Biomedical subjects

M E Safar

Publications and source records attributed to M E Safar.

At least 91 records · Page 5Linked to original sources

PubMed1998

Influence of biochemical alterations on arterial stiffness in patients with end-stage renal disease.

The incremental elastic modulus of the common carotid and radial arteries is increased in patients with end-stage renal disease (ESRD), independently of blood pressure, wall stress, and the presence of atherosclerotic alterations. Whether biochemical factors may be involved in the arterial changes and related to renal dysfunction remain largely ignored. To assess this question, we measured aortic (carotid-femoral), upper-limb (carotid-radial), and lower-limb (femoral-tibial) pulse wave velocity (PWV) in 74 ESRD patients undergoing hemodialysis in comparison with 57 control subjects similar in age, sex ratio, and mean blood pressure. We evaluated arterial blood pressure by sphygmomanometry, aortic calcifications and cardiac mass by echography, and routine biochemical parameters, total plasma homocysteine, and plasma endothelin levels by standard techniques. In the population of patients with ESRD, on the basis of multiple stepwise regression analysis, aortic PWV was positively and independently correlated with systolic blood pressure (P<.0001), age (P<.0001), prevalence of aortic calcification (P=.0004), and the prevalence of diabetes mellitus (P=.0043). Upper-limb PWV was influenced exclusively by mean blood pressure (P<.0001). Lower-limb PWV was positively and independently correlated with plasma total homocysteine (P=.0004) and plasma endothelin (P=.0187) only. At any vascular site, PWV was not independently correlated with tobacco consumption; plasma levels of cholesterol, triglyceride, fibrinogen, or hemoglobin; body mass index; or the presence of bilateral nephrectomy. Finally, plasma homocysteine was independently correlated with cardiac mass (P=.0022). This study provides evidence that in ESRD patients, the stiffness of the arterial wall and cardiac mass are strongly influenced by biochemical factors related to the kidney alterations and are independent of age and blood pressure level. Increased plasma endothelin and homocysteine may be specifically involved in the vascular damage of lower limbs.

Adult↗

PubMed1998

Recent advances on large arteries in hypertension.

The most classic hemodynamic concept explaining the increased mean arterial pressure in hypertension reflects an increased total peripheral resistance dynamically and an increased wall-to-lumen ratio to suppress smaller arteries. However, a more current consideration takes into account not only that steady component but also the pulsatile component of blood pressure, a point that importantly modifies the traditional hemodynamic definition. Whereas mean arterial pressure is almost constant along the arterial tree, the pulse pressure increases markedly from the more central to the peripheral arteries, indicating that in vivo each artery should be characterized according to its own blood pressure curve. This important concept implies major modifications in the methods used to investigate the relationships between mechanical factors and large artery structure and function. It therefore seems reasonable that in hypertension the large arteries should no longer be considered as passive conduits but rather in terms of their active behavioral response to the mechanical forces to which they are subjected. New investigational aspects in hypertension therefore now involve not only genetic, cellular, and molecular mechanisms but also transductional hemodynamic mechanisms reflecting changing patterns in the extracellular matrix that influence structural remodeling of the vessels.

Animals↗

PubMed1998

Static and dynamic mechanical properties of the carotid artery from normotensive and hypertensive rats.

