血液透析患者骨保护素细胞核因子кB受体活化因子配体与动脉僵硬度的关系

目的探讨血液透析患者颈-股脉搏波速度(CFPWV)和颈-桡脉搏波速度(CRPWV)的变化及与骨保护素(OPG)、细胞核因子кB受体活化因子配体(sRANKL)系统的关系。方法对北京大学人民医院血液净化中心2006年6—10月40例血液透析患者采用酶联免疫吸附法测定血清OPG、sRANKL,PWV测定仪测定外周动脉僵硬度,X线平片检测腹主动脉、股动脉及桡动脉部位血管钙化,计算血管钙化积分。结果 25例(64.1%)患者存在不同程度的血管钙化,中重度钙化者较轻度钙化者血清OPG高[(342.50±171.53)ng/L对(206.21±137.88)ng/L,P=0.025]、OPG/sRANKL比值高(454.65±455.63比135.31±136.81,P=0.035),sRANKL比较差异无统计学意义[(0.10±0.08)pmol/L对(0.12±0.08)pmol/L]。血液透析患者CRPWV及CFPWV均较对照组增高,差异有统计学意义[(9.48±1.80)m/s对(8.58±1.29)m/s,P=0.043]和[(13.42±3.26)m/s对(10.07±1.76)m/s,P<0.01]。血OPG较对照组高[(235.12±154.33)ng/L对(93.00±44.10)ng/L,P=0.01],sRANKL两组比较,差异无统计学意义[(0.12±0.08)pmol/L对(0.16±0.08)pmol/L]。相关分析发现CRPWV与舒张压、sRANKL呈正相关(r=0.389、0.349,P=0.025、0.040),控制年龄、血压因素后CRPWV仍然与sRANKL呈正相关(r=0.381,P=0.029)。多元线性回归分析显示血磷、sRANKL及钙磷乘积是CRPWV的独立影响因素,年龄是CFPWV的独立影响因素。结论血液透析患者外周动脉僵硬度增加,sRANKL独立于年龄和血压影响血液透析患者动脉僵硬度。     

应用超声检查评价高血压患者血管僵硬度与心功能的关系

目的 应用超声检查、评价高血压患者动脉僵硬度和心功能的关系.方法 分别检测、计算高血压组(167例)与对照组(165例)的心功能和颈动脉血管僵硬度参数,并进行两组间比较.结果 二尖瓣口舒张早期血流速度峰值(E峰)与左心室后壁二尖瓣环舒张早期速度峰值(e峰)比值(E/e)、Tei指数高血压组分别为(10.92±3.14)和(0.58±0.13),对照组分别为(7.70±1.56)和(0.45±0.09),两组差异有统计学意义(均P＜0.05);射血分数两组间差异无统计学意义(P＞0.05).血管僵硬度参数β、压力应变弹性系数、脉搏波传导速度(PWVβ)和动脉顺应性高血压组分别为(11.0±5.2)、(172.6±83.8)kPa、(7.8±1.6)m/s和(0.6±0.2)mm2/kPa.对照组分别为(7.5±3.0)、(97.1±45.4)kPa、(5.9±1.3)m/s和(0.8±0.3)mm2/kPa,两组差异有统计学意义(均P＜0.05).E/e与压力应变弹性系数和PWVβ呈正相关(γ分别为0.316和0.296,P＜0.05),Tei指数与压力应变弹性系数、增大指数和PWVβ呈正相关(γ分别为0.278、0.300和0.323,P＜0.05或P＜0.01);射血分数与血管僵硬度参数无相关性.结论 高血压引起动脉僵硬度增高,心功能障碍;动脉硬化可作为早期心功能障碍预测指标之一.     

Different effects of pravastatin and cerivastatin on the media of the carotid arteries as assessed by integrated backscatter ultrasound.

