the lipid profile.

Adult↗
PubMed2000

Drug treatment of hypertension: the reduction of pulse pressure does not necessarily parallel that of systolic and diastolic blood pressure.

Drug treatment of hypertension reduces systolic and diastolic blood pressure according to a well-established dose-response curve. Whether there is a parallel decrease in mean blood pressure and pulse pressure has not been investigated in the past Recent analysis of the literature and personal work indicates that, during drug treatment of hypertension, a significant decrease in systolic and diastolic blood pressure may be associated with an unchanged pulse pressure, a situation that might contribute to maintaining cardiovascular risk.

Antihypertensive Agents↗
PubMed2000

Therapeutic studies and arterial stiffness in hypertension: recommendations of the European Society of Hypertension. The Clinical Committee of Arterial Structure and Function. Working Group on Vascular Structure and Function of the European Society of Hypertension.

BACKGROUND: Increased pulse pressure and arterial stiffness are identified as predictors of cardiovascular risk in older hypertensive populations, particularly that of myocardial infarction. Because increased pulse pressure involves an increase in systolic (SBP) and a decrease in diastolic blood pressure (DBP), and because the former promotes cardiac hypertrophy and the latter alters coronary perfusion, a drug regimen reducing pulse pressure and decreasing arterial stiffness might further reduce cardiovascular risk. Under conventional treatment, normalization of DBP (< or = 90 mmHg) is not consistently associated with normalization of SBP (< or = 140 mmHg). THERAPEUTIC DESIGNS: In individuals older than 50 years, the goal of antihypertensive treatment should be, not only to decrease mean blood pressure (to less than 100 mmHg), but also to decrease pulse pressure (to less than 50 mmHg). Using appropriate pharmacological tools, trials should test whether an active decrease in arterial stiffness might produce an attenuation of the age-related increase in SBP and decrease in DBP, thus delaying the age-related increase in pulse pressure and decreasing further cardiovascular risk. This procedure requires concomitant non-invasive evaluations of aortic stiffness. CONCLUSION: The studies that are required in hypertension should use two different approaches: novel titrations of conventional drugs to achieve a decrease in either SBP or pulse pressure, and development of new drugs acting selectively on the large artery wall, to facilitate the conduct of subsequent controlled trials.

Antihypertensive Agents↗
PubMed2000

Arterial mechanical changes in children with familial hypercholesterolemia.

Atherosclerosis is preceded by a phase of changes in the arterial wall that could have functional consequences even before the appearance of atheromatous changes. We hypothesized that early alterations of the mechanical properties of the arterial wall could precede clinical and echographic modifications. We used an automatic, computerized, ultrasonic procedure to evaluate geometric and mechanical characteristics of the common carotid artery (CCA) in normotensive children with primary familial class IIA hypercholesterolemia (FH; n=30; mean+/-SD age, 11+/-2 years old; mean+/-SD systolic/diastolic blood pressure, 109+/-9/55+/-7 mm Hg). These subjects were compared with age-matched, nonobese control subjects (n=27; 11+/-3 years old; 112+/-10/55+/-7 mm Hg). Noninvasive ultrasonic measurements were performed by the same investigator to measure the CCA luminal systolic and diastolic diameters and intima-media thickness (IMT). The cross-sectional compliance, cross-sectional distensibility, and the incremental elastic modulus of the CCA wall were then calculated. Finally, we assessed the degree of reactive hyperemia in the brachial artery produced after distal cuff occlusion and release. The changes in brachial arterial diameter in response to reactive hyperemia (endothelium-dependent dilation) and to glyceryltrinitrate (endothelium-independent dilation) were then measured. In patients with FH, we observed a significant reduction of systodiastolic variations in diameter (by 20%, P:<0.001) without a significant difference in IMT. Cross-sectional compliance and cross-sectional distensibility were significantly reduced in FH subjects (by 15%, P:<0.05 and 19%, P:<0.01, respectively). In parallel, the incremental elastic modulus was significantly increased (by 27%, P:<0.01) in children with FH. No correlation was evident between the carotid incremental modulus and either IMT or plasma low density lipoprotein cholesterol level. There was no difference in diameter of the brachial artery at rest in control and FH subjects (3.0+/-0.5 versus 3.0+/-0.4 mm). The reactive hyperemia and glyceryltrinitrate dilation were also similar in the 2 groups. However, the flow-mediated dilation of the brachial artery was smaller in the FH subjects (4.2+/-2.9%) than in controls (9.0+/-3.1%, P:<0.001). In FH, endothelium-dependent dilation was negatively correlated with the plasma low density lipoprotein cholesterol level (P:<0.04). These results indicate that increased stiffness of the CCA wall in children with FH is independent of blood pressure and could be related to endothelial dysfunction. Thus, alterations in CCA wall mechanics could be early and easily measurable markers of atheromatous changes in the arterial wall.