Several recent results obtained in hypertensive animals and subjects under in vivo isobaric conditions do not confirm the classic view of stiffer arteries in hypertensive subjects. We compared the mechanical behavior of in situ isolated common carotid arteries from normotensive Wistar-Kyoto rats (WKY) and age-matched spontaneously hypertensive rats (SHR) under both static and dynamic conditions for transmural pressure ranging from 50 to 200 mm Hg. The static pressure (P)-diameter (D) relationship was shifted to higher values of diameters in the SHR mainly because of a larger unstressed carotid diameter (Do) in hypertensive rats. The carotid mechanical strain, calculated as (D-Do)/Do, was significantly reduced in SHR at pressure levels between 100 and 200 mm Hg. The static carotid compliance and distensibility were markedly smaller in SHR than in WKY carotid arteries, indicating a stiffer wall in hypertensive animals. In contrast, carotid compliance and distensibility were similar under dynamic conditions close to the in vivo pulse pressure (frequency, 300 bpm; peak amplitude of the oscillatory pressure, 20 to 25 mm Hg). However, marked differences in dynamic compliance- and distensibility-strain relationships in SHR and WKY are evidence of clearly different arterial wall material properties in both strains. We therefore conclude that larger lumen carotid arteries in hypertensive rats could compensate for a stiffer arterial wall, resulting in similar dynamic compliance and distensibility in normotensive and hypertensive rats.

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

Determination of total effective vascular compliance in patients with sepsis syndrome.

Changes in capacitance vessels have important consequences on cardiac filling pressure and fluid volume distribution in patients with sepsis syndrome. Vascular compliance may be evaluated from the slope of the relationship between changes in total blood volume (deltaTBV) and changes in central venous pressure (deltaCVP) during acute volume expansion (450 ml of gelatin fluid over 6 min), i.e., from the deltaTBV/deltaCVP ratio. The mean ratio (ml x mm Hg-1 x kg-1) was 2.03 +/- 0.21 in control subjects, 1.43 +/- 0.25 in mechanically ventilated patients without sepsis syndrome, and 0.94 +/- 0.24 in mechanically ventilated patients with sepsis syndrome (p < 0.0001 versus the other two groups). Based on echocardiographic determinations, cardiac performance was constantly found within the normal range (cardiac output ranged from 5.6 +/- 1.2 to 6.7 +/- 2.0 L/min in nonseptic patients from 6.8 +/- 1.9 to 7.8 +/- 2.2 in septic patients). Effective compliance of the total vascular bed is therefore reduced in patients with sepsis syndrome, independently of the hemodynamic modifications due to mechanical ventilation.

Adolescent↗

PubMed1998

Plasma insulin and ankle on brachial systolic blood pressure ratio in overweight men with hypertension.

BACKGROUND: Hypertension is often associated with multiple metabolic abnormalities included in the insulin resistance syndrome. In hypertensive individuals, the ratio between ankle and brachial systolic blood pressure (ABI) is considered to be an independent cardiovascular risk factor. Insulin resistance has not been studied in relation to ABI ratio in men with essential hypertension and who are moderately overweight. OBJECTIVE: To identify whether a decrease in the ABI ratio is associated with the degree of abdominal obesity and, hence, with the biochemical characteristics of resistance to insulin. METHODS: In 166 overweight men with mild-to-moderate essential hypertension, insulinaemia was measured using radioimmunoassay. The ABI ratio was measured by using a pressure cuff of appropriate diameter, a standard mercury sphygmomanometer and a Doppler probe. Patients with diabetes or arteriosclerosis obliterans of the lower limbs, or both, were excluded from the study. RESULTS: The ABI ratio was significantly associated with the degree of abdominal obesity, but also with plasma triglycerides and cholesterol, low high-density lipoprotein cholesterol, plasma glucose and insulin. In a multiple regression analysis, the ABI ratio was significantly and negatively associated with only two variables: age and plasma insulin. This result was independent of age and drug treatment of hypertension. CONCLUSION: Because alterations in the ABI ratio may be considered markers of the changes in the structure and function of the arteries of lower limbs, the study provides evidence that plasma insulin, independently of atherosclerotic occlusive lesions, can significantly influence the status of conduit arteries of the lower limbs.

Adult↗

PubMed1998

Factors determining cardiac hypertrophy in hypertensive patients with or without peripheral vascular disease.

