C-reactive protein and arterial stiffness in older adults: the Rotterdam Study

Arterial stiffness is one of the characteristics of vascular aging. Increases in pulse pressure, which reflect an increase in the stiffness of the large arteries, are associated with elevated C-reactive protein (CRP) levels. This may suggest a role of inflammation in the development of arterial stiffness. We investigated the relation between measures of arterial stiffness and CRP within the framework of the Rotterdam Study, a population-based cohort study including subjects aged 55 years and older. The carotid-femoral pulse wave velocity and the distensibility coefficient of the carotid artery were used as measures of arterial stiffness. Data on both arterial stiffness and CRP were available for 866 participants. In adjusted models, levels of CRP were linearly associated with pulse wave velocity (regression coefficient 0.088, 95% CI 0.006-0.170). Adjusted mean values of pulse wave velocity were significantly different across tertiles of CRP, being higher in the highest tertile of CRP. However, no significant association between CRP and carotid distensibility was observed.     

Aortic Distensibility in Normotensive, Untreated and Treated Hypertensive Patients

Background: Compared with normotensive subjects, untreated hypertensive patients show a decrease of their aortic distensibility. Whether antihypertensive treatment, by reducing blood pressure and changing functional and/or structural abnormalities of the arterial wall, may prevent or reverse the arterial damage due to the accelerated ageing process remains unclear. The objective of the present study was to determine, using a cross-sectional approach, whether aortic distensibility as measured by pulse wave velocity, in treated hypertensive patients whose diastolic blood pressure had been normalised for several months, was significantly improved over that of untreated hypertensive patients.

Methods: Carotid femoral pulse wave velocity was measured in 124 normotensive subjects and 388 hypertensive patients. The latter group included 164 treated patients with well controlled diastolic blood pressure and 224 untreated hypertensive subjects. The three groups did not differ in other cardiovascular risk factors.

Results: In each group there was a significant relationship between age and pulse wave velocity. When compared with untreated hypertensives, treated hypertensives with well controlled diastolic blood pressure had significantly lower blood pressure and pulse wave velocity according to age. However, although diastolic blood pressure of well controlled hypertensives was not significantly different from that of normotensive subjects, the aortic distensibility of the controlled hypertensives remained reduced showing two characteristics: a faster increase in pulse wave velocity with age and a negative relationship with HDL-cholesterol.

Conclusion: These results suggest that long-term antihypertensive treatment and control of blood pressure using only diastolic blood pressure criteria may not fully reverse arterial alteration associated with hypertensive vascular disease.     

Arterial stiffness, cardiovagal baroreflex sensitivity and postural blood pressure changes in older adults: the Rotterdam Study

OBJECTIVE: Arterial stiffness may be involved in the impairment of the arterial baroreflex. In the present study the associations between arterial stiffness and cardiovagal baroreflex sensitivity (BRS) and between BRS and postural blood pressure (BP) changes were investigated within the framework of the Rotterdam Study. METHODS: Arterial stiffness was determined by aortic pulse wave velocity and the carotid distensibility coefficient. Continuous recording of the R-R interval and finger BP was performed with the subject resting supine, and BRS was estimated from the spontaneous changes in systolic BP and corresponding interbeat intervals. Measures of aortic stiffness or carotid distensibility and BRS were available in 2490 and 2083 subjects, respectively. The association between arterial stiffness and ln BRS was investigated by multivariate linear regression analysis and then by analysis of covariance, comparing BRS by quartiles of arterial stiffness. RESULTS: The mean age of the subjects was 71.7 +/- 6.6 (41.7% men). Aortic stiffness was negatively associated [beta = -0.029; 95% confidence interval (CI): -0.040, -0.019] and the carotid distensibility coefficient positively associated with BRS (beta = 0.017; 95% CI: 0.010, 0.024). An orthostatic decrease in systolic BP was absent in 1609 subjects, between 1 and 10 mmHg in 502 and >10 mmHg in 269 subjects, with corresponding mean values (95% CI) of ln BRS of 1.47 (1.44-1.51), 1.43 (1.37-1.49) and 1.36 (1.28-1.44) ms/mmHg (test for trend P < 0.019). An orthostatic decrease in diastolic BP was absent in 1123 subjects, 1-10 mmHg in 1057 and >10 mmHg in 209 subjects, with corresponding mean values of ln BRS of 1.49 (1.45-1.53), 1.41 (1.37-1.45) and 1.45 (1.36-1.54) ms/mmHg (P < 0.04). CONCLUSION: In a large population of older subjects, arterial stiffness appears to be an independent determinant of impaired BRS. Within the same population, impaired BRS was associated with orthostatic BP changes.     

