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Biomedical subjects

A Benetos

Publications and source records attributed to A Benetos.

At least 37 records · Page 2Linked to original sources
PubMed2001

Telomere length as an indicator of biological aging: the gender effect and relation with pulse pressure and pulse wave velocity.

Chronological age is the primary determinant of stiffness of central arteries. Increased stiffness is an independent indicator of cardiovascular risk. The aim of this study was to determine whether telomere length, a possible index of biological aging, provides a better account than chronological age for variation in arterial stiffness, evaluated by measuring pulse pressure and aortic pulse wave velocity. The study population included 193 French subjects (120 men, 73 women), with a mean age of 56+/-11 years, who were not on any antihypertensive medications. Telomere length was evaluated in white blood cells by measuring the mean length of the terminal restriction fragments. Age-adjusted telomere length was longer in women than in men (8.67+/-0.09 versus 8.37+/-0.07 kb; P=0.016). In both genders, telomere length was inversely correlated with age (P<0.01). Multivariate analysis showed that in men, but not in women, telomere length significantly contributed to pulse pressure and pulse wave velocity variations. In conclusion, telomere length provides an additional account to chronological age of variations in both pulse pressure and pulse wave velocity among men, such that men with shorter telomere length are more likely to exhibit high pulse pressure and pulse wave velocity, which are indices of large artery stiffness. The longer telomere length in women suggests that for a given chronological age, biological aging of men is more advanced than that of women.

Age Factors↗
PubMed2001

Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients.

Although various studies reported that pulse pressure, an indirect index of arterial stiffening, was an independent risk factor for mortality, a direct relationship between arterial stiffness and all-cause and cardiovascular mortality remained to be established in patients with essential hypertension. A cohort of 1980 essential hypertensive patients who attended the outpatient hypertension clinic of Broussais Hospital between 1980 and 1996 and who had a measurement of arterial stiffness was studied. At entry, aortic stiffness was assessed from the measurement of carotid-femoral pulse-wave velocity (PWV). A logistic regression model was used to estimate the relative risk of all-cause and cardiovascular deaths. Selection of classic risk factors for adjustment of PWV was based on their influence on mortality in this cohort in univariate analysis. Mean age at entry was 50+/-13 years (mean+/-SD). During an average follow-up of 112+/-53 months, 107 fatal events occurred. Among them, 46 were of cardiovascular origin. PWV was significantly associated with all-cause and cardiovascular mortality in a univariate model of logistic regression analysis (odds ratio for 5 m/s PWV was 2.14 [95% confidence interval, 1.71 to 2.67, P<0.0001] and 2.35 [95% confidence interval, 1.76 to 3.14, P<0.0001], respectively). In multivariate models of logistic regression analysis, PWV was significantly associated with all-cause and cardiovascular mortality, independent of previous cardiovascular diseases, age, and diabetes. By contrast, pulse pressure was not significantly and independently associated to mortality. This study provides the first direct evidence that aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in patients with essential hypertension.

Adult↗
PubMed2001

Cardiovascular mortality in hypertensive men according to presence of associated risk factors.

To evaluate the risk of cardiovascular disease (CVD) mortality in hypertensive men according to the presence of associated risk factors (ARFs). The population was composed of 29 640 normotensive men without ARFs (reference group) and 60 343 hypertensive men (with and without ARFs) who had a standard health checkup at the Centre d'Investigations Préventives et Cliniques between 1978 and 1988. Mortality data for a mean period of 14 years were analyzed. The following ARFs were considered: total cholesterol >/=2.5 g/L, personal history of diabetes, smoking (current smokers), body mass index >28 kg/m(2), and heart rate >80 bpm. CVD risk related to the presence of isolated hypertension (assessed in hypertensive subjects without ARFs versus the reference group) increased linearly from 15% at the age of 30 years to 134% at the age of 80 years. In hypertensive subjects, one additional ARF increased CVD risk by 56% (47% to 65%, P<0.01) in younger subjects but only by 4% (-8% to 17%, P=NS) in older subjects. The role of hypercholesterolemia and tobacco smoking in CVD mortality was significantly higher in hypertensive subjects aged <55 years than in hypertensive subjects aged >/=55 years (P<0.01), whereas the roles of tachycardia and obesity were not affected by age. In younger hypertensive subjects, evaluation of CVD risk and therapeutic strategies should target ARFS: In older subjects, the presence of high blood pressure levels seems to be the major determinant of CVD risk.