1. Coronary ischaemic disease and congestive heart failure are the principal causes of mortality in patients with peripheral vascular disease. Whether cardiac hypertrophy is present and even more pronounced in peripheral vascular disease than in other populations has never been explored.2.Twenty-five hypertensive patients were investigated, 11 without and 14 with peripheral vascular disease, matched for age, sex, mean arterial pressure and antihypertensive drug treatment. Cardiac mass was determined using echocardiography together with measurement of systemic blood pressure, ratio between ankle systolic pressure (ASP) and brachial systolic pressure (BSP), and standard biochemical parameters including natriuresis per 24 h.3. At the same mean arterial pressure, patients with peripheral vascular disease had a significantly higher cardiac mass (157+/-12 versus 116+/-6 g/m2; P<0.01), pulse pressure (81+/-5 versus 55+/-4 mmHg; P<0.01) and natriuresis (180+/-17 versus 144+/-6 mmol/24h; P<0. 01) than controls. Using univariate correlations, cardiac mass was positively associated with pulse pressure, mean arterial pressure and natriuresis, and negatively with the ASP/BSP ratio. On the basis of multivariate regression analysis, only natriuresis was positively correlated to cardiac mass.4. Patients with peripheral vascular disease develop a higher degree of cardiac hypertrophy in comparison with hypertensive subjects with the same level of mean arterial pressure. Sodium intake rather than mechanical factors seems to be the major modulating factor which influences the degree of cardiac hypertrophy.

Aged↗

PubMed1997

Systolic blood pressure revisited.

The clinical importance of systolic blood pressure (SBP) needs no emphasis. Its determinants are well known, but recent studies of one of these determinants, arterial distensibility, have led to results that now have clinical relevance. This review summarizes the role of arterial stiffness in ventricular-vascular coupling in the normal circulation and that disordered by aging and hypertension. The discussion defines the unfamiliar terms of compliance, distensibility and modulus and indicates how they are measured. Such measurements have increased our understanding of the parts played by the inhomogeneity of the arterial tree and reflected pressure waves in governing SBP. Elevated SBP is a recognized risk factor for cardiovascular complications among older patients, but when this elevation is due to a stiffened arterial tree, diastolic blood pressure (DBP) is necessarily reduced. Early epidemiologic studies in hypertension required a DBP > or = 90 mm Hg for hospital admission. They therefore excluded persons with high SBP, low DBP and very wide pulse pressure (PP). More recent inclusion of such patients has shown that elevation of SBP and PP is a strong predictor of cardiovascular risk. These considerations point to a possible redefinition of hypertension to include patients with lower DBP and to the inaccuracy but indispensability of the brachial artery pressure as a surrogate for aortic pressure--the pressure the heart sees. Finally, we review the known effects of available antihypertensive drugs on the arterial wall and indicate possible future directions of research stemming from wider understanding of the role of arterial distensibility in hypertension.

Antihypertensive Agents↗

PubMed1997

Association between increased plasma levels of aldosterone and decreased systemic arterial compliance in subjects with essential hypertension.

We previously observed that, in subjects with essential hypertension, acute ouabain constricts the brachial artery diameter in the presence of spironolactone treatment, a finding that is not observed in the absence of aldosterone antagonist and therefore suggests a specific effect of aldosterone on the arterial wall. To evaluate whether aldosterone excess may contribute to modulate arterial function, we investigated 56 patients with sustained essential hypertension in comparison with 36 normotensive controls. Systemic arterial compliance was measured from intraarterial blood pressure and cardiac output measurements using a classical Windkessel model to determine the elasticity of the proximal arterial tree. Radial artery compliance was determined using a previously described echo tracking technique. In hypertensive, but not in normotensive, subjects, systemic arterial compliance was strongly and negatively correlated with plasma aldosterone. The correlation was observed even after adjustment for age and blood pressure. Plasma potassium and renin activity did not interfere in the correlation. Acute administration of diltiazem did not change systemic compliance but significantly decreased plasma aldosterone, suggesting that, in the presence of calcium blockade, the same compliance was achieved for a lower plasma aldosterone level. Taken together, these findings strongly suggest that significant interactions exist between aldosterone and central conduit arteries and that aldosterone might modulate arterial function in subjects with essential hypertension.