Antihypertensive therapy increases cerebral blood flow and carotid distensibility in hypertensive elderly subjects

Many physicians are reluctant to lower blood pressure to recommended levels in elderly hypertensive patients because of concern about producing cerebral hypoperfusion. Because hypertension is associated with potentially reversible structural and functional alterations in the cerebral circulation that may improve with treatment, we investigated whether long-term pharmacological reduction of systolic blood pressure will improve, rather than worsen, cerebral blood flow and its regulation. Three groups of elderly subjects 65 years of age or older were studied prospectively: normotensive subjects (N=19), treated hypertensive subjects with systolic pressure <140 mm Hg (N=18), and uncontrolled hypertensive subjects with systolic pressure >160 mm Hg at entry into the study (N=14). We measured beat-to-beat blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasonography), finger arterial pressure (photoplethysmography), and pulsatile distensibility of the carotid artery (duplex Doppler ultrasonography) at baseline and after 6 months of observation or antihypertensive therapy. After baseline hemodynamic measurements, uncontrolled hypertensive subjects underwent aggressive treatment with lisinopril with or without hydroclorothiazide or, if not tolerated, nifedipine or an angiotensin receptor blocker to bring their systolic pressure <140 mm Hg for 6 months. The other 2 groups were observed for 6 months. After 6 months of successful treatment, uncontrolled hypertensive subjects had significant increases in cerebral blood flow velocity and carotid distensibility that was not seen in the other groups. Treatment reduced cerebrovascular resistance and did not impair cerebral autoregulation. Therefore, judicious long-term treatment of systolic hypertension in otherwise healthy elderly subjects does not cause cerebral hypoperfusion.     

Endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness over a 6-year period

Endothelial dysfunction and low-grade inflammation are associated with cardiovascular disease. Arterial stiffening plays an important role in cardiovascular disease and, thus, may be a mechanism through which endothelial dysfunction and/or low-grade inflammation lead to cardiovascular disease. We investigated the associations between, on the one hand, biomarkers of endothelial dysfunction (soluble endothelial selectin, thrombomodulin, and both vascular and intercellular adhesion molecules 1 and von Willebrand factor) and of low-grade inflammation (C-reactive protein, serum amyloid A, interleukin 6, interleukin 8, tumor necrosis factor-α and, soluble intercellular adhesion molecule 1) and, on the other hand, arterial stiffness over a 6-year period, in 293 healthy adults (155 women). Biomarkers were combined into mean z scores. Carotid, femoral, and brachial arterial stiffness and carotid-femoral pulse wave velocity were determined by ultrasonography. Measurements were obtained when individuals were 36 and 42 years of age. Associations were analyzed with generalized estimating equation and adjusted for sex, height, and mean arterial pressure. The endothelial dysfunction z score was inversely associated with femoral distensibility (β: -0.51 [95% CI: -0.95 to -0.06]) and compliance coefficients (β: -0.041 [95% CI: -0.076 to -0.006]) but not with carotid or brachial stiffness or carotid-femoral pulse wave velocity. The low-grade inflammation z score was inversely associated with femoral distensibility (β: -0.51 [95% CI: -0.95 to -0.07]) and compliance coefficients (β: -0.050 [95% CI: -0.084 to -0.016]) and with carotid distensibility coefficient (β: -0.910 [95% CI: -1.810 to -0.008]) but not with brachial stiffness or carotid-femoral pulse wave velocity. Biomarkers of endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness. This provides evidence that arterial stiffening may be a mechanism through which endothelial dysfunction and low-grade inflammation lead to cardiovascular disease.     

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.     