Biomechanical Phenomena↗
PubMed2000

Stiffness of carotid artery wall material and blood pressure in humans: application to antihypertensive therapy and stroke prevention.

BACKGROUND AND PURPOSE: Because epidemiological studies show that increased pulse pressure and carotid wall-material stiffness are predictors of cardiovascular mortality independent of age, atherosclerosis, and conventional risk factors, the relationships between carotid wall stiffness and blood pressure are important to the optimization of cardiovascular prevention. SUMMARY OF REVIEW: In middle-aged hypertensive patients, mean and pulse pressures are increased, and systolic and diastolic pressures are increased to the same degree as mean pressure. Carotid hypertrophy is associated with normal wall stress, but no increased stiffness of wall material has been reported. With age, the normal wall stress is associated with a larger diameter and a stiffer material of carotid but not peripheral arteries. The stiffer wall involves calcifications, large amounts of collagen, and fragmentation and rupture of elastic tissue, which results in increased pulse-wave velocity and alterations of amplitude and timing of wave reflections and thus causes a disproportionate increase in systolic and pulse pressure. During this period, acutely administered nitrates in elderly subjects are able to reduce selectively systolic and pulse pressures without altering diastolic and mean blood pressure and composition of the carotid wall. CONCLUSIONS: New therapeutic approaches acting mainly on the wall of large arteries are needed to treat hypertension in elderly patients and prevent stroke and myocardial infarction. These drugs could either selectively lower pulse pressure through changes in wave reflections (as nitrates do) or decrease arterial wall stiffness through modification of the composition of material (such as compounds that act on collagen cross-linking).

Aging↗
PubMed1999

Impact of aortic stiffness on survival in end-stage renal disease.

BACKGROUND: Damage to large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased arterial stiffness and intima-media thickness, together with increased pulse pressure, are the principal arterial alterations. Whether increased aortic pulse-wave velocity (PWV), a classic marker of increased arterial stiffness, may predict all-cause and/or cardiovascular mortality has never been investigated. METHODS AND RESULTS: A cohort of 241 patients with ESRD undergoing hemodialysis was studied between April 1987 and April 1998. The mean duration of follow-up was 72+/-41 months (mean+/-SD). Mean age at entry was 51.5+/-16.3 years. Seventy-three deaths occurred, including 48 cardiovascular and 25 noncardiovascular fatal events. At entry, together with standard clinical and biochemical analyses, patients underwent echocardiography and aortic PWV measured by Doppler ultrasonography. On the basis of Cox analyses, 2 factors emerged as predictors of all-cause and cardiovascular mortality: age and aortic PWV. Hemoglobin and low diastolic pressure interfered to a smaller extent. After adjustment for all the confounding factors, an OR for PWV >12. 0 versus <9.4 m/s was 5.4 (95% CI, 2.4 to 11.9) for all-cause mortality and 5.9 (95% CI, 2.3 to 15.5) for cardiovascular mortality. For each PWV increase of 1 m/s in our study population, all-cause mortality-adjusted OR was 1.39 (95% CI, 1.19 to 1.62). CONCLUSIONS: These results provide the first direct evidence that in patients with ESRD, increased aortic stiffness determined by measurement of aortic PWV is a strong independent predictor of all-cause and mainly cardiovascular mortality.

Adult↗
PubMed1999

[Current aspects of arterial hypertension. Doppler echocardiography. Value and indications].

