Stiffness of the common carotid artery in treated hypertensive patients.

Antihypertensive treatment, by lowering blood pressure and correcting functional and/or structural abnormalities of the arterial wall, may prevent the arterial damage due to the accelerated ageing process. The objective of the present study was to determine, using a cross-sectional approach, whether arterial distensibility of patients whose blood pressure had been normalized for several months by antihypertensive treatment, was significantly higher than that of untreated hypertensive patients. The properties of the vessel wall of the common carotid artery (CCA) were studied non-invasively, using an original pulsed ultrasound echo-tracking system based on Doppler shift, during a study comparing 46 normotensive subjects and 81 age-matched hypertensive patients. The latter group included 25 patients well controlled by antihypertensive treatment for at least 3 months and 56 untreated hypertensives. The three groups did not differ with respect to age, total and high-density lipoprotein cholesterol, blood glucose and smoking. In each group, there were significant relationships between age and CCA dimensional and functional data, including end-diastolic diameter, absolute and relative stroke changes in diameter and Peterson modulus, indicating a widening of the CCA with advancing age and a decrease in its buffering function. When compared with untreated hypertensives, well controlled hypertensives had significantly lower blood pressure and Peterson elastic modulus according to age. However, although blood pressure of well controlled hypertensives was not significantly different from that of normotensive subjects, their arterial distensibility remained altered compared with that of normotensive subjects (significant increase in Peterson elastic modulus). These results suggest that long-term antihypertensive treatment may not fully reverse arterial lesions due to the hypertensive disease.     

Acute reduction of blood pressure by nitroglycerin does not normalize large artery stiffness in essential hypertension

Stiffness of large elastic arteries is elevated in subjects with hypertension, an effect that could potentially be explained by increased distending pressure. We examined effects of an acute change in blood pressure on carotid-femoral pulse wave velocity and carotid artery distensibility (inversely related to stiffness) in normotensive control subjects (n=20, mean age 42) with mean arterial pressure (MAP) 84+/-1.7 mm Hg (mean+/-SE) and subjects with essential hypertension (n=20, mean age 45, MAP 104+/-2.0 mm Hg). Normotensive subjects received intravenous nitroglycerin (NTG) and angiotensin II to lower/increase blood pressure. Hypertensive subjects received NTG to lower blood pressure. Pulse wave velocity was 24% (95% CI: 12% to 35%) higher and carotid distensibility 47% (95% CI: 32% to 63%) lower in hypertensive subjects compared with controls. In normotensive subjects, acute changes in blood pressure produced expected changes in stiffness. However, in hypertensive subjects, despite reducing MAP by 22 mm Hg to the same level as in normotensive subjects, there was no detectable reduction in arterial stiffness: pulse wave velocity remained 24% (95% CI: 10% to 38%) higher and carotid distensibility 48% (95% CI: 31% to 63%) lower in hypertensive compared with normotensive subjects. Because blood pressure-independent effects of NTG are, if anything, to reduce stiffness, these results indicate that elevated carotid and aortic stiffness in hypertensive subjects is not explained by elevated blood pressure but relates to structural change in the arterial wall.     

Ascending aorta distensibility abnormalities in hypertensive patients and response to nifedipine administration.

PURPOSE: The purpose of the present investigation was to study the distensibility of the ascending aorta in patients with arterial hypertension and normal subjects before and after administration of a calcium antagonist, nifedipine. PATIENTS AND METHODS: The distensibility of the ascending aorta was measured before and after nifedipine administration in 22 male hypertensive patients and 12 age-matched male normotensive subjects. Aortic distensibility was calculated as a function of changes in aortic diameter and pulse pressure, using the formula: 2 x (pulsatile change in aortic diameter)/[(diastolic aortic diameter) x (aortic pulse pressure)]. Aortic diameters were measured by echocardiography and aortic pressures were obtained by catheterization of the ascending aorta. RESULTS: In the basal state, the distensibility of the ascending aorta and aortic strain were lower in hypertensive patients than in normotensive subjects (p < 0.001); the lower aortic distensibility, however, was associated with a greater distending pressure. A good inverse correlation (r = -0.81) was found between mean aortic pressure and aortic distensibility. The aortic distensibility was increased after nifedipine administration in both groups; this increase in aortic distensibility, however, was lower in the patients with hypertension compared with normotensive subjects (p < 0.001). CONCLUSIONS: Aortic distensibility is decreased in patients with arterial hypertension. Nifedipine administration increased the distensibility of the ascending aorta both in patients with arterial hypertension and in normotensive subjects. The increase of aortic distensibility after nifedipine administration was lower in hypertensive patients.     