老老年人群动态血压参数与动脉僵硬度的相关性

目的探讨老老年人群动态血压参数与动脉僵硬度的相关性。方法筛选年龄≥80岁的老老年人238例,以血压≥160/95 mm Hg(1 mm Hg=0.133 kPa)为标准,分为高血压组(134例)和对照组(104例),并进行臂-踝脉搏传导速度(baPWV)和24 h动态血压监测。用Pearson分析动态血压各参数与动脉僵硬度的相关性。结果高血压组baPWV高于对照组(P<0.05)。高血压组偶测收缩压,24 h、昼间和夜间收缩压、舒张压、脉压,收缩压负荷及舒张压负荷均高于对照组.夜间收缩压下降率、舒张压下降率低于对照组,差异有统计学意义(P<0.05,P<0.01)。baPWV与偶测血压;24 h收缩压、舒张压、脉压;昼间收缩压、舒张压、脉压、心率;夜间收缩压、舒张压、脉压;收缩压负荷、舒张压负荷呈正相关(P<0.05,P<0.01),而与夜间收缩压下降率呈负相关(P<0.01)。结论高血压是老老年人群动脉僵硬度增加的一个重要因素,动脉僵硬度与动态血压、脉压、心率及血压负荷相关。     

Angiotensin-converting enzyme gene polymorphism and common carotid stiffness. The Rotterdam study

The insertion/deletion (I/D) polymorphism of the ACE gene may be involved in structural arterial changes. Aim of the present study was to assess the relationship between the ACE I/D gene and vessel wall stiffness among older adults. The study was conducted within the Rotterdam study, a population-based cohort study including subjects aged 55 years and older. The II, ID and DD genotypes of the ACE gene were determined in all subjects. The distensibility coefficient (10(-3)/kPa) of the carotid artery and the carotid-femoral pulse wave velocity were measured during the third phase of the Rotterdam study (1997-1999) and were used as measure of arterial stiffness. Data on both carotid stiffness and the ACE genotype were available for 3001 participants. After adjustment for age and gender, subjects with the ID and DD genotype had higher carotid stiffness compared to subjects with II genotype (distensibility coefficient (10(-3)/kPa) 10.24 (95% CI, 10.06-10.43), 10.27 (95% CI, 10.02-10.52), 10.65 (95% CI, 10.37-10.93), respectively (ID versus II genotype, P = 0.017), (DD versus II genotype, P = 0.037)). In stratified analyses, the association was strongest in subjects younger than 70 years. No difference was seen for pulse wave velocity among genotypes. In conclusion, the results of this population-based study show that the ACE ID/DD genotypes are associated with higher common carotid stiffness.     

Late-life depression is associated with arterial stiffness: a population-based study

OBJECTIVES: To determine whether arterial stiffness is associated with depression in the elderly. DESIGN: Population-based cross-sectional study. SETTING: In Ommoord, a suburb of Rotterdam, the Netherlands. PARTICIPANTS: Three thousand seven hundred four subjects of the Rotterdam Study aged 60 and older. MEASUREMENTS: Arterial stiffness was assessed using the distensibility of the carotid artery and the carotid-femoral pulse wave velocity. All participants were screened for depressive symptoms with the Center for Epidemiologic Studies-Depression scale. Those with depressive symptoms had a psychiatric evaluation to establish a diagnosis of depressive disorders according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria. RESULTS: Participants with increased arterial stiffness were more likely to have depressive symptoms. Odds ratios (ORs) for depressive symptoms were 1.24 (95% confidence interval (CI) = 1.01-1.52) per standard deviation decrease in carotid distensibility and 1.17 (95% CI = 1.00-1.38) per standard deviation increase in aortic pulse wave velocity. The association was stronger for depressive disorders meeting DSM-IV criteria (OR = 1.44, 95% CI = 1.03-2.03; OR = 1.48, 95% CI = 1.16-1.90, respectively). Control for atherosclerosis, as measured by the ankle-to-brachial index or presence of plaques in the carotid artery, did not change the associations. CONCLUSION: This study shows an association between arterial stiffness and depression in the elderly. The findings are compatible with the vascular depression hypothesis. These data suggest that arterial stiffness may partly cause the proposed relationship between vascular factors and depression.     