BACKGROUND: Currently, there are various types of statins used in the treatment of hyperlipidemia and coronary artery disease. The purpose of this study was to compare the effects of a lipophilic statin (cerivastatin) with those of a hydrophilic statin (pravastatin) on the carotid arterial media using integrated backscatter (IB) ultrasound. Cerivastatin (C) has a strong anti-proliferative effect (APE) on smooth muscle cells (SMCs), whereas pravastatin (P) has a weak effect. METHODS AND RESULTS: The IB values in the media of 72 segments of carotid arteries were measured in 36 patients with hyperlipidemia before and after statin therapy or diet for 6 months (C, n=13: P, n=12: diet, n=11). In addition, IB values of 34 segments of carotid arteries were measured in 34 patients without coronary risk factors. Intima - media thickness (IMT) and arterial stiffness (stiffness beta) were measured by conventional echo at the same time. IB values did not significantly change in the P group (12.8+/-3.5 vs 12.7+/-2.7 dB), but decreased in the C group (12.1 +/-2.9 vs 10.0+/-2.7 dB, p<0.01). Also, stiffness beta did not significantly change in the P group (8.3+/-3.1 vs 7.6+/-2.5), but decreased in the C group (10.1+/-4.3 vs 7.9+/-3.3, p<0.05). IB values correlated with age (r=0.70, p<0.01) and stiffness beta (r=0.67, p<0.01) in the 34 patients without coronary risk factors. CONCLUSIONS: Statin therapy with cerivastatin, but not pravastatin, decreased the IB values of the carotid media and arterial stiffness. The difference between these 2 statins may be related to their effective dose range.     

Effect of 4 weeks of aerobic or resistance exercise training on arterial stiffness, blood flow and blood pressure in pre- and stage-1 hypertensives

The benefits of aerobic exercise (AE) training on blood pressure (BP) and arterial stiffness are well established, but the effects of resistance training are less well delineated. The purpose of this study was to determine the impact of resistance vs aerobic training on haemodynamics and arterial stiffness. Thirty pre- or stage-1 essential hypertensives (20 men and 10 women), not on any medications, were recruited (age: 48.2 +/- 1.3 years) and randomly assigned to 4 weeks of either resistance (RE) or AE training. Before and after training, BP, arterial stiffness (pulse wave velocity (PWV)) and vasodilatory capacity (VC) were measured. Resting systolic BP (SBP) decreased following both training modes (SBP: RE, pre 136 +/- 2.9 vs. post 132 +/- 3.4; AE, pre 141 +/- 3.8 vs. post 136 +/- 3.4 mm Hg, P = 0.005; diastolic BP: RE, pre 78 +/- 1.3 vs post 74 +/- 1.6; AE, pre 80 +/- 1.6 vs. post 77 +/- 1.7 mm Hg, P = 0.001). Central PWV increased (P = 0.0001) following RE (11 +/- 0.9-12.7 +/- 0.9 ms(-1)) but decreased after AE (12.1 +/- 0.8-11.1 +/- 0.8 m s(-1). Peripheral PWV also increased (P = 0.013) following RE (RE, pre 11.5 +/- 0.8 vs. post 12.5 +/- 0.7 ms(-1)) and decreased after AE (AE, pre 12.6 +/- 0.8 vs post 11.6 +/- 0.7 m s(-1)). The VC area under the curve (VC(AUC)) increased more with RE than that with AE (RE, pre 76 +/- 8.0 vs. post 131.1 +/- 11.6; AE, pre 82.7 +/- 8.0 vs. post 110.1 +/- 11.6 ml per min per s per 100 ml, P = 0.001). Further, peak VC (VCpeak) increased more following resistance training compared to aerobic training (RE, pre 17 +/- 1.9 vs. post 25.8 +/- 2.1; AE, pre 19.2 +/- 8.4 vs post 22.9 +/- 8.4 ml per min per s per 100 ml, P = 0.005). Although both RE and AE training decreased BP, the change in pressure may be due to different mechanisms.     

The association between low 25-hydroxyvitamin D and increased aortic stiffness

There is accumulating evidence that vitamin D exerts important pathophysiological effects on cardiovascular system. Low vitamin D was associated with increased cardiovascular risk in several reports. We studied the association between vitamin D and arterial stiffness in a random sample of 560 subjects selected from general population. Arterial stiffness was measured as aortic pulse-wave velocity (PWV) using Sphygmocor device. Serum 25-hydroxyvitamin D (25(OH)D) was measured using commercial kits. We found a clear negative trend in aortic PWV among 25(OH)D quartiles. Subjects in the bottom 25(OH)D quartile (<20?ng?ml(-1)) showed the highest aortic PWV (9.04?m?s(-1)), compared with 2nd-4th quartile (8.07?m?s(-1), 7.93?m?s(-1) and 7.70?m?s(-1), respectively; P for trend <0.0001). The association between 25(OH)D and aortic PWV remained significant after adjustment for age, gender and other potential confounders; subjects in the first 25(OH)D quartile had adjusted odds ratio 2.04 (1.26-3.30) for having aortic PWV 9?m?s(-1) (top quartile) in multiple regression. In conclusion, we found a clear significant and independent negative association between 25(OH)D and aortic PWV. Subjects with lowest vitamin D status showed the highest arterial stiffness.     