Adult↗
PubMed2001

Effects of valsartan on mechanical properties of the carotid artery in spontaneously hypertensive rats under high-salt diet.

The aim of this investigation was to evaluate the influence of a high-salt diet (HSD) on the effects of valsartan, an angiotensin II type 1 (AT(1)) receptor antagonist, on carotid arterial stiffness and structure in spontaneous hypertensive rats (SHR). Carotid arterial stiffness was studied in SHR receiving a HSD or a normal-salt diet (NSD) from the 10th to 20th week of age. Within each of the 2 groups, the animals received treatment with either placebo or valsartan (30 mg. kg(-1). d(-1)) administered on the 4th to 20th week of age. Arterial pressure, wall stress, incremental elastic modulus (Einc), medial cross-sectional area, and EIIIA fibronectin isoform were significantly increased in placebo-HSD rats compared with placebo-NSD rats with no change in the ratio of collagen to elastin. Valsartan reduced mean arterial pressure in both NSD and HSD rats but reduced pulse pressure only in NSD rats. In NSD rats, valsartan reduced Einc and medial cross-sectional area. In HSD, valsartan increased Einc and did not modify medial cross-sectional area and fibronectin. In valsartan-treated rats, the ratio of collagen to elastin was greater in HSD than in NSD rats. In conclusion, the effects of AT(1) blockade are greatly influenced by salt intake in SHR. Despite a reduction in mean arterial pressure in HSD rats, AT(1) blockade was not able to prevent the effects of a HSD on pulse pressure, carotid artery stiffness, and hypertrophy.

Animals↗
PubMed2001

Aortic pulse wave velocity predicts cardiovascular mortality in subjects >70 years of age.

Aortic pulse wave velocity (PWV) is a significant and independent predictor of cardiovascular mortality in subjects with essential hypertension and in patients with end-stage renal disease. Its contribution to cardiovascular risk in subjects 70 to 100 years old has never been tested. A cohort of 141 subjects (mean+/-SD age, 87.1+/-6.6 years) was studied in 3 geriatrics departments in a Paris suburb. Together with sphygmomanometric blood pressure measurements, aortic PWV was measured with a validated automatic device. During the 30-month follow-up, 56 patients died (27 from cardiovascular events). Logistic regressions indicated that age (P=0.005) and a loss of autonomy (P=0.01) were the best predictors of overall mortality. For cardiovascular mortality, aortic PWV was the major risk predictor (P=0.016). The odds ratio was 1.19 (95% confidence interval, 1.03 to 1.37). Antihypertensive drug treatment and blood pressure, including systolic and pulse pressure, had no additive role. In subjects 70 to 100 years old, aortic PWV is a strong, independent predictor of cardiovascular death, whereas systolic or pulse pressure was not. This prospective result will need to be confirmed in an intervention trial.

Aged↗
PubMed2000

A decrease in diastolic blood pressure combined with an increase in systolic blood pressure is associated with a higher cardiovascular mortality in men.

OBJECTIVES: The study evaluated the risk of cardiovascular mortality according to combined spontaneous (non-treatment-related) changes in both systolic and diastolic blood pressure (BP). BACKGROUND: Long-term longitudinal changes in blood pressure may be a more accurate determinant of cardiovascular risk since changes in systolic or diastolic blood pressure over a period of time reflect the evolution of arterial and arteriolar alterations. METHODS: Two independent French male cohorts were studied: the IPC cohort (Investigations Préventives et Cliniques) composed of 15,561 men aged 20 to 82 years who had had two visits spaced four to 10 years apart, and the Paris Prospective Study composed of 6,246 men aged 42 to 53 years, examined annually for a period of four years. None of the subjects were taking antihypertensive medication. Annual changes in BP were estimated, and subjects were divided into groups according to the increase, lack of change, or decrease of systolic or diastolic BP. Nine groups were formed by combining the changes of systolic and diastolic BP. Cardiovascular mortality was assessed for a mean period of 13.5 years for the IPC Study and 17 years for the Paris Prospective Study. RESULTS: In both cohorts, after adjustment for age and major risk factors, the group with an increase in systolic and a decrease in diastolic BP presented the highest relative risk of cardiovascular mortality compared to the group with no changes in either systolic or diastolic BP (relative risk: 2.07 [1.05 to 4.06] in the IPC Study and 2.16 [1.16 to 4.01] in the Paris Prospective Study). CONCLUSIONS: Assessment of spontaneous changes of BP over a long period of time can contribute to the evaluation of cardiovascular risk. Subjects whose systolic BP increased while their diastolic BP decreased had the highest cardiovascular risk independently of absolute values of BP or other risk factors.