Rapid baroreceptor resetting in chronic hypertension. Implications for normalization of arterial pressure

The purpose of this study was to examine the ability of baroreceptors of renal hypertensive rabbits to reset rapidly during acute changes in arterial pressure. The carotid sinus (CS) was vascularly isolated and baroreceptor activity was recorded during slow ramp increases in CS pressure in hypertensive (one-kidney, one wrap; 127 +/- 3 mm Hg) and normotensive (one-kidney, no wrap; 85 +/- 3 mm Hg) rabbits anesthetized with chloralose. Control measurements were made after holding pressure for 10-15 minutes at the level of arterial pressure recorded before each experiment. Baroreceptor threshold pressure (Pth) was higher in hypertensives (78 +/- 4 mm Hg) compared with normotensives (55 +/- 3 mm Hg, p less than 0.05), and nerve activity was less in hypertensives over a wide range of pressure. CS distensibility (sonomicrometers) was not significantly different in the two groups. After increasing holding pressure from control by 30 and 60 mm Hg for 10-15 minutes, the extent of baroreceptor resetting (delta Pth/delta holding pressure x 100%) in normotensives was 39 +/- 6% and 33 +/- 2%, respectively, but only 14 +/- 5% and 9 +/- 3% in hypertensives (p less than 0.05). After decreasing holding pressure by 30 and 60 mm Hg, resetting was similar in normotensives (32 +/- 6% and 28 +/- 3%) and hypertensives (34 +/- 3% and 30 +/- 4%). In hypertensive rabbits, acute (10-15 minutes) exposure of baroreceptors to normotension (71 +/- 4 mm Hg) decreased Pth to 62 +/- 4 mm Hg and increased nerve activity to levels not significantly different from those of normotensive animals without altering CS distensibility.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac and vascular consequences of pre-hypertension in youth

Hypertension is associated with increased left ventricular mass (LVM) and carotid intima-media thickness (cIMT), which predict cardiovascular (CV) events in adults. Whether target organ damage is found in pre-hypertensive youth is not known. The authors measured body mass index, blood pressure, fasting glucose, insulin, lipids and C-reactive protein, LVM/height(2.7) (LVM index), diastolic function, cIMT, carotid stiffness, augmentation index, brachial artery distensibility, and pulse wave velocity (PWV) in 723 patients aged 10 to 23 years (29% with type 2 diabetes mellitus). Patients were stratified by blood pressure level (normotensive: 531, pre-hypertensive: 65, hypertensive: 127). Adiposity and CV risk factors worsened across blood pressure group. There was a graded increase in cIMT, arterial stiffness, and LVM index and decrease in diastolic function from normotension to pre-hypertension to hypertension. In multivariable models adjusted for CV risk factors, status as pre-hypertension or hypertension remained an independent determinant of target organ damage for LVM, diastolic function, internal cIMT, and carotid and arterial stiffness. Pre-hypertension is associated with cardiovascular target organ damage in adolescents and young adults.     

Impaired fasting glucose is associated with increased arterial stiffness in elderly people without diabetes mellitus: the Rotterdam Study

OBJECTIVES: To study the association between impaired fasting glucose (IFG) and arterial stiffness in older adults. DESIGN: Cross-sectional population-based study. SETTING: The Rotterdam Study, a Dutch population-based cohort study. PARTICIPANTS: Two thousand nine hundred eighty-seven subjects aged 60 and older. MEASUREMENTS: Arterial stiffness assessed by measuring common carotid arterial distensibility and glucose status classified into three categories: normal fasting glucose (NFG) (fasting glucose <6.1 mmol/L), IFG (fasting glucose 6.1-6.9 mmol/L), and diabetes mellitus (DM). RESULTS: In the total cohort, common carotid distensibility decreased with increasing impairment of glucose metabolism. Subjects younger than 75 with IFG were comparable with subjects with NFG with respect to arterial stiffness. Subjects aged 75 and older with IFG had stiffer arteries than subjects with NFG, reaching the same arterial stiffness as subjects with DM. For subjects younger than 75, mean difference in distensibility coefficient between subjects with NFG and with IFG was 0.1 (95% confidence interval (CI)=-0.04-0.05, P=.88) and between subjects with NFG and with DM was 1.2 (95% CI=0.7-1.7, P<.001). For subjects aged 75 and older, the mean difference between these groups was 0.7 (95% CI=0.2-1.2, P=.007) and 0.8 (0.3-1.4; P=.002), respectively. In the total cohort, fasting glucose was strongly associated with carotid distensibility (beta-coefficient=-0.29, P<.001). CONCLUSION: IFG is related to arterial stiffness in elderly subjects. An advanced stage of arterial stiffness, comparable with that of subjects with DM, is only reached at the age of 75.     

Carotid plaques, but not common carotid intima-media thickness, are independently associated with aortic stiffness.

