Biomedical subjects

A Benetos

Publications and source records attributed to A Benetos.

At least 73 records · Page 4Linked to original sources

PubMed1996

Prevalence and circadian variations of ST-segment depression and its concomitant blood pressure changes in asymptomatic systemic hypertension.

Coronary artery disease is a major complication of hypertension; one of its manifestations is silent ischemia. The aim of this study was to assess the prevalence and circadian distribution of ST-segment depression together with concomitant blood pressure (BP) and heart rate variations. One hundred patients (male:female ratio 1:1) with a mean age (+/- SD) of 51 +/- 8 years underwent ambulatory monitoring using the combined AMP 5600 monitor which simultaneously records a continuous Holter electrocardiogram and intermittent noninvasive BP measurements at 15-minute intervals, with extra measurements triggered by detection of a horizontal or downsloping ST depression (> 1 mm and >60 seconds). Cardiovascular risk factors were fully evaluated in all patients; accurate and reliable echocardiogram enabled left ventricular mass index to be calculated in 52 patients. Twenty-three patients (15 men and 8 women) experienced a total of 72 episodes of ST depression. Duration of such episodes (mean +/- SD) was 132 +/- 65 seconds and amplitude was 1.51 +/- 0.55 mm. Circadian distribution showed 2 peaks: on awakening and in the late afternoon periods. The mean ambulatory BP load was greater in the patients with than without ST-segment depression for both systolic and diastolic BP (135 +/- 14 vs 129 +/- 15 and 84 +/- 8 vs 79 +/- 10 mm Hg, respectively; p < 0.01). Plasma glucose (5.83 +/- 0.70 vs 5.46 +/- 0.71 mmol/L; p = 0.04) and self-related work-related stress levels (22% vs 13%; p = 0.03) were also higher in patients with ST-segment depression. There were no significant differences between groups for clinical parameters, left ventricular mass index, and other cardiovascular risk factors. During ST depression episodes, systolic BP increased by 9 +/- 15 mm Hg, diastolic BP by 7 +/- 11 mm Hg, and heart rate by 5 +/- 17 beats/min. Thus, 24-hour Holter electrocardiographic monitoring showed ST depression episodes in 23 of 100 hypertensive patients (23%); ambulatory BP load was greater in these patients. BP variations, and mainly its elevation, may trigger such episodes of ST-segment depression.

Adult↗

PubMed1996

Influence of the angiotensin II type 1 receptor gene polymorphism on the effects of perindopril and nitrendipine on arterial stiffness in hypertensive individuals.

Angiotensin-converting enzyme inhibitors improve arterial stiffness independently of blood pressure reduction. Since we have recently shown that in hypertensive individuals the A1166C polymorphism of the angiotensin II type 1 receptor (AT1-R) is an independent determinant of aortic stiffness, we designed the present study to assess the influence of this polymorphism on the changes of aortic stiffness after chronic treatment with the angiotensin-converting enzyme inhibitor perindopril and the calcium channel blocker nitrendipine. Forty perindopril- and 42 nitrendipine-treated hypertensive individuals were studied. We evaluated aortic stiffness by measuring the carotid-femoral pulse wave velocity. Carriers of the AT1-RC allele showed higher baseline values of pulse wave velocity than AA homozygotes (P < .05). In the perindopril group, a threefold greater reduction in pulse wave velocity was observed in carriers of the C allele than in AA homozygotes (-2.85 +/- 0.62 versus -0.94 +/- 0.32 m/s, respectively; P < .001), whereas in the nitrendipine group, pulse wave velocity decreased only in AA homozygotes and not in AT1-R C carriers (-1.38 +/- 0.35 versus +0.04 +/- 0.60 m/s, respectively; P < .01). These results indicate that according to the AT1-R A1166C genotype, an angiotensin-converting enzyme inhibitor and a calcium channel blocker affect pulse wave velocity in opposite ways. Since some evidence shows that increased pulse wave velocity may enhance cardiovascular risk, it might be useful for physicians to consider the AT1-R genotype when prescribing an angiotensin-converting enzyme inhibitor or calcium channel blocker to a hypertensive individual.

Adult↗

PubMed1996

Aortic collagen, aortic stiffness, and AT1 receptors in experimental and human hypertension.