Clinical Implications of White Coat Hypertension

Objective: To determine the clinical implications of mild white coat hypertension (WCH).

Subjects and methods: We studied 102 subjects (54 men, 48 women). 51 of whom were normotensive and 51 slightly hypertensive. None had ever received antihypertensive therapy. An ambulatory blood pressure (ABP) record (Accutracker II), a 24-h electrocardiogram and an echocardiogram were obtained from each, and each was examined by funduscopy. WCH subjects were compared with sustained hypertension (SH) subjects and with normotensives.

Results: Fifty-three percent of the hypertensives qualified as WCH. The ultrasonographic characteristics and the ABP variables of the WCH group differed significantly from those of normotensives, but not from those of the SH group. The prevalence of left ventricilar hypertrophy (LVH) in the SH group (62.5%) did not differ significantly from its prevalence in the WCH group (40.7%). but the prevalence among normotensives (17.6%) was significantly lower than in either of the other two groups. The WCH and SH groups did not differ significantly as regards the prevalence of hypertensive retinopathy (33.3%) in the former, 58.3% in the latter). For no non-LVH, nonretinopathic subject, whether norniotensive or hypertensive, were more than 18% of daytime diastolic ABP measurements ≥90mmHg. Ultrasonographic findings were no better correlated with ABP than with in-clinic BP measurements. Fundus findings correlated well with in-clinic BP and with numerous ABP parameters. Retinopathy, with or without LVH, was efficiently predictable among hypertensives on the basis of body mass index and the 24-h maximum of systolic BP.

Conclusions: Myocardiac remodelling and vascular retinopathy develop early and in parallel in hypertensives, and both developments appear to involve determinants including body mass index and 24-h maximum systolic BP. WCH subjects, as defined by current ABP-based criteria, have cardiac and retinovascular Characteristics different to normotensive subjects. Stricter criteria are needed to discriminate between hypertensives with and without the systemic developments that constitute the immediate source of risk to the hypertensive individual.     

Blood pressure normalization is associated with normal left ventricular mass but not carotid geometry: the ICARe Dicomano Study

OBJECTIVE: While many studies have examined the relation between antihypertensive treatment and ventricular hypertrophy, relatively few data are available regarding changes in arterial structure due to blood pressure reduction. Therefore, we compared normotensive to untreated hypertensive subjects to uncontrolled (treated with elevated blood pressure values) or controlled (treated with normal blood pressure values) hypertensive older subjects. PATIENTS: Community-dwellers (age >or= 65 years) of a small town in Italy (Dicomano) underwent extensive clinical examination, echocardiography, carotid ultrasonography, and applanation tonometry. Of the 614 participants, 173 subjects were normotensive; among the hypertensive subjects, 225 were untreated (51%), 177 (40%) were uncontrolled, and only 39 (9%) were controlled. RESULTS: The majority of treated hypertensive subjects were on monotherapy (82%). Subjects with a history of coronary artery disease or stroke were more frequently treated. Controlled hypertensives had left ventricular mass index similar to normotensives but lower than uncontrolled and untreated hypertensives. There were no differences among the three hypertensive groups in carotid artery structure. Only the pressure-independent stiffness index was reduced in the treated hypertensive subjects compared to untreated hypertensives, with no difference between controlled and uncontrolled subjects. CONCLUSIONS: In our community-based, older population, antihypertensive treatment was associated with a normal left ventricular mass only when blood pressure was well controlled. In contrast, carotid artery remodeling and atherosclerosis were independent of antihypertensive treatment as well as of achievement of satisfactory blood pressure control. However, antihypertensive treatment was associated with significantly higher carotid compliance even in the absence of detectable changes in carotid structure.     