OBJECTIVE: It has been suggested that non-invasive aortic stiffness measurements can be used as an indicator of atherosclerosis. The relationships of arterial stiffness with arterial wall hypertrophy and atherosclerosis however, have rarely been investigated in large-scale studies. The present study reports the associations of carotid arterial structure assessed by B-mode ultrasound with carotid-femoral pulse-wave velocity in hypertensive and non-hypertensive subjects. DESIGN AND METHODS: Free health examinations were performed on 564 subjects (age 58.2 +/- 10.8 years, 31.9% of women, 53.2% of all were hypertensive). Carotid-femoral pulse-wave velocity (PWV) was used to assess aortic stiffness. Carotid ultrasound examination included measurements (at sites free of plaques) of intima-media thickness (IMT) at the common carotid arteries (CCA), CCA-lumen diameter, and assessment of atherosclerotic plaques in the extracranial carotid arteries. RESULTS: Subjects with carotid plaques had significantly higher mean sex-adjusted values of PWV than those without carotid plaques (12.7 +/- 0.2 versus 11.1 +/- 0.1 m/s, P < 0.001). Multivariate analyses showed that this association was independent of sex, age, height, body mass index, mean blood pressure, pulse pressure, diabetes, hypercholesterolaemia and smoking habits (P < 0.009). PWV was positively associated with CCA-IMT and CCA-lumen diameter in sex-adjusted analysis (partial correlation coefficients (r ) were respectively 0.39 and 0.42, P < 0.001 for each). However, the association of PWV with CCA-IMT, but not that with CCA-lumen diameter, disappeared after further adjustment for age and blood pressure measurements (mean blood pressure and/or pulse pressure). CONCLUSION: This study shows that there is a differential association of PWV with CCA-IMT and carotid plaques. The nature of the independent positive association between atherosclerosis and arterial stiffness should be thoroughly investigated.     

Nebivolol increases arterial distensibility in vivo

Arterial stiffness is a key determinant of cardiovascular risk in hypertensive patients. beta-Blockers appear to be less effective than other drugs in improving outcome in hypertensive patients, and a potential explanation may be that beta-blockers are less effective in reducing arterial stiffness. The aim of this study was to assess the direct effect of beta-blockade on pulse wave velocity (PWV), a robust measure of arterial distensibility, using a local, ovine, hind-limb model. In addition, we hypothesized that the vasodilating beta-blocker nebivolol, but not atenolol, would increase arterial distensibility in vivo. All studies were conducted in anesthetized sheep. PWV was recorded in vivo using a dual pressure-sensing catheter placed in the common iliac artery. Intraarterial infusion of nebivolol reduced PWV by 6+/-3% at the higher dose (P<0.001), but did not alter mean arterial pressure (change of -1+/-3 mm Hg, P=0.1). In contrast, atenolol had no effect on PWV (P=0.11) despite a small drop in mean pressure (change of -5+/-3 mm Hg, P<0.01). Infusion of glyceryl trinitrate led to a dose-dependent fall in PWV, and 2 nmol/min produced a similar reduction in PWV to the higher dose of nebivolol (500 nmol/min). The effect of nebivolol on PWV was significantly attenuated during coinfusion of N(G)-monomethyl-L-arginine (P=0.003) and also during coinfusion of butoxamine (P=0.02). These results demonstrate that nebivolol, but not atenolol, increases arterial distensibility. This effect of nebivolol is mediated through the release of NO via a beta2 adrenoceptor-dependent mechanism. Thus, nebivolol may be of benefit in conditions of increased large artery stiffness, such as isolated systolic hypertension.     

Static versus dynamic distensibility of the carotid artery in humans

In clinical studies, the elastic behavior of central arteries is usually assessed by measuring dynamic distensibility. In this study, we aimed to investigate how dynamic and static distensibility of the common carotid artery (D(dyn) and D(stat), respectively) are related in 28 healthy volunteers of 20-71 years. The carotid diameter and its change with the pressure pulse were measured using an ultrasound echo-tracking device. Arterial blood pressure was measured by Finapres and carotid pressure was determined by applanation tonometry. D(dyn) was determined at rest using the pressure pulse, while D(stat) was determined during pressor responses induced by handgrip or cold pressor test. Data are given as mean +/- 1 SD. In younger subjects (<35 years), D(stat) did not differ from D(dyn) (7.0 +/- 3.4 vs. 6.5 +/- 2.1 x 10(-3) x mm Hg(-1), respectively), whereas in older subjects (>35 years), D(stat) was significantly higher than D(dyn) (3.8 +/- 1.4 vs. 2.1 +/- 0.9 x 10(-3) x mm Hg(-1), p < 0.001). For all subjects, D(stat) and D(dyn) decreased with increasing age and mean arterial pressure (MAP). Using stepwise multiple regression analysis, the strongest predictor of D(stat) proved to be MAP, while that of D(dyn) was age. D(stat) was found to be linearly related to the hysteresis loop area of the pressure-diameter relation (r = 0. 94), i.e. to vessel wall viscosity. It is concluded that, with increasing age, static distensibility overestimates the distension capacity of large arteries.     