Converting-enzyme inhibitors decrease the collagen content of the arterial wall in various models of hypertension in rats. Angiotensin II induces collagen production in culture cells. Whether the decrease in collagen induced by converting-enzyme inhibition is due in vivo to pressure mechanisms or to nonhemodynamic factors or a combination of both remains the subject of discussion. In this review, it will be shown that (i) converting-enzyme inhibition prevents the accumulation of aortic collagen in hypertensive rats independently of blood pressure changes, (ii) prevention of aortic collagen accumulation in hypertensive rats is obtained through blockade of angiotensin II formation involving AT1 receptors, and (iii) in hypertensive humans, increased aortic stiffness is associated with AGTR1 receptor polymorphism independently of age and blood pressure.

Angiotensin II↗

PubMed1995

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.

Adult↗

PubMed1995

Carotid artery mechanical properties of Dahl salt-sensitive rats.

We evaluated the mechanical properties of the carotid artery in anesthetized Dahl rats with or without long-term treatment with the diuretic compound indapamide. The mechanical properties of the carotid artery were evaluated by establishing pressure-volume curves in situ in vivo before and after total relaxation of arterial smooth muscle by potassium cyanide. Dahl salt-sensitive and salt-resistant rats were fed either a low (0.4%) or high (7%) NaCl diet for 5 weeks. In each group, half the rats received for the same period of time oral treatment with indapamide (3 mg/kg per day). Blood pressure, heart rate, and pressure-volume curves were studied at the end of the 5-week period. In untreated Dahl salt-sensitive rats, the pressure-volume curve of the carotid artery was shifted to the right compared with that in untreated Dahl salt-resistant rats. The finding was observed even after potassium cyanide and regardless of the NaCl diet (P < .01 between Dahl salt-sensitive and -resistant rats). Indapamide was able to prevent the development of hypertension in Dahl salt-sensitive rats receiving a high NaCl diet (185 +/- 7 versus 146 +/- 8 mm Hg in untreated and treated Dahl salt-sensitive rats with a high NaCl diet, P < .0005). In the other groups, indapamide had no effect on blood pressure. Indapamide treatment increased carotid arterial static compliance in Dahl salt-sensitive rats with a high or low NaCl diet and to a lesser extent in Dahl salt-resistant rats. The increase was observed even after total relaxation of carotid arterial smooth muscle by potassium cyanide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Common carotid artery stiffness and patterns of left ventricular hypertrophy in hypertensive patients.

The aim of this study was to determine the relationship between the lumen diameter and function of the common carotid artery, a vessel representative of the capacitance portion of the circulation, and the different patterns of left ventricular hypertrophy in uncomplicated essential hypertensive patients. Carotid luminal diastolic cross-sectional area, distensibility, and compliance were derived from measurements by a high-definition echotracking system. Left ventricular dimensions were from echocardiography. The 86 hypertensive patients included 31 who had never been treated (group 1), 31 in whom treatment had been stopped for at least 2 weeks (group 2), and 24 treated patients (group 3). In multivariate analysis of the population as a whole, the following relations were statistically independent of age, blood pressure, gender, and group: Left ventricular end-diastolic volume index was positively correlated to carotid luminal cross-sectional area (r = .46, P < .0001) and compliance (r = .47, P < .0001); left ventricular mean wall thickness and mass-volume ratio were negatively correlated to distensibility (r = -.68, P < .0001; r = -.46, P < .0001, respectively) and compliance (r = -.40, P < .0001; r = -.37; P < .001, respectively); and left ventricular mass index was positively correlated to luminal cross-sectional area (r = .23, P < .02) and negatively to distensibility (r = -.26, P < .01). These results indicate that geometric and functional changes in the common carotid artery accompany geometric changes in the left ventricle. More specifically, they suggest that a reduction in distensibility paralleled cardiac concentric hypertrophy and remodeling, whereas an increase in arterial volume paralleled increased left ventricular cavity size.

Adult↗

PubMed1995

Influence of angiotensin II type 1 receptor polymorphism on aortic stiffness in never-treated hypertensive patients.