Adult↗

PubMed1997

Non-invasive evaluation of arterial abnormalities in hypertensive patients.

ARTERIAL ABNORMALITIES IN HYPERTENSION: Morbidity and mortality in hypertension are mainly determined by arterial lesions which may occur in different regional circulations (e.g. kidney, cerebral, coronary circulations, causing nephro-angiosclerosis, stroke or myocardial infarction, respectively). Despite arterial heterogeneity, structural and functional abnormalities are usually observed at an early stage of hypertension in both large and small arteries. These alterations modify physiological and mechanical properties of the arterial wall, which may become clinically evident by increasing arterial pulsatility or pulse pressure; the alterations facilitate the establishment and progression of atherosclerosis and arteriosclerosis. METHODS OF ASSESSING ARTERIAL ABNORMALITIES: Several non-invasive techniques can be used to assess haemodynamic properties of arteries: (1) casual and ambulatory blood pressure measurements can be used to evaluate pulse pressure; (2) pulse pressure can be measured directly in different sites of the arterial tree using the Tonometer device; (3) ultrasound techniques can be applied, including Doppler signals to assess the arterial flow, video-echo signals to analyse the arterial structure such as the intimal-medial thickness and echo-tracking systems for direct measurements of arterial wall distension and thickness; (4) pulse wave velocity is widely used as index of arterial distensibility; this parameter, assessed by the Complior device, has shown that hypertensive patients have decreased arterial distensibility and that antihypertensive treatment does not always reverse this abnormality. TREATMENT: It is important to evaluate the effect of cardiovascular risk-reduction measures on the arterial wall. Large therapeutic trials are necessary to show whether an evaluation of arterial abnormalities can identify patients with a high cardiovascular risk and contribute to their treatment and prognostic improvement.

Arteries↗

PubMed1997

Sodium, survival, and the mechanical properties of the carotid artery in stroke-prone hypertensive rats.

BACKGROUND: Reduction in sodium intake improves the survival of stroke-prone spontaneously hypertensive rats (SHR-SP) without causing any change in their blood pressure. OBJECTIVE: To investigate whether the diuretic indapamide improves survival of SHR-SP and whether changes in the structure and the function of large arteries are associated with survival. EXPERIMENTAL DESIGN: Forty-eight hypertensive rats aged 6 weeks were divided into three groups: a control SHR-SP group (n = 24) and a control spontaneously hypertensive rat (SHR) group (n = 12), with 1% saline drinking water; and an indapamide-treated SHR-SP group (n = 12) with 1% saline drinking water administered 1 mg/kg per day indapamide via their food. At the end of a 12-week follow-up period, pulsatile changes in blood pressure and common carotid artery diameter (measured by high-resolution echo-tracking techniques) were determined and aortic histomorphometry was performed. RESULTS: By the end of the study 58% of the SHR-SP control group rats had died. There were no deaths in the other two groups. In these two groups the mean blood pressure (217+/-10 and 212+/-7 mmHg), carotid diameter and distensibility (0.48+/-0.09 and 0.61+/-0.22 mmHg[-1]), arterial thickness (116+/-4 and 116+/-3 microm), and collagen content of the arterial wall were identical. In the SHR-SP control group the mean blood pressure was significantly lower (168+/-9 mmHg), the carotid distensibility was higher (1.47+/-0.35 mmHg[-1]), and the arterial thickness (138+/-5 microm) and collagen content were substantially higher than those in the other two groups. In the study population as a whole, for a given mean arterial pressure the carotid distensibility was identical in the three groups, although the arterial thickness was substantially greater in the SHR-SP control group rats. CONCLUSIONS: The study provides evidence that the diuretic compound indapamide improved the survival of SRH-SP even though their blood pressure was higher than that of untreated animals, and that genetic sensitivity to sodium, rather than blood pressure, influences the changes in arterial structure.