Relationship between arterial stiffness and myocardial damage in patients with newly diagnosed essential hypertension

BackgroundArterial stiffness increases in hypertensive individuals. Arterial stiffness is associated with impairment of systolic and diastolic myocardial function in hypertension (HT). However, the relationship between arterial stiffness and serum heart-type fatty acid-binding protein (H-FABP) levels, a sensitive marker of myocardial damage, has not been previously examined in patients with HT. We investigate the relationship between serum H-FABP levels and arterial stiffness in patients with newly diagnosed HT.MethodsWe studied 46 (48.5 +/- 10.6, years) never-treated patients with HT and age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. H-FABP levels were determined in all subjects. We evaluated arterial stiffness and wave reflections of study population, using applanation tonometry (Sphygmocor). Carotid-femoral pulse wave velocity (PWV) was measured as indices of elastic-type, aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections.ResultsCarotid-femoral PWV (10.5 +/- 2.2 vs. 8.7 +/- 1.6, m/s, P = 0.0001) and AIx@75 (22.7 +/- 9.5 vs. 15 +/- 11, %, P = 0.001) were significantly higher in patients with HT than control group. H-FABP levels were increased in hypertensive patients compared with control group (21.1 +/- 14.8 vs. 12.9 +/- 8.5, ng/ml, P = 0.002). In multiple linear regression analysis, we found that the body mass index (beta = 0.42, P = 0.0001) and carotid-femoral PWV (beta = 0.23, P = 0.03) were significant determinants of H-FABP levels.ConclusionArterial stiffness is associated with serum H-FABP levels, a sensitive marker of myocardial damage, in patients with newly diagnosed HT.American Journal of Hypertension (2008). doi 10.1038/ajh.2008.235American Journal of Hypertension (2008); 21, 9, 989-993. doi 10.1038/ajh.2008.235.     

Arterial stiffness is related to insulin resistance in nondiabetic hypertensive older adults

Hypertension, diabetes, obesity, and aging are associated with increased arterial stiffness. Both insulin resistance and hyperglycemia may contribute to the development of arterial stiffness. Older nondiabetic hypertensive adults were recruited to test the following hypotheses: (1) insulin resistance is associated with arterial stiffness, and (2) this relationship is independent of glucose tolerance status. Aortic pulse wave velocity (PWV), pulse pressure (PP), insulin sensitivity index (S(I), measured by insulin-assisted frequently sampled iv glucose test), glucose tolerance status, and abdominal fat mass were assessed in 37 older (23 male, 14 female, mean age 69.4 +/- 5.9 yr), nondiabetic, hypertensive adults after a 4-wk antihypertensive medication withdrawal. Both PWV and PP were negatively correlated with S(I) (r = -0.49, P = 0.002, and r = -0.38, P = 0.02, respectively). The mean PWV and PP in those with normal glucose tolerance were not significantly different from those with impaired glucose tolerance (9.8 +/- 2.4 vs. 10.0 +/- 3.1 m/sec, P = 0.79 and 71 +/- 17 vs. 72 +/- 18 mm Hg, P = 0.80, respectively). In multiple regression analysis, PWV and PP remained independently correlated with S(I) (P < 0.05) after adjusting for age, gender, fasting glucose, glucose tolerance status, body mass index, or abdominal fat mass. These results suggest that in hypertensive, nondiabetic, older adults, insulin resistance is associated with arterial stiffness independent of glucose tolerance status.     