Several clinical and experimental studies have suggested a significant role of angiotensin II in the development of alterations of small and large arteries. The present study was designed to assess the contribution of polymorphism (corresponding to an A1166-->C transversion) of the angiotensin II type 1 receptor (AT1) gene to aortic stiffness. One hundred thirty-four never-treated hypertensive patients were included in the study. Aortic distensibility was evaluated by measuring carotid-femoral pulse wave velocity. Age, systolic and diastolic pressure, and metabolic parameters were similar in the three genotypes. Pulse wave velocity was 11.4 +/- 2.5 m/s in AT1 AA homozygotes, 12.5 +/- 3.2 m/s in AC heterozygotes, and 14.7 +/- 4.0 m/s in CC homozygotes (P = .003, P < .001 after adjustment for age, blood pressure, and body mass index). Moreover, an interaction was found between AT1 genotype and the ratio of total to high-density lipoprotein cholesterol in terms of the development of aortic stiffness. Thus, a positive correlation was observed between the ratio of total to high-density lipoprotein cholesterol and pulse wave velocity in AC and CC (r = .42, P < .001) but not AA patients. These results suggest that the AT1 gene is involved in the development of aortic stiffness in hypertensive patients and could modulate the effects of lipids on large arteries.

Adult↗

PubMed1995

Aortic distensibility and structural changes in sinoaortic-denervated rats.

The purpose of the present study was to determine the effects of chronic sinoaortic denervation on the mechanical properties and composition of the abdominal aorta in Wistar rats. We used a high-resolution echotracking system to determine in situ under physiological conditions of blood flow and arterial wall innervation the aortic diameter-, compliance-, and distensibility-pressure curves in 16-week-old anesthetized rats that had been denervated at 10 weeks of age for 6 weeks (n = 8). Compared with sham-operated rats (n = 8) we observed a marked reduction of baroreflex response and increase in overall mean blood pressure variability as measured by standard deviation and spectral analysis in sinoaortic-denervated rats. Mean blood pressure was not affected by sinoaortic denervation in both conscious and anesthetized rats. Sinoaortic denervation significantly shifted the distensibility-pressure curve toward lower levels of distensibility, indicating a decreased aortic distensibility for a given level of arterial pressure. Sinoaortic denervation produced a significant increase of aortic wall cross-sectional area and collagen content, one of the less-distensible components of the arterial wall. These results suggest that intact arterial baroreceptors are necessary for maintaining normal functional and structural properties of large arteries in rats. The reduction in arterial distensibility in chronic sinoaortic-denervated rats may have resulted from different factors, including the initial hypertensive phase, aortic wall hypertrophy, and increase in collagen content. The changes in aortic wall structure and related reduction in aortic distensibility, in addition to other mechanisms, might have been direct consequences of an increased blood pressure variability.

Animals↗

PubMed1995

Assessment of arterial distensibility by automatic pulse wave velocity measurement. Validation and clinical application studies.

Pulse wave velocity is widely used as an index of arterial distensibility. The aim of this study was to evaluate the accuracy of a new automatic device to measure it and then to analyze the major determinants of pulse wave velocity by application of this device in a large population. We evaluated the accuracy of on-line and computerized measurement of pulse wave velocity using an algorithm based on the time-shifted and repeated linear correlation calculation between the initial rise in pressure waveforms compared with the reference method (manual calculation) in 56 subjects. The results, analyzed according to the recommendations of Bland and Altman, showed a mean difference of -0.20 +/- 0.45 m/s for the mean carotid-femoral pulse wave velocity values (reference method, 11.05 +/- 2.58 m/s; automatic device, 10.85 +/- 2.44 m/s). The interreproducibility and intrareproducibility of measurements by each method were analyzed with the use of the repeatability coefficient according to the British Standards Institution. The interobserver repeatability coefficient was 0.947 for the manual method and 0.890 for the automatic, and intraobserver repeatability coefficients were 0.938 and 0.935, respectively. We evaluated the major determinants of the carotid-femoral pulse wave velocity measured by the automatic method in a separate study performed in 418 subjects of both sexes without any cardiovascular treatment or complication (18 to 77 years of age; 98 to 222 mm Hg systolic and 62 to 130 mm Hg diastolic pressure).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1995

Aortic distensibility in normotensive, untreated and treated hypertensive patients.