Persistent remodeling of resistance arteries in type 2 diabetic patients on antihypertensive treatment

We hypothesized that resistance arteries from diabetic patients with controlled hypertension have less remodeling than vessels from untreated hypertensive subjects. Eight normotensive subjects (aged 44+/-3 years, 3 men; values are mean+/-SEM), 19 untreated hypertensive subjects (46+/-2 years, 9 men), and 23 hypertensive subjects with type 2 diabetes mellitus under antihypertensive treatment (58+/-1 years, 15 men) were studied. Resistance arteries dissected from gluteal subcutaneous tissue were assessed on a pressurized myograph. Most diabetic patients (70%) were being treated with angiotensin-converting enzyme inhibitors. Although systolic blood pressure was still above the normotensive range in these patients (144+/-2 versus 150+/-3 mm Hg in hypertensive and 114+/-4 mm Hg in normotensive subjects), diastolic blood pressure was well controlled (83+/-2 mm Hg) and significantly lower compared with that in untreated hypertensives (100+/-1 mm Hg; P<0.001) but higher than in normotensives (76+/-3 mm Hg; P<0.05). Thus, pulse pressure was higher in diabetic patients (P<0.05). The media-to-lumen ratio of resistance arteries was greater in hypertensives (0.083+/-0.002) compared with normotensive controls (0.059+/-0.003; P<0.05) and was even higher in diabetic hypertensive subjects (0.105+/-0.004; P<0.001 versus normotensive controls). The medial cross-sectional area was greater in diabetic and hypertensive patients compared with normotensive controls (P<0.001). Acetylcholine-induced relaxation was impaired in vessels from hypertensive patients and from patients with both diabetes mellitus and hypertension (P<0.05 versus normotensive controls), whereas endothelium-independent vasorelaxation was similar in all groups. Despite effective antihypertensive treatment, resistance arteries from hypertensive diabetic patients showed marked remodeling, greater than that of vessels from untreated, nondiabetic, hypertensive subjects, in agreement with the high cardiovascular risk of subjects suffering from both diabetes and hypertension.     

Effect of smoking on blood viscosity and arterial rigidity in normal and hypertensive subjects

The purpose of the study was to assess whether cigarettes smoking could induce blood hyperviscosity and arterial rigidity in 30 normotensive and 70 hypertensive men aged from 24 to 65 years. Of those, 20 normotensive and 20 hypertensive were cigarettes smokers, while the remaining subjects were non smokers. Age and weight were similar in the 4 groups of subjects. A couette viscometer with coaxial cylinders allowed the measurements of blood viscosity over a wide range of shear rates (0.033 to 241 sec-1) mimicking the flow condition of the circulation, and two strain gauge transducers permitted the measurements of the brachial to radial pulse wave velocity as an index of arterial wall distensibility. In normotensive subjects cigarettes smoking increased pulse wave velocity from 7.1 + 1 to 9.2 + 0.6 m/sec. (P less than 0.05) as well as blood viscosity, which increased both at higher shear rates (+10% from 52 to 241 sec-1, P less than 0.05) and lower shear rates (+20% from 11.2 to 0.2 sec-1, P less than 0.02). In hypertensives, cigarettes smoking increased pulse wave velocity (9.8 + 0.3 to 11.3 + 0.4; P less than 0.05) and blood viscosity (4% at higher shear rate P less than 0.05 and 10% at lower shear rates P less than 0.02). Although hypertensive patients had increased pulse wave velocity and blood viscosity compared to normotensive controls, these variables were not significantly different when hypertensive non smokers were compared to normotensive. The present study demonstrated that cigarettes smoking produced in normotensive and hypertensive men significant rheological disturbances of flow and wall arteries.2     