Adrenalectomy improves arterial stiffness in primary aldosteronism

BackgroundAldosterone has been shown to substantially contribute to the accumulation of different types of collagen fibers and growth factors in the arterial wall, which increase wall stiffness. We previously showed that arterial wall stiffness is increased in primary aldosteronism (PA) independently of concomitant hypertension. This study was aimed at assessing the effects of specific treatment of PA on the arterial stiffness.MethodsTwenty-nine patients with confirmed PA (15 with aldosterone-producing adenoma treated by unilateral laparoscopic adrenalectomy, 14 treated with spironolactone (mainly idiopathic aldosteronism) were investigated by Sphygmocor applanation tonometer (using measurement of carotid-femoral pulse wave velocity (PWV) and augmentation index (AI)) at the time of the diagnosis and then approximately 1 year after the specific treatment.ResultsThe office blood pressure (BP) decreased from 167 +/- 18/96 +/- 9 to 136 +/- 12/80 +/- 7 mm Hg after adrenalectomy (P = 0.001), and from 165 +/- 21/91 +/- 13 to 151 +/- 22/88 +/- 8 mm Hg (not significant (n.s.)) on spironolactone. The mean 24-h BP decreased from 150 +/- 18/93 +/- 11 mm Hg to 126 +/- 17/80 +/- 10 mm Hg after adrenalectomy (P < 0.01), and from 155 +/- 16/94 +/- 12 to 139 +/- 18/88 +/- 8 mm Hg (n.s.) on spironolactone. The PWV significantly decreased after surgery from 9.5 +/- 2.7 m/s to 7.6 +/- 2 m/s (P = 0.001), and the AI (recalculated for heart rate 75/min) decreased significantly from 27 +/- 10 to 19 +/- 9% (P < 0.01). On the other hand, we did not find significant change of arterial stiffness indices in patients treated with spironolactone (PWV: 9.3 +/- 1.6 m/s vs. 8.8 +/- 1.3 m/s (n.s.); AI: 25 +/- 9% vs. 25 +/- 8% (n.s.)).ConclusionsSurgical but not conservative treatment of PA led to a significant decrease of BP and arterial stiffness parameters.American Journal of Hypertension (2008). doi:10.1038/ajh.2008.243American Journal of Hypertension (2008); 21, 10, 1086-1092. doi 10.1038/ajh.2008.243.     

The T-allele of the C825T polymorphism is associated with higher arterial stiffness in young healthy males

Arterial stiffening is the major cause of increasing systolic blood pressure in arterial hypertension. Increased arterial stiffness is one major mechanism responsible for morbidity and mortality in hypertension. A C825T polymorphism was identified in the gene encoding the G-protein beta3 subunit (GNB3), and an association of the T-allele with hypertension was demonstrated in several studies. In order to identify a pathogenetic link between hypertension and arterial stiffness, we compared two indices of arterial stiffness, pulse wave velocity (PWV) and augmentation index, in young, healthy men with and without the 825T-allele under resting conditions. PWV was determined from pressure tracing over carotid and femoral arteries in 99 subjects (CC: n=43; CT&TT: n=56). Augmentation index was derived in 72 subjects (CC: n=30; CT&TT: n=42) by pulse wave analysis using radial applanation tonometry. Carriers of the 825T-allele exhibited a significantly higher PWV compared to subjects with the CC genotype (6.0+/-0.1 m/s (TC&TT) vs 5.7+/-0.1 m/s (CC); P=0.0251). There was also a significant difference (P = 0.0448) in augmentation index between carriers of the T-allele (CT&TT: 3.4+/-2.9%) and controls with the CC -genotype (-5.0+/-4.1 %). There was no difference in any other anthropometric (age, height, weight, body mass index) or haemodynamic (heart rate, peripheral and central blood pressure). In summary, the C825T polymorphism is associated with higher arterial stiffness in young, healthy males. Arterial stiffening may pathogenetically contribute to the development of hypertension in carriers of the T-allele.     

Does Aerobic Exercise Mitigate the Effects of Cigarette Smoking on Arterial Stiffness?