Animals↗

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↗

PubMed1997

Arterial mechanics predict cardiovascular risk in hypertension.

Systolic and diastolic blood pressures are the exclusive mechanical factors considered as predictors of cardiovascular risk for members of populations of normotensive and hypertensive subjects. However, if hypertension is considered as a mechanical factor acting on the arterial wall with deleterious consequences, the totality of the blood pressure curve should be considered in order to investigate the risk. The purpose of this review is to show that in addition to systolic and diastolic blood pressures, other hemodynamic indexes with particular relevance for cardiac complications and that originate from pulsatile pressure should be taken into account, namely brachial pulse pressure, pulse pressure amplification, early wave reflections, and pulse wave velocity.

Adult↗

PubMed1997

Arterial stiffness in hypertensive subjects with or without end-stage renal disease.

Therapeutic trials have shown that the response to antihypertensive drug treatment is heterogeneous, with substantially higher effects of cardiovascular prevention for the cerebral than for the coronary circulation. This finding suggests that the response of large conduit arteries to elevated blood pressure may vary greatly between the different compartments of the arterial bed. Recent in vivo non-invasive studies in humans suggest that the stiffness of large arteries in subjects with essential hypertension differs greatly according to the vascular territory involved. Operational arterial stiffness, i.e., measured at the mean blood pressure of the hypertensive population by comparison with normotensive subjects, is increased in central arteries (carotid artery, aorta) but normal in peripheral muscular arteries (femoral artery, radial artery). On the other hand, when hypertensive and normotensive subjects are compared for the same blood pressure, arterial stiffness appears to be normal for the radial artery but decreased for the femoral artery and the aorta. In the case of carotid arteries, isobaric arterial stiffness is normal in subjects with uncomplicated essential hypertension but decreased in hypertensive patients with end-stage renal disease. Thus, important differences may be observed according to the territory involved, suggesting that the response to drug treatment of hypertension may be influenced not only by the blood pressure reduction itself but also by the regional properties of each particular vascular bed and the presence of advanced renal disease.

Arteries↗

PubMed1997

Role of angiotensin II and bradykinin on aortic collagen following converting enzyme inhibition in spontaneously hypertensive rats.

We previously showed that chronic angiotensin-converting enzyme (ACE) inhibition prevented the increase in aortic collagen in spontaneously hypertensive rats (SHRs) independently of blood pressure reduction. The aim of the present study was to determine whether the effects of ACE inhibition on aortic fibrosis were due to inhibition of angiotensin II formation, preservation of bradykinin, or a combination of both. Four week-old SHRs were treated for 4 months with the ACE inhibitor quinapril, quinapril with the bradykinin B2 receptor antagonist Hoe 140, or the angiotensin II AT1 receptor antagonist CI996. Control SHR and Wistar-Kyoto (WKY) rats received a placebo for the same period of time. At the end of the treatment, as compared to conscious SHR and WKY controls, quinapril completely prevented the development of hypertension, whereas quinapril-Hoe 140 and the AT1 receptor antagonist produced only a partial reduction of blood pressure. In relation with blood pressure changes, aortic hypertrophy was significantly prevented by quinapril but not by quinapril-Hoe 140 or CI996. In contrast, aortic collagen accumulation was completely prevented by all three treatments. The study provides evidence that in young live SHRs, the prevention of aortic collagen accumulation is independent of blood pressure changes and bradykinin preservation and involves exclusively angiotensin II inhibition through AT1 receptors.

Angiotensin II↗

PubMed1997

Prevention of aortic fibrosis by spironolactone in spontaneously hypertensive rats.