Increased skin capillary density in treated essential hypertensive patients

BACKGROUND: Microvascular rarefaction is a hallmark of essential hypertension. We measured the skin capillary density in nondiabetic hypertensive subjects with effective antihypertensive treatment and evaluated possible correlations with arterial blood pressure (BP). METHODS: This cross-sectional observational study included 76 (55 +/- 1 years) consecutive outpatients with essential hypertension under chronic antihypertensive drug treatment (BP < 140/90 mm Hg), 24 age- and sex-matched patients with recently discovered and never-treated hypertension and 70 normotensive (BP < 140/90 mm Hg) age- and sex-matched healthy controls. We used intravital video-microscopy to measure basal and maximal (during venous congestion) skin capillary densities in the dorsum of the fingers. Aortic stiffness was evaluated using pulse wave velocity and central aortic pressure calculated from radial artery applanation tonometry. RESULTS: Baseline and maximal capillary densities (number/mm2) were significantly lower (59.6 +/- 2.0 and 62.0 +/- 1.9) in untreated than in treated hypertensive patients (74.0 +/- 1.4 and 79.4 +/- 1.5; P < .001) and than in normotensives (68.2 +/- 1.5 and 72.4 +/- 1.5; P < .001). Based on multiple regression analysis, after adjustment to tobacco consumption, aortic (and not brachial) systolic BP was inversely correlated with basal and postocclusive capillary densities in normotensive subjects. In hypertensives, this correlation disappears and capillary density was influenced by two independent variables, antihypertensive drug treatment and overweight. CONCLUSIONS: In nondiabetic hypertensive patients, capillary density is reduced in association with a cluster of cardiovascular risk factors involving tobacco consumption and obesity. The finding of an increased capillary density in effectively treated antihypertensives suggests that a cause-to-effect relationship between BP and capillary density should be evaluated in a long-term prospective follow-up.     

Pulse wave velocity as an index of arterial stiffness: a comparison between newly diagnosed (untreated) hypertensive and normotensive middle-aged Malay men and its relationship with fasting insulin

BACKGROUND: Arterial stiffness, an aging process which is accelerated by hypertension, is emerging as a useful index of vascular health. There are evidences to suggest that hyperinsulinaemia may be an independent risk factor for coronary artery disease, besides its possible pathogenic role in essential hypertension. The main objectives of this study were to compare arterial stiffness between untreated hypertensives and normotensives and to investigate the relationship between fasting serum insulin and arterial stiffness. METHODS: A cross-sectional observational study was designed. Forty normotensive (median age 47 +/- 6 yrs.) and twenty untreated hypertensive Malay men (median age 50 +/- 7 yrs.) without clinical evidence of cardiovascular complications were selected. Pulse wave velocity measured using the automated Complior machine was used as an index of arterial stiffness. Other measurements obtained were blood pressure, body mass index, fasting insulin, cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, glucose and creatinine level. RESULTS: The blood pressure and pulse wave velocity (PWV) were significantly higher in the hypertensives compared to the normotensives (blood pressure 169/100 mm Hg +/- 14/7 vs. 120/80 mm Hg +/- 10/4, p < 0.001; PWV 11.69 m/s +/- 1.12 vs. 8.83 m/s +/- 1.35, p < 0.001). Other variables such as body mass index, fasting insulin, cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides and haematocrit were comparable among the two groups. Within each group, there was a significant positive correlation between pulse wave velocity and systolic blood pressure (r = 0.76, p < 0.001 in normotensives; r = 0.73, p < 0.001 in hypertensives) and mean arterial pressure (r = 0.74, p < 0.001 in normotensives; r = 0.73, p < 0.001 in hypertensives). No correlation was noted between pulse wave velocity and diastolic blood pressure, age, body mass index, fasting insulin level, cholesterol, HDL-cholesterol, LDL-cholesterol or triglyceride levels. CONCLUSION: Arterial stiffness as determined by PWV is increased in newly diagnosed untreated hypertensive subjects even before clinically evident cardiovascular disease. However, arterial stiffness is not correlated with the fasting insulin level in normotensives and newly diagnosed hypertensives.     