DETECTION OF LEFT VENTRICULAR HYPERTROPHY: High blood pressure can lead to left ventricular hypertrophy and is an independent risk factor of cardiovascular disease. Echocardiography can be used to measure left ventricular mass based on equations established from anatomoclinical studies. Echocardiography can also give a precise map of the left ventricle allowing a prognostic classification: poor prognosis, concentric remodeling, eccentric hypertrophy, concentric hypertrophy. INDICATIONS: Doppler-echocardiographic analysis of left ventricular filling provides information on systolic function and is clearly indicated in case of symptomatic hypertension, or associated cardiopathies or electrocardiographic abnormalities. Indications should be discussed in case of moderate hypertension in order to evaluate the cardiovascular risk. LIMITATIONS AND PERSPECTIVES: Because of the low reproducibility, Doppler-echocardiography is not useful for follow-up of established left ventricular hypertrophy in hypertensive patients, all the more so since it has not been established that regression is associated with improved cardiovascular prognosis.

Echocardiography, Doppler↗
PubMed1999

Arterial structural changes with verapamil in spontaneously hypertensive rats.

Reducing pulse pressure might be more powerful than reducing mean arterial pressure to obtain regression of vascular hypertrophy. However, this hypothesis has never been investigated in the conduit arteries of intact hypertensive animals. A group of 4-week-old spontaneously hypertensive rats (SHR) was treated with the calcium-entry blocker verapamil (50 mg/kg) for 16 weeks and compared with untreated SHR and control Wistar Kyoto (WKY) normotensive rats of the same age. At the end of the experiment, intraarterial thoracic aorta blood pressure was measured both in the conscious and anesthetized animals. Carotid artery diameter and stiffness (echo-tracking techniques) and aortic histomorphometry were determined in parallel. With verapamil, pulse pressure, but not mean arterial pressure, was significantly decreased but did not reach the normotensive values. Carotid internal diameter, medial thickness, and collagen content were significantly reduced by comparison with SHR and did not differ from the values of the WKY group. A significant positive and independent correlation was observed between pulse pressure and medial thickness in the overall population. The study shows that, in SHR chronically treated with verapamil, structural changes may be completely prevented without any change in mean arterial pressure. The parallel change in pulse pressure might suggest that mechanosensitive elements within the vascular wall may be selectively sensitive to the dynamic aspects of physical forces and are able to convert frequency and amplitude information into cellular responses that lead to vascular remodeling.

Animals↗
PubMed1999

Plasma insulin, plasminogen activator inhibitor, and ankle-brachial systolic blood pressure ratio in overweight hypertensive subjects.

BACKGROUND: In hypertensive subjects, the ratio between ankle and brachial systolic blood pressure (ABI) has been shown to be an independent risk factor for cardiovascular diseases, particularly in the elderly. Plasma insulin may be an important interconnecting factor explaining this observation. PURPOSE: In a population of middle-aged subjects with essential hypertension and moderate overweight, we identified whether the decrease in the ABI ratio was associated with the clinical and biochemical factors involved in resistance to insulin. Patients with diabetes and/or arteriosclerosis obliterans of the lower limbs were excluded from the population. Subjects were or were not on antihypertensive therapy. RESULT: On the basis of univariate correlations, the ABI ratio was found to be significantly and negatively associated not only with the degree of abdominal fat distribution, but also with the usual biological features of resistance to insulin: plasma triglycerides and cholesterol; plasma glucose and insulin; and plasminogen activator inhibitor (PAI) antigen. In a multivariate analysis in subjects with untreated hypertension, the ABI ratio was significantly and negatively associated with only three variables: age, plasma insulin and PAI antigen. In treated hypertensive subjects, only the role of age and insulin remained significant. CONCLUSION: Since the alterations of the ABI ratio may be considered as a marker of the changes in the structure and function of arteries of the lower limbs, the study provides evidence that plasma insulin and PAI antigen, independently of the presence of significant atherosclerotic occlusive lesions, are susceptible to alter the pressure wave transmission in conduit arteries of the lower limbs.

