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B Pannier

Publications and source records attributed to B Pannier.

At least 37 records · Page 2Linked to original sources
PubMed1998

Assessment of the acute arterial effects of converting enzyme inhibition in essential hypertension: a double-blind, comparative and crossover study.

In subjects with essential hypertension, angiotensin-converting enzyme (ACE) inhibition increases arterial diameter, compliance and distensibility of peripheral muscular arteries in association with blood pressure reduction. Whether pulse pressure amplification is modified by ACE inhibition and whether changes in compliance and distensibility are due to a drug effect on the arterial wall, to the blood pressure reduction or to a combination of both factors, is largely ignored. In a randomised, double-blind crossover trial, we used the ACE inhibitor quinapril as a marker to evaluate the changes in: pulse pressure amplification (applanation tonometry), carotid compliance and distensibility (echo-tracking technique), and aortic distensibility (measured from pulse wave velocity). Quinapril decreased in the same extent carotid and brachial pulse pressure, thus causing a resetting of pulse pressure amplification toward normal values. Carotid compliance and distensibility as well as aortic distensibility increased significantly. Based on three-way analysis of variance, it was shown that, whereas the changes in carotid stiffness were exclusively due to blood pressure reduction and not to a drug-induced relaxation of the arterial wall, the changes in aortic distensibility were due to the combination of both factors. Thus, using an atraumatic non-invasive procedure, it was possible to show that: (i) ACE inhibition is able to maintain pulse pressure amplification, an important factor contributing to reduce the afterload of the heart; and (ii) ACE inhibition alters the hypertensive arterial wall in a very heterogeneous manner, with a maximal drug effect on muscular large arteries like the abdominal aorta, and not on elastic arteries like the carotid artery and the thoracic aorta.

Adult↗
PubMed1998

Nitric oxide synthase gene polymorphisms, blood pressure and aortic stiffness in normotensive and hypertensive subjects.

BACKGROUND: Genetic studies may help us to understand the mechanisms underlying the involvement of various neuro-humoral factors in the regulation of the mechanical properties of large arteries. We have shown previously that the angiotensin II type 1 receptor gene polymorphism was a strong determinant of aortic stiffness in hypertensives. OBJECTIVE: To assess the contribution of two polymorphisms of the endothelial nitric oxide synthase gene to aortic stiffness in normotensive and hypertensive subjects in the same cohort. METHODS: We studied 309 untreated hypertensive and 123 normotensive subjects. Aortic stiffness was evaluated by measuring the carotid-femoral pulse-wave velocity non-invasively. The endothelial nitric oxide synthase gene polymorphisms G10-T at intron 23 (GIN23T) and G298-T at exon 7 (Glu298Asp) were determined in each subject. RESULTS: The distributions of genotypes and allele prevalences of the endothelial nitric-oxide synthase G10-T polymorphisms among hypertensive and normotensive subjects were similar. In contrast, the prevalence of the nitric oxide synthase 298G allele was higher in the hypertensive group than it was among normotensive subjects. We found no association of the endothelial nitric oxide synthase genotypes with blood pressure levels or pulse-wave velocity for either population. CONCLUSIONS: The present results do not suggest that two common polymorphisms of the endothelial nitric oxide synthase gene are involved in the regulation of aortic stiffness in hypertensive and normotensive individuals. The higher prevalence of endothelial nitric oxide synthase 298G allele among hypertensives suggests that this gene is involved in essential hypertension but this observation needs further confirmation.

Adolescent↗
PubMed1998

Large artery structure and function in hypertension and end-stage renal disease.