Adult↗
PubMed2000

Pressure-independent contribution of sodium to large artery structure and function in hypertension.

BACKGROUND: Sodium sensitivity is usually studied in terms of change of blood pressure (BP) but the specific effects on conduit arteries have not been addressed. EXPERIMENTAL STUDIES: In genetic models of hypertension, chronically increased sodium diet is associated with aortic hypertrophy and development of extracellular matrix independent of BP. These alterations, often associated with increased stiffness and secretory properties of vascular smooth muscle, are reversed by lowering sodium intake and/or giving diuretics, independently of BP changes. The arterial changes are chronically modulated by hormonal counterregulatory mechanisms since, when sodium intake is high, bradykinin blockade produces more carotid hypertrophy, and when sodium intake is normal, less aortic collagen accumulates because of AT(1)-receptor blockade. CLINICAL STUDIES: In longitudinal studies on hypertensive subjects, increased sodium intake not only increases BP but also decreases brachial artery diameter, implying pressure-independent mechanisms acting on the arterial wall. The antihypertensive effect of diuretics is associated with little change of arterial geometry and stiffness, probably resulting from marked angiotensin-induced increase of arterial stiffness. This latter effect is blocked by converting-enzyme inhibition. All these arterial changes may be genetically modulated since in salt-sensitive hypertensives, increased sodium intake is associated with decreased arterial distensibility, and in some hypertensive subjects, a polymorphism of the AT(1)-receptor gene has been described in association with increased aortic stiffness and is reversed by converting-enzyme inhibition independent of BP. CONCLUSION: In genetic models of human and rat hypertension, increased sodium intake is associated with specific alterations of the structure and function of conduit arteries involving extracellular matrix, but independent of BP and atherosclerosis.

Aged↗
PubMed2000

Association between 24-hour ambulatory heart rate and arterial stiffness.

Clinical and experimental studies point to a positive association between carotid-femoral pulse wave velocity (PWVcf) and casual heart rate. However, an association with 24-h ambulatory heart rate has never been investigated. Twenty-four hour ambulatory heart rate and PWVcf (automatic computerised technique) were simultaneously measured in 213 subjects with untreated mild-to-moderate essential hypertension. It was found that mean ambulatory heart rate was higher in women than in men but the difference reached statistical significance only in those below 50 years of age during night-time measurements. As well as age and blood pressure, 24-h ambulatory heart rate was also an independent factor influencing PWVcf. Independent of gender, the relationship between PWVcf and ambulatory heart rate was stronger in patients over 50 years of age. Casual heart rate was not a significant determinant of PWVcf in this population. In conclusion, ambulatory heart rate contribution to explain pulse wave velocity is more important than casual heart rate. The relationship between 24-h heart rate and pulse wave velocity is stronger for subjects older than 50 years of age independent of gender.

Adolescent↗
PubMed2000

Efficacy, safety, and effects on quality of life of bisoprolol/hydrochlorothiazide versus amlodipine in elderly patients with systolic hypertension.