BACKGROUND: Compared with normotensive subjects, untreated hypertensive patients show a decrease of their aortic distensibility. Whether antihypertensive treatment, by reducing blood pressure and changing functional and/or structural abnormalities of the arterial wall, may prevent or reverse the arterial damage due to the accelerated ageing process remains unclear. The objective of the present study was to determine, using a cross-sectional approach, whether aortic distensibility as measured by pulse wave velocity, in treated hypertensive patients whose diastolic blood pressure had been normalised for several months, was significantly improved over that of untreated hypertensive patients. METHODS: Carotid femoral pulse wave velocity was measured in 124 normotensive subjects and 388 hypertensive patients. The latter group included 164 treated patients with well controlled diastolic blood pressure and 224 untreated hypertensive subjects. The three groups did not differ in other cardiovascular risk factors. RESULTS: In each group there was a significant relationship between age and pulse wave velocity. When compared with untreated hypertensives, treated hypertensives with well controlled diastolic blood pressure had significantly lower blood pressure and pulse wave velocity according to age. However, although diastolic blood pressure of well controlled hypertensives was not significantly different from that of normotensive subjects, the aortic distensibility of the controlled hypertensives remained reduced showing two characteristics: a faster increase in pulse wave velocity with age and a negative relationship with HDL-cholesterol. CONCLUSION: These results suggest that long-term antihypertensive treatment and control of blood pressure using only diastolic blood pressure criteria may not fully reverse arterial alteration associated with hypertensive vascular disease.

Adolescent↗

PubMed1995

Proximal and distal pulse pressure after acute antihypertensive vasodilating drugs in Wistar-Kyoto and spontaneously hypertensive rats.

OBJECTIVE: In a previous study (J Hypertens 1993, 11:135-139) our group showed that in anaesthetized rats, although pulse pressure increased from the proximal (common carotid artery) to the distal (terminal aorta) portion of the aorta in normotensive Wistar-Kyoto (WKY) rats, such a pulse pressure gradient was not observed in spontaneously hypertensive rats (SHR) which had identical values of proximal and distal pulse pressure. The purpose of the present study was to show, in awake SHR, in comparison with awake WKY rats, that the lack of pulse pressure gradient might be functionally reversed after acute administration of vasodilating agents. METHODS: The drugs (administered intra-arterially) were an angiotensin converting enzyme inhibitor (perindoprilat; 2 mg/kg), a calcium antagonist (nicardipine; 30 micrograms/kg), a peripheral vasodilator (hydralazine; 200 micrograms/kg) and placebo (isotonic saline). Blood pressure was evaluated invasively. RESULTS: In untreated rats it was noticed that pulse pressure increased physiologically from the proximal to the distal part of the aorta for the same mean arterial pressure in WKY rats, whereas no pulse pressure gradient was observed in SHR. With acute drug administration, marginal modifications were observed in WKY rats, but mean arterial pressure was reduced significantly in SHR (hydralazine > perindoprilat > nicardipine). Proximal pulse pressure was decreased significantly with perindoprilat or nicardipine but was unchanged with hydralazine. Distal pulse pressure was unchanged, except for an increase in the nicardipine-treated group. Heart rate was increased significantly by hydralazine. CONCLUSION: The results show that, although all of the drugs studied decreased mean arterial pressure in SHR, only the calcium antagonist nicardipine and the angiotensin converting enzyme inhibitor perindoprilat reduced proximal pulse pressure. This dissociation between the effects on mean arterial pressure and proximal and distal pulse pressure can be explained by the preferential action of the different antihypertensive agents on large arteries and wave reflections, producing different patterns in the pulsatile component of the heart load.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

[Relation between cardiac hypertrophy and changes in the large arterial trunks. Role of the renin-angiotensin system].

The raised mean arterial pressure observed in hypertension increases the stress on the walls of large arteries by increasing the mechanical forces to which they are submitted. Cardiac and arterial wall hypertrophy seem to be adaptive mechanisms tending to reduce the stress in each musculo-elastic unit of the cardiovascular system. However, this adaptation only partially explains the development of cardiovascular hypertrophy. Cardiovascular changes are sometimes observed before the increase in blood pressure, as in normotensive children of hypertensive parents. Moreover, a dissociation has been shown between the antihypertensive effects of different antihypertensive agents. For the same reduction in mean arterial pressure, some drugs are associated with a greater regression in these changes than others. At present, it is acknowledged that other factors than mean arterial pressure may cause these changes. For example, the pulse pressure is a major factor, independent of mean arterial pressure, in developing cardiovascular hypertrophy. The activation of hormonal systems, especially the angiotensin converting enzyme system, influences cardiovascular structure. Therefore, hyperactivity of the renin-angiotensin system may stimulate the growth factor responsible for cardiac and arterial hypertrophy.