The cardiovascular complications in hypertension are ascribed to two different but associated alterations, namely atherosclerosis and arteriosclerosis. Whereas the former disturbs principally the conduit function and the delivery of an adequate blood flow to peripheral organs and tissues, the latter disturbs the cushioning function of large arteries, inducing an inadequate increase in systolic and pulse pressure. Arteriosclerosis represents a clinical form of accelerated ageing process and is characterized by a diffuse dilation and hypertrophy of large conduit arteries and stiffening of arterial walls. Independently from the ageing, structural changes are associated with several haemodynamic alterations such as increased in blood flow and flow velocity, and increased parietal stress due to increased arterial diameters and/or intraarterial pressure. The principal consequences of arterial stiffening are: (1) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand; (2) altered coronary perfusion and blood flow distribution; and (3) decreased perfusion reserve during haemodynamic stress. In the absence of controlled studies, it is difficult to propose therapeutic interventions aimed to prevent or treat arterial abnormalities in hypertensive patients. It has been shown that long-term administration of either calcium channel blockers and angiotensin converting enzyme inhibitors led to an improvement of vessel wall elasticity. Nevertheless, these studies did not conclude whether the improvement of elastic properties were due only to decrease in blood pressure or to alterations in intrinsic properties of arterial walls. More investigations should be necessary to investigate this important problem.

Animals↗
PubMed1998

Mechanisms of the cardiovascular deconditioning induced by tail suspension in the rat.

The aim of the present work was to obtain insights into the pathophysiology of cardiovascular deconditioning (CVD) induced by tail suspension (TS) in the rat: during TS, when central venous pressure (CVP) has been normalized (E. Martel, P. Champéroux, P. Lacolley, S. Richard, M. Safar, and J. L. Cuche. J. Appl. Physiol. 80: 1390-1396, 1996), and during simulated orthostatism (SO), when transient episodes of hypotension and bradycardia are disclosed, bradycardia with SO represents a response that seems peculiar to the rat compared with humans. According to basic physiology, a reduced activity of the sympathetic system induced by increased CVP was suspected but was not supported by data obtained through spectral analysis of blood pressure (BP) and heart rate (HR) variability or measurements of plasma catecholamine concentration during TS. Nonetheless, indirect evidence was obtained. During SO, plasma catecholamine concentration was lower in TS rats than in controls, suggesting a reduced synthesis of catecholamines, itself secondary to reduced activity of the sympathetic system. Furthermore, after 48 h of TS, the number of binding sites and affinity of alpha-receptors in rat aorta were increased, compatible with a reduced level of neurotransmitter in the synaptic cleft. A second series of experiments was carried out to study hypotension and bradycardia in TS rats during SO. Hypersensitivity of serotonergic mechanisms was suspected. Two 5-HT3 receptor antagonists (ondansetron and MDL-72222) blocked hypotension and restored tachycardia, basic features of orthostatic adaptation of the circulatory system. Response to the 5-HT3 receptor agonist was measured through dose-response curves of BP and HR after injection of 2-methylserotonin. After low doses, hypotension (10 micrograms/kg) and bradycardia (3 and 10 micrograms/kg) were significantly greater in 48-h TS rats than in controls. Thus CVD in the rat induced by TS appears to implicate at least two mechanisms: reduced activity of the sympathetic system and hypersensitivity of serotonergic mechanisms.

Animals↗
PubMed1998

Carotid arterial stiffness as a predictor of cardiovascular and all-cause mortality in end-stage renal disease.

Damage of large arteries is a major contributory factor to the high pulse pressure observed in patients with end-stage renal disease. Whether incremental modulus of elasticity (Einc), a classic marker of arterial stiffness, can predict cardiovascular mortality has never been investigated. A cohort of 79 patients with end-stage renal disease undergoing hemodialysis was studied between September 1995 and January 1998. Mean age at entry was 58+/-15 years. The duration of follow-up was 25+/-7 months, during which 10 cardiovascular and 8 noncardiovascular fatal events occurred. At entry, carotid Einc was calculated from measurements of diameter, thickness (echo-tracking technique), and pulse pressure (tonometry). Based on Cox analyses, 2 dominant factors emerged as predictors of all-cause and cardiovascular mortality: increased Einc and decreased diastolic blood pressure. Lipid abnormalities and the presence of previous cardiovascular events interfered to a smaller extent. After adjustment for confounding variables, the odds ratio for Einc >/=1 kPa-3 was 9.2 (95% confidence interval, 2.4 to 35.0) for all-cause mortality. These results provide the first direct evidence that in patients with end-stage renal disease undergoing hemodialysis, arterial alterations, as determined from carotid Einc, are strong independent predictors of all-cause and cardiovascular mortality.