BACKGROUND: Several studies have shown the benefits of antihypertensive treatment in elderly patients in terms of cardiovascular morbidity and mortality rate reduction. Low-dose drug combinations may be of interest in treating older subjects. A randomized, multicenter, double-blind, parallel group study was conducted to compare the efficacy and safety of bisoprolol 2.5 mg/hydrochlorothiazide 6.25 mg (n = 84) to amlodipine 5 mg (n = 80) in isolated systolic hypertension in patients older than 60 years. METHODS: After a 2- to 4-week placebo washout period, both drugs were administered once daily and taken for 12 weeks. Blood pressure was measured 24 hours after treatment administration. RESULTS: Systolic and diastolic blood pressure changes from baseline to week 12 were similar for both the bisoprolol and amlodipine groups (-20. 0/-4.5 mm Hg and -19.6/-2.4 mm Hg, respectively). Overall adverse events for bisoprolol and amlodipine were 39% and 40%, respectively. Changes in quality of life scores were +2.5 for bisoprolol and +3.2 for amlodipine, with a positive change indicating improvement. CONCLUSIONS: This study demonstrates comparable efficacy and tolerability of bisoprolol 2.5 mg/hydrochlorothiazide 6.25 mg and amlodipine 5 mg. The low-dose combination of bisoprolol and hydrochlorothiazide may be an appropriate alternative for elderly patients with systolic hypertension.

Adrenergic beta-Antagonists↗
PubMed2000

How can hypertensive patients be better treated? The contribution of combination therapy.

Recent studies demonstrated that target blood pressure (BP) in treated hypertensive patients should be below 140 mmHg for systolic blood pressure (SBP) and below 90 mmHg for diastolic blood pressure (DBP). However, population studies from several countries have demonstrated that in clinical practice the proportion of controlled hypertensive patients is less than 30%. In order to elucidate these questions in France we analysed a large population of 145,000 subjects examined at the Centre d'Investigations Préventives et Cliniques in Paris (IPC). Among those with high BP at the time of their IPC visit, only 20% received an antihypertensive treatment. Among those receiving an antihypertensive treatment, less than 27% (24% in men and 30% in women) presented with BP values less than 140 mmHg for SBP and less than 90 mmHg for DBP. This analysis also showed that 72% of hypertensive patients presented with at least one modifiable associated cardiovascular risk factor and that more than 30% of hypertensive men and more than 25% of hypertensive women presented with at least two associated risk factors. The use of combination therapies could help to increase the percentage of well-controlled hypertensive subjects. It has been shown that in order to reach this BP level, combination therapy should be used in more than two-thirds of the treated subjects. The trandolapril-verapamil combination is the first fixed combination of an angiotensin-converting enzyme inhibitor and a non-dihydropyridine calcium-channel blocker. Administered once daily, this combination reduces BP more than a classic monotherapy. The effects of the trandolapril-verapamil combination on risk factors are either neutral (metabolic parameters), or even beneficial (reduction in heart rate).

Adolescent↗
PubMed1999

Arterial structural changes with verapamil in spontaneously hypertensive rats.

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

Animals↗
PubMed1999

Determinants of left ventricular mass in a French male population.

The aim of this analysis was to study the determinants of left ventricular mass evaluated by echocardiography. A total of 843 healthy men aged 47-61 years, who had a standard health check-up at the Centre d'Investigations Preventives et Cliniques (IPC Center), were included in the study. None of the subjects were being treated for cardiovascular disease at the time of their visit and each had a standard clinical and biological examination. The answers to a lifestyle questionnaire, weight at 20 years and family history were recorded. All subjects had an echocardiogram to evaluate left ventricular mass. Left ventricular mass values were adjusted for height using the ratio of left ventricular mass to height. Current body mass index, systolic and diastolic blood pressure, brachial circumference, triglycerides and a family history of sudden death were positively associated with this ratio (p < 0.01). Physical activity and tobacco consumption were associated with left ventricular mass. Body mass index at 20 years, variation of body mass index since that age, systolic blood pressure and family history of sudden death explain 21% of the ratio of left ventricular mass/height (body mass index at 20 years: 11.8%; variation of body mass index: 5.1%; systolic blood pressure: 2.3%; and family history of sudden death: 0.4%). The other factors explain only 1.4% of this variance and were not significantly associated with the ratio of left ventricular mass to height. Body mass index at 20 years was the strongest determinant of left ventricular mass, suggesting that left ventricular mass at middle age is in large measure determined much earlier in life. A family history of sudden death before the age of 60 years is also an important determinant of left ventricular mass, independent of obesity. These factors must be taken into account in order to prevent an increase in left ventricular mass.

Age Factors↗
PubMed1999

Associations between heart rate and other risk factors in a large French population.