Left ventricular filling in treated essential hypertension. A study using Doppler echocardiography

The first stigmata of left ventricular involvement in hypertension are changes in diastolic filling. Early detection of these abnormalities is important as some antihypertensive agents may have beneficial effects on left ventricular distensibility and filling, in addition to lowering the blood pressure. This study compares parameters of left ventricular filling recorded by pulsed Doppler echocardiography in 44 treated hypertensives (average blood pressure: 157 +/- 20/93 +/- 12 mmHg) without any other coronary risk factors with 33 age-matched (52 +/- 13 years and 48 +/- 13 years) control normotensive subjects (average blood pressure: 130 +/- 11/80 +/- 7 mmHg). The main findings were an increase of the peak. A wave velocity after atrial contraction and of the A/E ratio in the hypertensive group (66 +/- 16 cm/s vs 53 +/- 14 cm/s, p less than 0.05 and 0.99 +/- 0.34 vs 0.78 +/- 0.24, p less than 0.05, respectively). These changes were more pronounced in patients with left ventricular hypertrophy. The rapid filling phase was unchanged (maximum E wave velocity = 68 +/- 18 cm/s vs 70 +/- 14 cm/s). The influence of age on peak A wave velocity and A/E ratio was obvious in control subjects and hypertensives without left ventricular hypertrophy r = 0.80; p less than 0.05). The age factor was not significant in the presence of left ventricular hypertrophy (r = 0.18). A weak linear correlation was observed between the peak A wave velocity, diastolic septal thickness (r = 0.44; p = 0.04) and left ventricular mass (r = 0.44; p = 0.05) in hypertensive patients with left ventricular hypertrophy.     

Racial differences in aortic stiffness in normotensive and hypertensive adults.

OBJECTIVE: To investigate whether differences exist in the mechanical properties of large arteries between white and black subjects. DESIGN: Eighty-two white (49 normotensive and 33 untreated hypertensive) and 38 black (24 normotensive and 14 untreated hypertensive) adult male volunteers were studied in a cross-sectional study. METHODS: Carotid-femoral pulse wave velocity was measured as an index of arterial stiffness, using a recently developed non-invasive automatic device, and compared between white and black subjects before and after the adjustment for age. The slope of regressions for pulse wave velocity and systolic blood pressure were also compared between racial groups. RESULTS: In the normotensive group, white subjects presented higher mean values of pulse wave velocity than blacks while the opposite behavior was found in the hypertensive group. After adjustment for age, significant differences in pulse wave velocity between whites and blacks became evident in the normotensive (whites 8.15 +/- 0.04 versus blacks 7.75 +/- 0.02 m/s; P < 0.001) and hypertensive (whites 8.88 +/- 0.02 versus blacks 9.30 +/- 0.17 m/s; P < 0.001) groups. Linear regression analysis for age-adjusted pulse wave velocity and systolic blood pressure showed that the slope was significantly greater in blacks than in whites (0.040 +/- 0.002 versus 0.019 +/- 0.001 m/s; P < 0.001). CONCLUSION: These data indicate that there is a greater pressure-dependent increase in aortic stiffness in blacks than in whites. This finding points towards major differences in mechanical properties of large arteries between these racial groups.     

Arterial stiffness and kidney function

The vascular hallmark of subjects with end-stage renal disease undergoing hemodialysis is increased aortic stiffness, a phenomenon independent of mean arterial blood pressure, wall stress, and standard cardiovascular risk factors such as plasma glucose, cholesterol, obesity, and smoking. These observations suggest that subtle links might associate arterial stiffness and kidney function in normotensive and hypertensive populations. Recently, aortic pulse wave velocity and creatinine clearance have been shown to be statistically associated in subjects with plasma creatinine < or =130 micromol/L, again independently of mean arterial blood pressure and classical cardiovascular risk factors. This association was even shown to predominate in subjects younger than age 55 years. In addition, acceleration of aortic pulse wave velocity with age was more important in these subjects than in untreated normotensive control individuals, and the phenomenon was consistently predicted by baseline plasma creatinine values. Among all antihypertensive drugs, angiotensin-converting enzyme inhibitors only were shown to exhibit a significant and independent effect on aortic stiffness. The use of these drugs was significantly associated with improvement of large aortic stiffness in subjects treated for hypertension. In conclusion, increased stiffness of central arteries is independently associated with reduced creatinine clearance in subjects with mild to severe renal insufficiency, indicating that kidney diseases may interact not only with small but also with large conduit arteries, independently of age, blood pressure level, and classical cardiovascular risk factors. Whether sodium, divalent ionic species (calcium, phosphates), and the renin-angiotensin-aldosterone system play a role in such alterations remains to be elucidated.     