Aged↗
PubMed1998

Further study on the carotid baroreflex system in the cardiovascular deconditioning induced by head-down tilt.

HYPOTHESIS: The responses of the carotid baroreflex and of the peripheral sympathetic system to stimulations induced by either lower body negative pressure (LBNP -40 mmHg) or cold pressor test were investigated in eight volunteers before and after 48 h in the -6 degrees head-down tilt (HDT). METHODS: Geometry (diastolic diameter and pulsatile distention) and dynamics (cross-sectional compliance and tangential tension) of the bulb and the common carotid artery were investigated using ultrasonic devices, echotracking and aplanation tonometry. The activity of the sympathetic system was evaluated through measurements of plasma concentrations of catecholamines (CAs) and 3,4-dihydroxyphenyl glycol (DHPG). RESULTS: During LBNP -40 mmHg, the pulsed tangential tension was decreased and the pressure amplification, induced by the reflexion of the pressure wave, was increased with no difference between before and after HDT. Since cross-sectional compliance and distensibility coefficient remained unchanged and the carotid contour of the waveform unaltered, it is concluded that the carotid reflexogenic area reads the same message during LBNP whether the cardiovascular system was deconditioned or not. Nonetheless, during LBNP after 48 h HDT, the heart rate accelerated faster and CAs and DHPG concentrations increased out of proportion, suggesting that the peripheral sympathetic activity was more reactive after HDT than before. Finally, forearm vascular resistances were measured in response to cold pressor test; they increased in the same proportion after HDT when compared with before. CONCLUSION: Results indicate that the carotid baroreflex and the peripheral sympathetic system were not deficient after 48 h HDT.

Adolescent↗
PubMed1997

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

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

Adult↗
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

Cardiac and arterial interactions in end-stage renal disease.

Although cardiac hypertrophy is a frequent complication of end-stage renal disease (ESRD), relatively little is known about large arterial geometry and function in vivo in these patients, and the relationship between arterial changes and cardiac hypertrophy is unknown. Common carotid artery (CCA) intima-media thickness and internal diameter and left ventricular geometry and function were determined by ultrasound imaging in 70 uncomplicated ESRD patients and in 50 age-, sex-, and blood pressure-matched controls. Arterial distensibility and compliance were determined from simultaneously recorded CCA diameter and stroke changes in diameter and CCA pressure waveforms, obtained by applanation tonometry, and also by the measurement of carotid-femoral pulse wave velocity. Compared with control subjects, ESRD patients had greater left ventricular diameter (P < 0.01), wall thicknesses and mass (P < 0.001), increased CCA diameter (6.25 +/- 0.87 vs. 5.55 +/- 0.65 mm; P < 0.001), larger CCA intima-media thickness (777 +/- 115 vs. 678 +/- 105 microns; P < 0.001) and intima-media cross-sectional area (17.5 +/- 4.5 vs. 13.4 +/- 3.3 mm2; P < 0.001). In uremic patients, arterial hypertrophy was associated with decreased CCA distensibility (17.8 +/- 8.8 vs. 24.0 +/- 12.7 kPa-1.10(-3); P < 0.001) and compliance (5.15 +/- 2 vs. 6.0 +/- 2.5 m2.kPa-1.10(-7); P < 0.05), accelerated carotid-femoral pulse wave velocity (1055 +/- 290 vs. 957 +/- 180 cm/seconds; P < 0.001), early return and increased effect of arterial wave reflections (20.5 +/- 15.4 vs. 9.2 +/- 18.4%; P < 0.001). The latter phenomenons were responsible for increased pulsatile pressure load in CCA (58.3 +/- 21 vs. 48 +/- 17 mm Hg; P < 0.01) and were associated with a decreased subendocardial viability index (157 +/- 31 vs. 173 +/- 30%; P < 0.001). The CCA diameter was correlated with the left ventricular diameter (P < 0.01), and a significant correlations existed between CCA wall thickness or CCA intima-media cross-sectional area and left ventricular wall thicknesses and/or left ventricular mass (P < 0.01). In multivariate analysis, these relationships were independent regarding age, sex, blood pressure and body surface area. The present study documents parallel cardiac and vascular adaptation in ESRD, and demonstrates the potential contribution of structural and functional large artery alterations to the pathogenesis of left ventricular hypertrophy and functional alterations.