OBJECTIVES: In a large general French population of 100,000 subjects, the relationship of resting heart rate with age, gender, demographic parameters, physical activity and classical risk factors was evaluated. POPULATION AND METHODS: A population composed of all the subjects who had a free health check-up at the IPC Centre between 1992 and 1995 (62,353 men and 35,371 women) was analysed. Heart rate was considered either as a continuous parameter or as a qualitative parameter. The study population was divided into four heart rate classes: < 65, 65-74, 75-84 and > or = 85 beats/min. RESULTS: Women had significantly higher heart rate values than men, and this gender difference was constant in the different age groups. In both genders, heart rate was positively associated with blood pressure, triglycerides, glycaemia and physical inactivity, and negatively with body height Heart rate was also correlated with total cholesterol but only in men. The only factor having opposite effects on heart rate in men and women was tobacco smoking (positive in men and negative in women). Among untreated hypertensive men, 21.3% had a heart rate > or = 85 beats/min compared with only 4.0% among normotensive men. In women, these percentages were 23.6 and 7.6%, respectively. Subjects with untreated mild hypertension or uncontrolled treated hypertension also showed increased rates of tachycardia compared to normotensives. CONCLUSIONS: The present analysis, performed in a large French population, shows that high heart rate is associated with several other risk factors, especially hypertension, suggesting that tachycardic subjects have a high risk profile.

Adult↗
PubMed1999

Influence of heart rate on mortality in a French population: role of age, gender, and blood pressure.

-The aim of the present study was to assess the effects of high heart rate on mortality in different subgroups in a French population according to age, gender, and blood pressure levels. We studied 19 386 subjects (12 123 men, 7263 women), aged 40 to 69 years, who had a routine health examination at the Centre d'Investigations Préventives et Cliniques (IPC) between 1974 and 1977. Heart rate (HR) measured by ECG was classified into 4 groups: HR1, <60; HR2, 60 to 80; HR3, 81 to 100; and HR4, >100 bpm. Mortality data were recorded for the period of 1974 through 1994. In both sexes, HR was a significant predictor of noncardiovascular mortality. In men, the relative risk (95% confidence interval) for cardiovascular death after adjustment for age and other risk factors in the HR2, HR3, and HR4 groups was 1.35 (1.01 to 1.80), 1.44 (1.04 to 2.00), and 2.18 (1.37 to 3.47), respectively, when compared with HR1. In women, HR did not influence cardiovascular mortality. The association of HR with cardiovascular mortality in men was (1) related to a strong association with coronary but not cerebrovascular mortality, (2) independent of age and hypertension, and (3) influenced by the level of pulse pressure; in patients with high pulse pressure (>65 mm Hg), accelerated HR was not associated with increased cardiovascular mortality. In conclusion, in a large French population, accelerated resting HR represents an independent predictor of noncardiovascular mortality in both genders, and of cardiovascular mortality in men, independent of age and the presence of hypertension. Further investigations are needed to explain the complex interactions between HR, pulse pressure, and cardiovascular complications.

Adult↗
PubMed1999

Genotype-phenotype relationships for the renin-angiotensin-aldosterone system in a normal population.

The renin-angiotensin-aldosterone system plays an important role in blood pressure regulation by influencing salt-water homeostasis and vascular tone. The purpose of the present study was to search for associations of single nucleotide polymorphisms on 3 major candidate genes of this system with the plasma concentrations of the corresponding renin-angiotensin-aldosterone system components considered as quantitative phenotypes. Genotyping was performed in 114 normotensive subjects for different variants of the angiotensinogen (AGT) gene (C-532T, G-6A, M235T), the angiotensin I-converting enzyme (ACE) gene [4656(CT)(2/3)], the aldosterone synthase (CYP11B2), and the type 1 angiotensin II receptor (AT1R) gene (A1166C) by hybridization with allele-specific oligonucleotides (ASO) or enzymatic digestion of polymerase chain reaction products. Plasma levels of AGT, ACE, angiotensin II (Ang II), aldosterone, and immunoreactive active renin were measured according to standard techniques. Platelet binding sites for Ang II were analyzed by the binding of radioiodinated Ang II to purified platelets. B(max) and K(D) values of the Ang II binding sites on platelets of each individual were calculated to examine a possible relationship between these parameters and the AT1R genotype. A highly significant association of the ACE 4656(CT)(2/3) variant with plasma ACE levels was observed (P<0.0001). ANOVA showed a significant effect of the AGT C-532T polymorphism on AGT plasma levels (P=0.017), but no significant effect was detectable with the other AGT polymorphisms tested, such as the G-6A or the M235T. A significant effect association was also found between the C-344T polymorphism of the CYP11B2 gene and plasma aldosterone levels, with the T allele associated with higher levels (P=0.02). No genotype effect of the AT1R A1166C polymorphism was detected either on the B(max) or the K(D) value of the Ang II receptors on platelets.