Assessment of arterial distensibility in patients with cardiac syndrome X

This study aims to investigate arterial distensibility by using carotid-femoral (aortic) pulse wave velocity measurements in patients with cardiac syndrome X. The authors studied 10 patients with cardiac syndrome X (mean age 49.4 +/-7.5, 39 to 67 years old, 3 men) and 10 healthy subjects (mean age 50.0 +/-10.5, 38 to 70 years old, 3 men). Carotid-femoral pulse wave velocity measured by a Complior Colson device was calculated for each patient. The carotid-femoral pulse wave velocity was increased in patients with cardiac syndrome X as compared with age-matched control subjects (10.25 +/-1.28 vs 8.95 +/-0.89 m/s, p = 0.01). In contrast, there were no significant differences in the age, weight, height, body mass index, waist/hip ratio, systolic blood pressure, diastolic blood pressure, mean blood pressure, pulse pressure, and heart rate (p=0.76,p=0.17,p=0.36,p=0.08, p=0.21,p=0.14,p=0.89,p=0.30,p=0.10, p = 0.36, respectively). No significant correlation was found between pulse wave velocity and age, sex, height, weight, heart rate, systolic blood pressure, diastolic blood pressure, mean blood pressure, and pulse pressure in the studied groups (p>0.05). The arterial distensibility was decreased in patients with cardiac syndrome X. The deterioration in these patients showed that this disease might be a more generalized disturbance of the vasculature. Measurements of carotid-femoral pulse wave velocity may provide a simple and noninvasive technique to identify patients at increased risk of vascular disease.     

From 'optimal' to 'borderline' blood pressure in subjects under chronic antihypertensive therapy

OBJECTIVES: The ESH2003 report (J Hypertens 2003, 21:1011-1053) has classified brachial blood pressure into six groups reflecting the consistently increasing cardiovascular risk caused by high blood pressure. Chronically treated hypertensive individuals with well-controlled blood pressure retain higher cardiovascular risk than normotensive untreated individuals. Differences between these groups in arterial stiffness, pressure wave reflections and central blood pressure, which are all predictors of cardiovascular risk independently of peripheral blood pressure, have never been studied. METHODS: A cohort of 216 treated subjects with controlled hypertension was compared with 105 never-treated normotensive controls, according to the ESH2003 blood pressure groups. Aortic stiffness (pulse wave velocity; PWV), carotid wave reflections (augmentation index; AI) and carotid pressures were measured non-invasively, by pulse wave analysis. Systolic blood pressure (SBP) and pulse pressure (PP) amplification between brachial and carotid arteries were estimated. RESULTS: The distribution of subjects in each subgroup of the untreated and treated populations was: 'optimal', 21 versus 43; 'normal', 44 versus 77; 'borderline', 40 versus 96. Brachial blood pressure, carotid SBP and PP did not differ between the two populations, but a constant interaction between blood pressure classification and treatment effect on PWV, AI and blood pressure amplification was found. Compared with untreated subjects, treated subjects had higher AI and lower blood pressure amplification (in the optimal group) and higher PWV (in the borderline group). CONCLUSION: 'Optimal' to 'borderline' blood pressure control in chronically treated hypertensive individuals is associated with impaired properties of the large and small arteries. These results suggest that antihypertensive treatment strategies with more beneficial effects on arterial properties are needed.     