Adult↗
PubMed1996

Antihypertensive effects and arterial haemodynamic alterations during angiotensin converting enzyme inhibition.

OBJECTIVE: To assess the respective roles of the anti-hypertensive and blood pressure-independent effects of angiotensin converting enzyme (ACE) inhibition in the changed arterial haemodynamics observed in hypertensive patients with end-stage renal disease (ESRD) treated by haemodialysis. DESIGN AND METHODS: Twelve hypertensive patients with ESRD were included in a double-blind, cross-over study comparing a single 20 mg dose of the ACE inhibitor quinapril versus placebo. Two study periods each of 172 h duration were separated by a 2-week placebo period. Repeated measurements of the following parameters were performed: brachial artery systolic blood pressure (SBP); diastolic blood pressure and mean blood pressure (using a mercury sphygmomanometer); carotid artery SBP and pulse pressure (by applanation tonometry); aortic stiffness (by pulse wave velocity); and the effect of arterial wave reflections in the common carotid artery (the augmentation index, by applanation tonometry). A radioimmunoassay was used to determine plasma angiotensin II levels. Quinaprilat pharmacokinetics were studied using a specific assay. Two-way (time-treatment) analysis of variance for repeated measures, analysis of covariance for two within-factors and a covariate changing with the level of the factor time (pressures measured at each time) and baseline values of the studied parameter as a second covariate were used for statistical analysis. RESULTS: Quinapril treatment induced a long-lasting decrease in arterial wave reflections, which was still observable 172 h after quinapril administration and still present after removing the effect of the decrease in blood pressure. The effect on wave reflections was associated with a more pronounced and sustained decrease in carotid SBP and pulse pressure than that in brachial SBP and pulse pressure. Quinapril administration also induced a long-lasting decrease in aortic pulse wave velocity, but this effect was entirely dependent on parallel changes in blood pressure. Arterial haemodynamic changes were not related to plasma angiotensin II or quinaprilat levels. CONCLUSIONS: The results of this controlled study indicate that, in ESRD patients, ACE inhibition results in a long-lasting, blood pressure-independent decrease in arterial wave reflections. The consequence of this was a decrease in pulsatile pressure load in the central arteries with increased aortic distensibility. The increased aortic distensibility resulted from the decrease in blood pressure. The observed arterial haemodynamic alterations suggest that ACE inhibition induced alterations in arterial wave reflections in the distal parts of the arterial tree.

Adult↗
PubMed1995

Carotid arterial hemodynamics in response to LBNP in normal subjects: methodological aspects.

Pulsatile changes in blood pressure and arterial diameter were studied noninvasively with applanation tonometry and echo-tracking techniques at the sites of the common carotid artery (CCA) and the carotid arterial bulb (CAB) in 12 healthy volunteers. Determinations were performed before and during application of -10 and -40 mmHg lower body negative pressure (LBNP) to investigate noninvasively the tensile forces acting on the CAB. Together with significantly decreased mean arterial pressure, increased heart rate, forearm vascular resistance, and plasma norepinephrine, the -40 mmHg LBNP stimulus produced the following significant changes in CCA and CAB hemodynamics: 1) for the same decrease in mean arterial pressure, a greater decrease in carotid than in brachial pulse pressure was observed (P < 0.01) due to a significant change in pressure wave transmission and in the timing of the carotid backward pressure wave; and 2) a highly significant decrease in pulsatile changes in diameter and tangential tension occurred, with a greater decrease in systolic than in diastolic tangential tension. Subsequently, cyclic tangential tension decreased more substantially than mean tangential tension. The cyclic changes in tension were quite significant after -40 mmHg LBNP but were already observed for mild -10 mmHg LBNP in which mean systemic blood pressure and heart rate were not modified. During -10 and -40 mmHg LBNP, CCA and CAB compliance and distensibility were unchanged. This study provides evidence that the autonomic nervous system activation produced by the LBNP procedure is associated with significant changes in pressure-wave amplification and in cyclic tensile forces acting on the CAB. These changes, which may occur even for mild LBNP, should be taken into account when interpreting results of the LBNP procedure in humans.