Adult↗
PubMed1999

Changes in arterial structure and function under trandolapril-verapamil combination in hypertension.

BACKGROUND AND PURPOSE: Converting enzyme inhibition and calcium blockade alter large arteries in hypertension. However, the heterogeneity of the response according to the site of cardiovascular measurements has never been investigated. METHODS: In a double-blind study, we compared for 180 days 3 hypertensive patient groups treated with verapamil, trandolapril, or their combination. Using echo-Doppler technique and applanation tonometry, we independently measured mean pressure, local pulse pressure, arterial diameter, and distensibility at 3 arterial sites (brachial and common carotid arteries and abdominal aorta), as well as cardiac and carotid wall structure. RESULTS: Mean and pulse pressure decreased significantly to a greater extent with the drug combination. Regarding arterial and cardiac hemodynamics, significant and similar changes were noted in the 3 groups: decreases in abdominal aorta and carotid but not brachial diameter; increases in carotid artery, abdominal aorta, and brachial distensibility even after adjustment to mean blood pressure reduction; and more substantial regression of cardiac mass than carotid wall thickness. CONCLUSIONS: This study shows that both compounds and more significantly combination therapy decreased mean and pulse pressures measured independently and that the changes in diameter, thickness, and stiffness were influenced primarily by the site of cardiovascular measurements, resulting in a predominant increase in distensibility of muscular arteries, little change in carotid wall thickness, but a significant regression of cardiac hypertrophy.

Adult↗
PubMed1999

[Rigidity of large arteries and cardiovascular risk. epidemiological aspects and genetic determinants].

Most of the morbid events due to hypertension and other risk factors are related to alterations of the large arteries of the brain, the heart or the kidney. Historically large arteries have been considered as passive conduits of blood, and physicians, surgeons and pathologists were mainly interested on their anatomical lesions such as rupture, stenosis, aneurysm, or thrombosis. However we know that large arteries are not passive conduit tubes but are characterized by elastic properties and are able to synthesize many vasoactive substances. These properties make the arterial wall a major modulator of the blood pressure and more generally of the cardiovascular regulation. Aging, environmental and genetic factors are responsible for structural and functional changes of the arterial wall media (hypertrophy, extracellular matrix accumulation, calcium deposits) and of the vascular endothelium (decrease in the release of vasodilators and increased synthesis of vasoconstrictors), all that leading to a diminution of elasticity and increased stiffness. The alteration of large arteries elasticity has deleterious effects on the heart upstream being responsible for an inadequate increase in systolic pressure and a relative decrease in aortic diastolic pressure at any given value of mean arterial pressure. The elevation in systolic pressure causes a disproportionate increase in end-systolic stress, which is the principal hemodynamic factor which promotes the development of cardiac hypertrophy, increased ventricular oxygen consumption, and left ventricular hypertrophy and can compromise capacity for coronary perfusion. Clinical and epidemiological studies have raised the possibility that subjects with stiffer arteries have wide pulse pressure, and that stiffening of large arteries is associated with excess morbidity and mortality independently of mean blood pressure. In addition to its etiologic role in cardiovascular disease, increased arterial stiffness may serve as an early marker for the diagnosis of asymptomatic atherosclerotic lesions, or for the evaluation of the severity of these lesions. In this review we report data from clinical, epidemiological and genetic studies, suggesting that arterial stiffness may be considered as a significant marker and/or an independent cardiovascular risk factor. This new concept should lead physicians to evaluate arterial stiffness for the prognosis and treatment of cardiovascular patients.

Aldosterone↗