Central Aortic Stiffness is Increased in Patients With Heart Failure and Preserved Ejection Fraction

BackgroundHypertension is an important risk factor for the development of heart failure with preserved ejection fraction. Although heart failure in hypertensive patients is usually ascribed to intrinsic myocardial abnormalities, noncardiac factors may contribute.Methods and ResultsUsing arterial tonometry and Doppler echocardiography, we assessed arterial stiffness and cardiac diastolic function in 53 individuals with ejection fraction >=0.50, including 23 with hypertension but no heart failure, 16 with hypertension and heart failure, and 14 healthy, normotensive controls. Relative to healthy controls and hypertensives, subjects with heart failure had higher systolic blood pressure, body mass index, creatinine, and left ventricular mass. Diastolic function, as estimated by myocardial relaxation velocity, was not different among the 3 groups. Peripheral arterial stiffness was similar across all groups, but key measures of central aortic stiffness (carotid-femoral pulse wave velocity, characteristic impedance, forward wave amplitude) steadily increased with progression from healthy to hypertensive to heart failure despite adjustment for body mass index, systolic blood pressure, and renal function and were positively correlated with both left ventricular mass and filling pressure.ConclusionsWe conclude that patients with heart failure and preserved ejection fraction have increased central aortic stiffness relative to age-matched healthy and hypertensive subjects without heart failure. These changes exceed differences in diastolic function and suggest that abnormal ventricular-vascular coupling may contribute to the pathophysiology of heart failure with preserved ejection fraction.     

Arterial stiffness assessed by pulse wave analysis in essential hypertension: relation to 24-h blood pressure profile

BACKGROUND: Arterial stiffness is a risk factor for cardiovascular morbidity and mortality and appears to be increased in arterial hypertension. The purpose of the present study was to relate systemic arterial stiffness assessed by pulse wave analysis to variables of 24-h ambulatory blood pressure monitoring (ABPM) in patients with essential hypertension. METHODS: Seventy-two subjects with untreated mild to moderate arterial hypertension underwent evaluation with 24-h ambulatory blood pressure monitoring. In the same subjects, applanation tonometry and pulse wave analysis was performed for evaluation of systemic arterial stiffness expressed as augmentation index and estimated aortic pulse wave velocity. RESULTS: Clinic systolic blood pressure, mean heart rate during 24-h blood pressure monitoring and height were independent predictors of augmentation index and estimated aortic pulse wave velocity. The 41 patients with blunted reduction in nighttime blood pressure (nondippers) showed higher mean systolic blood pressure (p=0.02), lower systolic and diastolic blood pressure variability (p<0.001), higher pulse pressure during 24-h monitoring (p=0.05) and higher estimated aortic pulse wave velocity (p=0.03), indicating stiffer arteries in this group. CONCLUSIONS: These results suggest that blood pressure change from day- to nighttime is an important determinant of arterial stiffness assessed by pulse wave analysis; this association could contribute to the higher cardiovascular risk in nondippers.     

Indirect, noninvasive evaluation of pressure wave transmission in essential hypertension

Blood pressure, carotid-femoral and brachioradial pulse wave velocities were measured in 123 male subjects: 32 normal subjects and 91 age-matched patients with sustained essential hypertension. The ratio between brachioradial (BR) and carotid-femoral (CF) pulse wave velocities was used as a marker of pressure wave amplitude changes from the aorta to the brachial artery. The ratio was similar in normotensive and hypertensive subjects and decreased with age to the same extent in both populations. In older subjects, the decrease in the ratio indicated that the amplitude of pulse pressure was quite similar in the aorta and the brachial artery whether the subjects were normotensives or hypertensives. The study provided evidence that adaptive changes occur in the arterial (aortic) wall in hypertension, for the effects of age on pressure wave transmission are similar in normal subjects and hypertensive patients. Such findings may be of prime importance in understanding the brachial blood pressure readings of patients with hypertension.     