Arteries↗

PubMed1994

Life survival and cardiovascular structures following selective beta-blockade in spontaneously hypertensive rats.

The aim of this study was to assess life survival, and arterial and cardiac structural changes following chronic selective beta-blockade in spontaneously hypertensive rats (SHR). Twenty-two SHR aged 3 months and 20 SHR aged 18 months were treated with the beta 1-blocking agent bisoprolol (10 mg/kg/day) or placebo for a period of 2 months. At the end of this period left and right ventricular weight and morphometric parameters of five different arterial segments (thoracic and abdominal aorta, renal, mesenteric, and carotid arteries) were evaluated. In younger SHR, systolic blood pressure (tail-cuff method) was significantly lower in drug-treated animals (225 +/- 15 v 185 +/- 10 mm Hg in placebo-treated animals; P < .001); left ventricular weight was significantly lower in drug-treated rats (0.845 +/- 0.02 v 0.932 +/- 0.03 g; P < .05); medial thickness was significantly lower in the bisoprolol-treated rats at the site of the thoracic (-22%) and abdominal (-17%) aorta, and mesenteric artery (-29%); in the renal and carotid arteries, no change in medial thickness was observed. In older SHR, cardiovascular morbidity and mortality were significantly higher (P < .01) in the placebo group. In bisoprolol-treated animals, systolic blood pressure did not change and was even significantly higher than in controls. Heart weight and medial thickness of the thoracic aorta and the renal arteries were significantly lower in the Bisoprolol group. These results provide evidence that 2 months of selective beta-blockade in adult SHR has an important antihypertrophic cardiac and vascular effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed1994

Arterial pulse wave and calcium-channel blockers in hypertension.

In contrast to mean blood pressure, arterial pulsatility represented by pulse pressure (PP) varies from heart to periphery. It depends on the stiffness of large arteries and the degree of arteriolar vasoconstriction. The central pulsatility, directly linked to left ventricular work, cannot be accurately evaluated by measurement of brachial PP. Moreover, the pulse wave reflection, when arriving in systole, increases the late-systolic pressure and the left ventricular afterload, particularly in older and hypertensive subjects. Analysis of the central pressure curve recorded by an accurate noninvasive method (applanation tonometry) may improve the hemodynamic evaluation of antihypertensive drugs. Calcium blockers reduce cardiac afterload in hypertension by their arteriolar vasodilating properties, by improving the compliance of large arteries, and also by reducing the central influences of the reflection wave, as shown after single administration and particularly after chronic treatment with calcium blockers.

Arteries↗

PubMed1994

Effects of bradykinin B2 receptor antagonism on the hypotensive effects of ACE inhibition.

1. The aim of this study was to determine the participation of endogenous bradykinin (BK) in the antihypertensive effects of the angiotensin converting enzyme inhibitor (ACEI), perindoprilat, in the spontaneously hypertensive rat (SHR) on different salt diets. 2. Conscious SHRs receiving either a low or a high NaCl diet were used in order to evaluate the respective roles of angiotensin II suppression and bradykinin stimulation in the acute hypotensive effects of perindoprilat. Two different B2 receptor antagonists (B 4146 and Hoe 140) were used after bolus administration of 7 mg kg-1 of the ACEI, perindoprilat. In separate animals, Hoe 140 was administered before the injection of perindoprilat. In other experiments, the effects of Hoe 140 on the hypotensive effects of the calcium antagonist, nicardipine, were tested. 3. The different NaCl diets had no effect on baseline blood pressure. Hoe 140 injection before ACE inhibition did not modify blood pressure. Perindoprilat caused more marked hypotension in the low salt-fed rats than in the high salt animals (P < 0.01). Administration of Hoe 140 or B4146 after perindoprilat significantly reduced the antihypertensive effects of perindoprilat in the different groups, but this effect was more pronounced in high salt-fed rats. However, in SHRs receiving Hoe 140 before perindoprilat, the antihypertensive effect of perindoprilat was completely abolished in both high or low salt diet rats. In separate experiments we confirmed that Hoe 140 did not affect the hypotensive efficacy of the calcium antagonist, nicardipine. 4. Our study shows that inhibition of endogenous bradykinin degradation participates in the acute antihypertensive effects of perindoprilat in SHRs. The role of bradykinin is more pronounced following exposure to a high salt diet i.e., when the renin-angiotensin system is suppressed. Blockade of bradykinin B2 receptors by Hoe 140 before administration of perindoprilat completely abolished the hypotensive effect of perindoprilat suggesting an increased role of bradykinin in the onset of hypotensive action of ACE inhibitors. However, the exact mechanism of this interaction remains unclear.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1994