Advanced glycation end-products and arterial stiffness in hypertension

BACKGROUND: The formation of advanced glycation end-products is associated with arterial stiffness in experimental models and alagebrium (formerly known as ALT-711), an advanced glycation end-product cross-link breaker, has been shown to reduce arterial stiffness in elderly subjects. METHODS: We related plasma concentrations of advanced glycation end-products (AGEs), measured using a noncompetitive immunoassay, and markers of aortic stiffness-pulse wave velocity (PWV) and augmentation index (AIx), a measure of aortic wave reflection-in 46 subjects, aged 47 +/- 2 years, comprising 30 untreated hypertensive and 16 normotensive subjects. Results were analyzed using univariate and multiple logistic regression analysis. RESULTS: Plasma AGEs were significantly higher in hypertensive than in normotensive subjects (7.8 +/- 1 v 3 +/- 1 mug/ml; P < .0001). There was a significant relationship between plasma AGEs and aortic PWV (r = 0.49, P < .01), but not with AIx. In a stepwise regression model age, plasma AGE levels, smoking status, and total cholesterol explained 67% of the variability in PWV. For AIx, the only variables that entered the model were age, gender, and heart rate (R(2) = 0.53, P < .0001) with no contribution from plasma AGEs. CONCLUSIONS: Concentration of plasma AGEs is significantly higher in hypertensive than in normotensive subjects and related to aortic stiffness independent of age and blood pressure, with no relationship with aortic wave reflection. Plasma AGEs may play a blood pressure-independent role in large but not small vessel remodeling in essential hypertension.     

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.     

Pulse pressure in sustained essential hypertension: a haemodynamic study

Central and forearm haemodynamics were studied in 73 middle-aged male subjects: 14 normotensive controls and 59 patients with sustained essential systolic/diastolic hypertension. Hypertensives were divided into two groups: pulse pressure within the normal range (40-60 mmHg; group I) or above 60 mmHg (group II) for the same level of mean arterial pressure (MAP). Indices of systemic and forearm arterial compliance and distensibility for the same age and MAP were reduced to the same extent in group I and II. In contrast, the peak systolic blood flow velocity of the brachial artery, cardiac output (CO) and stroke volume (SV) were significantly greater in group II than in group I. Systemic and forearm vascular resistances were significantly increased in group I but remained within the normal range in group II. The study provided evidence that, in middle age, there is a group of hypertensive patients characterized by a disproportionate increase in pulse pressure for the level of MAP. The elevation of the pulsed component of blood pressure (BP) reflects a relative hyperkinesia with an increase in CO and arteriolar vasodilatation. The subsequent increase in systolic pressure is produced by a combination of reduced arterial distensibility and increased SV.     

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     

Age and blood pressure levels modify the functional properties of central but not peripheral arteries

The effect of age and blood pressure on the carotid and the radial artery distensibilities was investigated. Patients referred to the outpatient clinic of the Department of Internal Medicine and Geriatric Medicine were asked to participate in the study. The carotid and radial artery distensibility coefficients were measured. Linear regression analyses were performed to investigate the associations between determinants and arterial distensibility. The mean age of the participants was 72.3 years, and 41.5% were men. Carotid distensibility decreased with age in adjusted models (beta = -0.317; 95% confidence interval [CI], -0.241, -0.055), whereas the radial distensibility did not decrease. Levels of systolic blood pressure and mean arterial pressure were associated with decreasing levels of carotid distensibility, whereas the diastolic blood pressure and pulse pressure were not associated (beta = -0.571; 95% CI, -0.404, -0.007; beta = -0.410; 95% CI, -0.308, -0.101, respectively). In conclusion, age and blood pressure levels are associated with the distensibility of the central arteries but not with that of the peripheral arteries.