Adult↗
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

Influence of sex on arterial hemodynamics and blood pressure. Role of body height.

Systolic pressure is lower in premenopausal women than in age-matched men, but underlying alterations are not well characterized. Aging and body size alter arterial function, influencing pressure wave propagation and amplification in peripheral and central arteries. To assess the possibility that systolic pressure differences in women are related to smaller body size, we studied arterial function in 119 men and 104 women. Premenopausal and postmenopausal women were compared with age-matched men. The following parameters were measured: ankle-arm pressure index (Doppler), aortic and arterial distensibility (pulse wave velocity), systolic pressure and the effect and time delay of arterial wave reflections in the common carotid artery (applanation tonometry), and diameters of the abdominal aorta and aortic bifurcation and their ratio (aortic tapering, echography). Premenopausal women had lower brachial (P < .05) and ankle (P < .01) systolic pressures than age-matched men, whereas the ankle-arm pressure index was higher in men (P < .01). In the overall population the ankle-arm index was positively correlated with body height (P < .001). Carotid systolic pressure was similar in women and men, with an increased effect and earlier return of wave reflections in women (P < .01). The effect of wave reflections was inversely correlated with body height (P < .001) and positively associated with aortic tapering (P < .001), which was increased in women (P < .01). In premenopausal women the distensibility of brachial and femoral arteries was higher than in age-matched men (P < .01), whereas aortic distensibility was not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Cardiac hypertrophy, aortic compliance, peripheral resistance, and wave reflection in end-stage renal disease. Comparative effects of ACE inhibition and calcium channel blockade.

BACKGROUND: We wished to assess the respective roles of the antihypertensive and blood pressure (BP)-independent effects of antihypertensive drugs on arterial hemodynamics and left ventricular hypertrophy (LVH) in end-stage renal disease (ESRD) patients. METHODS AND RESULTS: In a double-blind study, 24 ESRD patients with LVH were randomized to 12 months' administration of either the angiotensin-converting enzyme (ACE) inhibitor perindopril (n = 14) or the calcium channel blocker nitrendipine (n = 10). Repeated measurements of the following parameters were performed: BP (mercury sphygmomanometry), left ventricular mass (LVM, echocardiography), cardiac output (aortic cross-section and velocity integral), total peripheral resistance (cardiac output and mean BP), aortic and large-artery compliance (pulse wave velocity, Doppler flowmeter), and arterial wave reflections (augmentation index, applanation tonometry). Radioimmunoassay was used to determine plasma renin activity, aldosterone, and plasma catecholamine levels. Two-way (time-treatment) ANOVA for repeated measures was used for statistical analysis. Perindopril and nitrendipine induced significant and similar decreases in BP, total peripheral resistance (P < .001), aortic and arterial pulse wave velocities (P < .001), and arterial wave reflections (P < .01). At baseline, the two groups had LVH mostly due to increased LV end-diastolic diameter (LVEDD) (perindopril, 54.3 +/- 1.4 and nitrendipine, 54.3 +/ 2.4 mm) with near-normal mean LV wall thickness (perindopril, 11.4 +/- 0.3 and nitrendipine, 11.2 +/- 0.4 mm). A decrease in LVM was observed only in patients receiving perindopril (from 317 +/- 18 to 247 +/- 21 g) (time-treatment interaction, P = .036). Nitrendipine had no significant effect on LVM (314 +/- 29 versus 286 +/- 32 g). The decrease in LVM observed with perindopril was associated with a reduction in LVEDD (49.9 +/- 1.6 versus 54.3 +/- 1.4 mm after 12 months) (time-treatment interaction, P = .04), while the mean LV wall thickness was unchanged (11.4 +/- 0.3 versus 10.5 +/- 0.5 mm). Cardiac alterations were not correlated with changes in BP or with alterations in plasma renin activity or aldosterone or catecholamine levels. CONCLUSIONS: In ESRD patients with LVH, ACE inhibition decreases LVM independently of its antihypertensive effect and of associated alterations in arterial hemodynamics. The decrease in LVM was due primarily to a decrease in LV volume, which may have resulted in these patients from chronic volume overload.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Arterial compliance and blood pressure.