The largest percentage of mortality from tobacco smoking is cardiovascular‐related. It is not known whether regular participation in exercise mitigates the adverse influence of smoking on vasculature. Accordingly, the authors determined whether regular aerobic exercise is associated with reduced arterial stiffness in men who smoke cigarettes. Using a cross‐sectional study design, 78 young men were studied, including sedentary nonsmokers (n=20), sedentary smokers (n=12), physically active nonsmokers (n=21), and physically active smokers (n=25). Arterial stiffness was assessed by brachial‐ankle pulse wave velocity (baPWV). There were no group differences in height, body fat, and systolic and diastolic blood pressure. As expected, both physically active groups demonstrated greater maximal oxygen consumption and lower heart rate at rest than their sedentary peers. The sedentary smokers demonstrated greater baPWV than the sedentary nonsmokers (11.8±1 m/s vs 10.6±1 m/s, P=.036). baPWV values were not different between the physically active nonsmokers and the physically active smokers (10.8±1 m/s vs 10.7±1 m/s). Chronic smoking is associated with arterial stiffening in sedentary men but a significant smoking‐induced increase in arterial stiffness was not observed in physically active adults. These results are consistent with the idea that regular participation in physical activity may mitigate the adverse effects of smoking on the vasculature.     

“Supranormal” Cardiac Function in Athletes Related to Better Arterial and Endothelial Function

Objective: Athlete's heart is associated with left ventricular (LV) hypertrophy (LVH), and “supranormal” cardiac function, suggesting that this is a physiological process. Hypertrophy alone cannot explain increase in cardiac function, therefore, other mechanisms, such as better ventriculo‐arterial coupling might be involved. Methods: We studied 60 male (21 ± 3 years) subjects: 27 endurance athletes, and a control group of 33 age‐matched sedentary subjects. We assessed global systolic and diastolic LV function, short‐ and long‐axis myocardial velocities, arterial structure and function and ventriculo‐arterial coupling, endothelial function by flow‐mediated dilatation, and amino‐terminal pro‐brain natriuretic peptide (NT‐proBNP) and biological markers of myocardial fibrosis and of oxidative stress. Results: Athletes had “supranormal” LV longitudinal function (12.4 ± 1.0 vs 10.1 ± 1.4 cm/s for longitudinal systolic velocity, and 17.4 ± 2.6 vs 15.1 ± 2.4 cm/s for longitudinal early diastolic velocity, both P < 0.01), whereas ejection fraction and short‐axis function were similar to controls. Meanwhile, they had better endothelial function (16.7 ± 7.0 vs 13.3 ± 5.3%, P < 0.05) and lower arterial stiffness (pulse wave velocity 7.1 ± 0.6 vs 8.8 ± 1.1 m/s, P = 0.0001), related to lower oxidative stress (0.259 ± 0.71 vs 0.428 ± 0.88 nmol/mL, P = 0.0001), with improved ventriculo‐arterial coupling (37.1 ± 21.5 vs 15.5 ± 13.4 mmHg.m/s³× 10³, P = 0.0001). NT‐proBNP and markers of myocardial fibrosis were not different from controls. LV longitudinal function was directly related to ventriculo‐arterial coupling, and inversely related to arterial stiffness and to oxidative stress. Conclusions: “Supranormal” cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo‐arterial coupling; athlete's heart is purely a physiological phenomenon, associated with “supranormal” cardiac function, and there are no markers of myocardial fibrosis. (Echocardiography 2010;27:659‐667)     

A1166C polymorphism of angiotensin II type 1 receptor, blood pressure and arterial stiffness in hypertension

OBJECTIVE: To study the association of the AC polymorphism of angiotensin II type 1 receptor gene (AGTR1) with blood pressure and central arterial stiffness in a population of hypertensive patients referred to hospital for further work-up. METHODS: One hundred and eighty-five patients, referred to our department from April 1998 to February 2002, were included. Blood pressure was measured by conventional and 24-h ambulatory methods, and arterial stiffness by carotid-femoral pulse wave velocity (PWV) determination. Genotyping for the AGTR1 AC polymorphism was performed by polymerase chain reaction. RESULTS: AGTR1 AC polymorphism was not associated with systolic or diastolic blood pressure, measured either by conventional (P=0.89 and P=0.67, respectively) or by 24-h ambulatory (P=0.57 and P=0.56, respectively) methods. Conversely, this polymorphism was significantly associated with PWV (P=0.006) and had a dose-allele effect, PWV increasing with the number of A alleles (10.6 +/- 2.4 m/s in CC, 11.9 +/- 2.5 m/s in AC and 12.7 +/- 2.7 m/s in AA patients, P=0.002). Multiple regression analysis showed that AC polymorphism was still independently associated with PWV (P=0.01) and was the third most important determinant of PWV after age (P <0.0001) and 24-h mean blood pressure (P <0.0001). CONCLUSION: In our study population, central arterial stiffness assessed by PWV was significantly and independently associated with the AC polymorphism, increased PWV being associated with the presence of the A allele. Further investigations are required for identification of the underlying mechanisms.     