Continuous improvement of arterial compliance beyond blood pressure decrease after 5 years of antihypertensive treatment

Pulse wave velocity is a reliable marker of arterial compliance. Stiffness of large and elastic arteries leads to a faster propagation of pulse wave. The aim of this study was to evaluate changes in arterial distensibility using antihypertensive drugs. This treatment focused on the inhibition of the renin-angiotensin-aldosterone system and the changes produced in blood pressure. Measurements were taken at baseline and throughout 60 months in 66 previously untreated hypertensive patients (22 men and 44 women, aged 54 +/- 9.5 years, range 38-73 years at baseline). All patients received either angiotensin-converting enzyme inhibitors or, in case of adverse effects, angiotensin receptor blockers. To control blood pressure, diuretics, calcium channel blocking agents, or beta blockers were added when appropriate. Statistical analysis was performed by means of ANOVA with alpha = 0.05. Systolic and diastolic blood pressure decreased during the first year without significant changes thereafter. There were no significant changes in pulse pressure. Pulse wave velocity showed a continuous and significant decrease throughout the follow-up period, but its reduction since the third year was more evident than the decrease in systolic and diastolic blood pressure (p < 0.0001 for both). This observation could be related to changes in arterial remodeling probably due to angiotensin-converting enzyme inhibition or renin angiotensin system blockade. Further investigations are needed to establish this relationship.     

Efficacy of various antihypertensive agents as evaluated by indices of vascular stiffness in elderly hypertensive patients.

When observed in elderly hypertensive patients, increased pulse pressure (PP) and arterial stiffness are known to be independent risk factors for cardiovascular diseases. Increased systolic blood pressure (SBP) leads to left ventricular hypertrophy, while decreased diastolic blood pressure (DBP) results in decreased coronary circulation. It is known that increased arterial stiffness is the major cause of increased PP. Thus basic morbid states of cardiac failure or ischemic heart diseases are more likely to develop in elderly hypertensive patients with increased PP and arterial stiffness, and there is need of antihypertensive drugs that decrease these effects in elderly hypertensives. In this study, we compared the effects of an angiotensin-receptor blocker (ARB: valsartan), an angiotensin-converting enzyme inhibitor (ACE-I: temocapril), and long-acting Ca antagonists (L- and N-type Ca channel blocker: cilnidipine; and L-type Ca channel blocker: nifedipine CR) on PP and arterial stiffness measured by pulse wave velocity in elderly hypertensive patients for 3 months. The ARB yielded the largest reductions in PP and brachial-ankle pulse wave velocity (baPWV), followed by the ACE-I and L- and N-type Ca channel blocker, while the L-type Ca channel blocker yielded no improvement. The effects on arterial stiffness and PP thus varied among the drug characteristics. Although ARB achieved the largest reduction in baPWV, this decrease was not associated with any reductions in PP, SBP, DBP, or mean blood pressure, as were the baPWV-decreases achieved by the other drugs, suggesting that ARB may further reduce the risk of arteriosclerosis in elderly hypertensive patients by decreasing arterial stiffness in addition to its antihypertensive effect.     

高血压不同部位大动脉缓冲功能不均一性的临床研究

目的：研究正常人和高血压患者不同部位动脉缓冲功能的变化。方法：对１２０例正常人和２０５例原发性高血压患者应用动脉搏波速度（Ｐｕｌｓｅ ｗａｖｅ ｖｅｌｏｃｉｔｙＰＷＶ）测定仪进行检测。颈动脉－股动脉ＰＷＶ（ＣＦＰＷＶ）、肱动脉－找动脉ＰＷＶ（ＢＲＰＷＶ）和股动脉－足背动脉ＰＷＶ（ＦＴＰＷＶ）分别为反映大动脉和中等动脉扩张性（Ｄｉｓｔｅｎｓｉｂｉｌｉｔｙ）的参数。并能敏感反映动脉缓冲功能的改变。结果：无论正常人还是高血压患者,ＣＦＰＷＶ与年龄和收缩压成正相关关系（Ｐ均小于０．００１）,而ＢＲＰＷＶ和ＦＴＰＷＶ并不随年龄和收缩压的改变而改变。结论：正常人和高血压患者不同部位动脉节段的缓冲功能发生不同的变化,大动脉扩张性降低,中等动脉无明显变化。对大动脉缓冲功能变化的早期检测和有效治疗具有重要的临床价值。