Angiotensin converting enzyme inhibition prevents the increase in aortic collagen in rats.

Four groups of 4-week-old spontaneously hypertensive rats were treated during 4 months with the angiotensin converting enzyme inhibitor quinapril at 1 mg/kg per day (Q1) or 10 mg/kg per day (Q10), hydralazine at 15 mg/kg per day (H), or placebo (P). In the first set of experiments, blood pressure was measured in conscious rats, and plasma and aortic angiotensin converting enzyme activities were evaluated. In the second set of experiments, histomorphometric parameters of the thoracic aorta were evaluated. Mean blood pressure was lower in the Q10 and H groups (136 +/- 16 and 149 +/- 11 mm Hg) compared with the P group (190 +/- 23 mm Hg) (P < .01). The Q1 group showed mean blood pressure values (171 +/- 15 mm Hg) lower than the P group (P < .05) but significantly higher than the Q10 and H groups (P < .01 and P < .05, respectively). Aortic medial cross-sectional area was significantly lower in the H and Q10 groups (455 +/- 61 and 487 +/- 57 x 10(3) microns 2) than in the P group (636 +/- 72 x 10(3) microns 2) (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1994

Heterogeneity of the arterial tree in essential hypertension: a noninvasive study of the terminal aorta and the common carotid artery.

The diameter and the stiffness of the distal portion of the abdominal aorta and of the common carotid artery were evaluated noninvasively in 72 subjects with mild to moderate hypertension by comparing 39 normotensive controls of same age and sex distribution. For each arterial segment, pulsatile changes of diameter were determined by a newly described echotracking technique and pulse pressure was evaluated by applanation tonometry and oscillometric methods. In both territories, distensibility of hypertensive subjects was significantly reduced but compliance was reduced only at the aortic level. Diastolic diameter was increased at the carotid but not at the aortic site. Multiple regression analysis indicated that whereas compliance and distensibility were strongly influenced by BP in the terminal aorta, age was the predominant factor influencing carotid arterial stiffness. Following 30 days of converting enzyme inhibition, the decrease of BP was associated with a normalisation of aortic compliance and distensibility whereas no change was observed at the site of the carotid artery. The study provides evidence that the response of the arteries to the changes of BP differ in the various parts of the arterial tree. This factor may influence the drug effect produced by chronic converting enzyme inhibition.

Adult↗

PubMed1994

Ambulatory blood pressure profile after carotid endarterectomy in patients with ischaemic arterial disease.

OBJECTIVE: To assess the circadian blood pressure profile observed 3 months after endarterectomy. DESIGN: Twenty-five patients undergoing unilateral or bilateral carotid endarterectomy were compared with a control population of 20 patients, matched for age, sex, weight and drug therapy. Casual mean blood pressure measured by mercury sphygmomanometry was similar in both groups. RESULTS: Non-invasive ambulatory blood pressure monitoring showed that, whereas mean arterial pressure was identical in both groups, the group undergoing surgery had a significant increase in pulse pressure and its variability over 24 h. Such abnormalities predominated during the nocturnal period, in which the reduction in systolic blood pressure was less pronounced in the operated group than in controls. For all parameters there was no significant difference between subjects with unilateral or bilateral endarterectomy. CONCLUSION: This study provides evidence that patients with carotid endarterectomy were characterized in the long term by an increase in the pulsatile component of blood pressure and its variability, in association with a disturbance in the physiological circadian rhythm. Such findings were not identified using casual blood pressure measurements.

Aged↗