Adult↗
PubMed1999

Hypothesis on isolated systolic hypertension in the elderly.

Although a number of studies have been focused on systolic-diastolic hypertension, few investigations have been performed on isolated systolic hypertension, particularly in the fields of pathophysiology, aetiology and drug treatment. In this article, several hypotheses are presented on this subject

Aged↗
PubMed1999

Evidence for a common defect associated with pressure in the aorta of two hypertensive rat strains.

1. Thoracic aortas of normotensive (Wistar-Kyoto (WKY) and Lyon normotensive (LN)) and hypertensive (spontaneously hypertensive rats (SHR) and Lyon hypertensive (LH)) rats from two groups (Japanese (WKY rats and SHR) and Lyon (LN and LH rats)) were compared using organ chambers. Changes in endothelium and smooth muscle reactivity to noradrenaline (NA), carbamylcholine and N omega-nitro-L-arginine (L-NNA) were analysed to distinguish between changes in reactivity that are associated with the presence of hypertension and those that are dependent on group (Japanese vs Lyon). 2. Aortas of hypertensive rats had lower pD2 values for NA than aortas from normotensive rats. These differences were associated with hypertension (P < 0.005 and P < 0.01) and group (P < 0.005 and P < 0.005) in presence or absence of endothelium, respectively, whereas no difference was seen in the maximal developed tension in response to NA. 3. Aortas also differed by a reduced ability to relax in response to carbamylcholine in hypertensive rats; this effect is hypertension (P < 0.05) and group (P < 0.005) dependent, without any change in carbamylcholine pD2 values. 4. Changes in maximum developed tension in the presence of L-NNA were found to be endothelium dependent and pressure and group independent. Furthermore, the change in tension induced by L-NNA appears significantly more pronounced in SHR than in LH rats (P < 0.05). 5. These results indicate that the common defect associated with hypertension appears to be linked to the endothelium through alpha-adrenoceptors and muscarinic receptors in both the Japanese and Lyon groups. However, SHR differs markedly from LH rats by having a higher developed tension in response to NA, this increased tension being counterbalanced by the release of nitric oxide, as observed in the presence of L-NNA.

Animals↗
PubMed1999

Influence of age and end-stage renal disease on the stiffness of carotid wall material in hypertension.

BACKGROUND: Incremental elastic modulus, which is the slope of the relationship between stress and strain of arterial vessels, is a marker of wall material stiffness. The radial artery incremental elastic modulus, which is not influenced by age, is normal or reduced in patients with essential hypertension but increased in patients with end-stage renal disease. Authors of studies on hypertension largely ignore the question of whether the incremental elastic modulus, measured in the common carotid artery as typical of a central artery site, differs according to age or to the presence of end-stage renal disease or both. SUBJECTS AND METHODS: The carotid incremental elastic modulus was measured in 208 hypertensive patients divided into four groups according to age (< or = or > 55 years) and the presence or absence of end-stage renal disease. The incremental elastic modulus was calculated from transcutaneous measurements of arterial internal diameter and wall thickness (echo-tracking device) and carotid pulse pressure (tonometry). Because the four groups of subjects had the same mean arterial pressure, the static incremental elastic modulus was calculated both in isobaric conditions and for the same wall stress. RESULTS: In nonuremic subjects, lumen diameter, wall thickness and the incremental elastic modulus were significantly (P < 0.001) increased in older subjects whereas compliance and distensibility were decreased. The mean (+/- SD) elastic modulus was 0.41 +/- 0.14 x 10(3) kPa in younger and 0.71 +/- 0.28 x 10(3) kPa in older subjects. In uremic subjects, the corresponding values were 0.48 +/- 0.30 and 0.90 +/- 0.49 x 10(3) kPa, and therefore higher than in nonuremic subjects, irrespective of age. Multiple regression analysis showed that age, mean arterial pressure and the presence of end-stage renal disease independently influenced carotid diameter, distensibility and the incremental elastic modulus. CONCLUSIONS: In hypertensive patients, the carotid incremental elastic modulus is increased independently in aging men and women and in the presence of uremia. This increase is not dependent on mechanical factors such as the level of mean blood pressure.

Adult↗