We have previously shown that long-term angiotensin-converting enzyme (ACE) inhibition prevents the increase in aortic collagen in spontaneously hypertensive rats (SHRs), independent of blood pressure reduction. More recently, we reported that the effects of ACE inhibition in the prevention of aortic collagen accumulation were related to the inhibition of angiotensin II actions on angiotensin II type 1 receptors. Aldosterone, the synthesis of which is mainly modulated by angiotensin II through type 1 receptor stimulation, is known to promote cardiac fibrosis in different experimental models. The aim of the present study was to determine whether inhibition of aldosterone formation was able to prevent aortic fibrosis in SHRs. For this purpose, we compared the effects of a 4-month treatment with the aldosterone antagonist spironolactone with the ACE inhibitor quinapril in 4-week-old SHRs. Control SHRs and Wistar-Kyoto (WKY) rats received placebo for the same period of time. At the end of treatment, in conscious SHRs vs WKY controls, quinapril completely prevented the development of hypertension, whereas spironolactone produced only a slight but significant reduction in blood pressure. Aortic hypertrophy was significantly prevented by ACE inhibition but not by spironolactone. On the contrary, aortic collagen accumulation was completely prevented by both quinapril and spironolactone. In the latter case, collagen density was significantly below that of WKY controls. These results show that in SHRs, spironolactone can markedly prevent aortic fibrosis in the presence of a very slight antihypertensive effect. It is suggested that ACE inhibition or type 1 receptor antagonist-induced prevention of aortic collagen accumulation is at least partially related to aldosterone inhibition.

Animals↗

PubMed1997

Mechanical stress of the carotid artery at the early phase of spontaneous hypertension in rats.

Common carotid artery (CCA) hypertrophy has long been recognized in the neonatal period of development in spontaneously hypertensive rats (SHR), but the mean circumferential and shear stresses acting on the arterial wall have never been investigated in vivo. We investigated intra-arterial blood pressure in conscious rats, CCA diameter (echotracking techniques), blood flow velocity (pulsed Doppler), wall thickness (histomorphometry), and ganglionic blockade (hexamethonium) in Wistar rats and SHR at 5 and 12 weeks of age. During this interval, weight gain was identical in the strains, whereas the increase in wall thickness and blood pressure was greater in SHR. CCA diameter was identical at week 5 and increased similarly at week 12 in both strains. During ganglionic blockade, a larger diameter was observed in SHR at week 5 for the same BP level, whereas equivalent values were observed at week 12. Blood flow velocity decreased with age but to a significantly greater extent in SHR. Mean circumferential stress and shear stress index were identical in both strains at week 12. However, from weeks 5 to 12, mean circumferential stress increased with age similarly in both strains, whereas the age-related decrease in mean shear stress index was much greater in SHR than Wistar rats. Thus, despite a higher blood pressure, SHR exhibit the same carotid diameter as Wistar rats during early development. Because the kinetics of shear stress are different in both strains, altered flow-dilatation mechanisms, and possibly resulting endothelial dysfunction, may be involved in the diameter changes.

Age Factors↗

PubMed1996

Carotid artery stiffness with applications to cardiovascular pharmacology.

1. Increased carotid stiffness is a characteristic feature of cardiovascular aging, hypertension and, to a lesser extent, atherosclerosis. 2. The pharmacological approach, using nitrates, converting enzyme inhibitors, calcium entry blockers and blockers of the autonomic nervous system, may decrease carotid stiffness through 3 different mechanism: passive decrease in blood pressure, active change in smooth muscle tone, and structural modifications of the carotid arterial wall. 3. In recent years, such changes have been studied in vivo, in both humans and rats, using original in situ carotid preparations and echotracking ultrasound techniques of high resolution, allowing to evaluate both static and dynamic stiffness. 4. This new approach for investigating arterial vessel through changes in both stiffness and thickness should provide a better evaluation of drug effects in cardiovascular pharmacology and new interpretations for cardiovascular events related to morbidity and mortality.

Aging↗