As a result of the dual function of arteries, the conduit and cushioning functions, arterial pressure has 2 components: the steady component, characterised by mean blood pressure, and the pulsatile component, characterised by pulse pressure. Arterial compliance mostly depends on arterial intrinsic elastic properties, and is a determinant of the propagation speed of the pulse pressure wave. Decreased arterial compliance is responsible for both an increase in the incident pressure wave and the higher effect of reflected pressure waves. This increases systolic pressure and ventricular afterload, and generates left ventricular hypertrophy. Arterial structural changes that accompany the aging process result in a loss of distensibility and compliance. In essential as well as in secondary hypertension, arterial compliance is reduced, and age-related structural changes of the arterial wall are accelerated. Whether the change in arterial compliance is a passive consequence of the increase in blood pressure or is related to changes in the arterial wall structure remains unclear. Calcium antagonists improve the distensibility and compliance of large and small arteries, contributing significantly to the improvement in the management of essential and secondary hypertension.

Animals↗
PubMed1993

Hypocaloric diet and antihypertensive drug treatment. A randomized controlled clinical trial.

OBJECTIVE: To compare the amount of drug quantified by a score needed to control blood pressure in two groups of overweight hypertensive patients, receiving or not receiving a hypocaloric diet. DESIGN: Randomized controlled clinical trial. SETTING: Two hospital outpatient hypertension clinics. PATIENTS: Fifty-four subjects with a DBP between 95 and 110 mmHg and a weight > or = 110% of the ideal weight. INTERVENTION: Allocation to either drug treatment (DT) or hypocaloric diet (HD). In the HD group, after 2 months, an antihypertensive drug was administered to the subjects with a DBP > or = 90 mmHg, following the same scheme protocol as in the DT group. Subjects were followed during 10 months by a clinician only in the DT group and by a clinician and a dietician in the HD group. MAIN OUTCOME MEASURES: Score of treatment: hydrochlorothiazide 25 mg [score = 1] with, as needed to obtain a DBP < 90 mmHg, the addiction of enalapril 10 mg [score = 2], 20 mg [score = 3], and nifedipine 40 mg [score = 4]. RESULTS: At the end of the trial, 5 subjects were lost to follow-up in the HD group and 1 in the DT group (p > 0.05). Mean weight loss was 5.9 kg (sd = 1.2) in the HD and 2.3 kg (sd = 0.7) in the DT group (p = 0.02). Mean decrease in DBP was 18 mmHg (sd = 7) and 15 mmHg (sd = 8) in HD and DT groups respectively (p = 0.36). Mean DBP was 84 mmHg (sd = 7.8) in the HD group and 85 mmHg (sd = 7.2) in the DT group. In the HD group, 8 (38.1%) subjects had a DBP < 90 mmHg without any drug treatment. The mean drug treatment score was 0.86 (sd = 0.91) in the HD and 1.52 (0.70) in the DT group (p = 0.01). CONCLUSION: This study shows that in overweight hypertensives, the quantity of drug needed to achieve an acceptable level of BP is nearly reduced by 50% when an efficient hypocaloric diet is prescribed simultaneously.

Adult↗
PubMed1993

Cardiac hypertrophy and arterial alterations in end-stage renal disease: hemodynamic factors.

Left ventricular (LV) hypertrophy is the most common cardiovascular alteration observed in end-stage renal disease patients. LV hypertrophy results from chronic flow and pressure overload and combines features of concentric and eccentric hypertrophy. The causes of chronic flow overload are the presence of AV shunt, salt and water overload, and anemia. The pressure overload is related to alterations of physical properties of large arteries characterized by an increased arterial and aortic stiffness. The systolic function of hypertrophied ventricle is preserved, but the diastolic filling is impaired. The ventricular hypertrophy progresses over the time on hemodialysis together with a progressive worsening of both systolic and diastolic functions.

Arteries↗