老年患者认知功能障碍与动脉僵硬度关系

目的 探讨老年患者认知功能障碍与动脉僵硬度的关系.方法 选择142例老年患者,以肢体动脉搏动波(PWV)作为评价动脉僵硬度指标,以简易精神状态量表(MMSE)作为认知功能评价指标,MMSE评分总分30分,评分<24分为认知功能障碍.对所有入选病例进行PWV检查及MMSE评分,根据MMSE评分将所有患者分为两组:认知功能正常组93例,认知功能障碍组49例.结果 认知功能障碍组较认知功能正常组PWV明显增高[(13.3±2.4)m/s与(11.8±2.2)m/s,t=3.775,P-0.000].经Logistic回归分析,MMSE评分与PWV呈显著相关.结论 动脉僵硬度增加是老年患者认知功能障碍重要危险因素.     

Color Doppler tissue imaging in assessing the elastic properties of the aorta and in predicting coronary artery disease

We hypothesized that the change in aortic elastic properties could directly be shown with color Doppler tissue imaging (CDTI), that these findings could be related to aortic stiffness and distensibility and that, through these, coronary artery disease (CAD) could be predicted. One hundred and twenty six patients (group I: 83 with CAD, mean age 54+/-10 years, 18 female, 65 male; group II: 43 without CAD, mean age 53+/-10 years, 27 female, 16 male) having been evaluated for coronary artery disease by angiography were examined by echocardiography. Arterial pressure was measured immediately before echocardiographic evaluation. Internal aortic systolic and diastolic diameters by M-mode echocardiography and aortic upper wall tissue velocities (Aortic S, E, A, m/sec) by CDTI were measured 3 cm above the aortic valve. Lateral mitral annulus tissue velocities (Annulus S, E, A, m/sec) were also recorded. Aortic distensibility (cm2 x dynes(-1)) and aortic stiffness index were calculated using formulas. In the statistical analyses, CAD risk factors and left ventricular ejection fraction were used for adjustment. Aortic stiffness (2.79+/-3.49 vs 1.62+/-1.31, P=0.03), distensibility (1.55+/-1.46 vs 2.37+/-3.08, P=0.04), and aortic S velocity (0.057+/-0.016 vs 0.064+/-0.015, P=0.02) differed significantly between groups I and II. After adjustment, while aortic stiffness and S velocity were still statistically different (P=0.04; P=0.03 respectively), the significance of the difference in aortic distensibility disappeared (P=0.051). Aortic stiffness and aortic S velocity (0.06 m/sec<) were important CAD determinants (Odds ratio=1.4 P=0.03; Odds ratio=3.6 P=0.01, respectively), but aortic distensibility was not. Aortic stiffness was correlated only with aortic S velocity (r=-0.28, P=0.01), and aortic distensibility had a significantly positive correlation with aortic S velocity (r=0.20, P=0.02). The interobserver and intraobserver correlation coefficients for aortic S velocities were 0.65 and 0.71, respectively (P<0.05). Elastic properties of the aorta can directly be assessed by reproducibly measuring the movements in the upper wall of the aorta by CDTI. Reduced aortic S velocity is associated with increased aortic stiffness. Increased aortic stiffness and reduced aortic S velocity are important predictors of CAD.     

Serum osteoprotegerin levels are associated with inflammation and pulse wave velocity

OBJECTIVE: We examined the association between serum osteoprotegerin (OPG) levels, systemic inflammation and arterial stiffness in normal and diabetic patients. PATIENTS AND MEASUREMENTS: The study subjects comprised 49 newly diagnosed diabetic patients and 72 age- and sex-matched normal glucose controls. Anthropometric parameters, blood pressure, fasting blood glucose (FBG), lipid profiles, serum OPG, high-sensitive C-reactive protein (hsCRP), interleukin-6 (IL-6) and brachial-ankle pulse wave velocity (baPWV) were measured. RESULTS: Serum OPG levels (6.1 +/- 1.4 vs. 5.4 +/- 1.3 pmol/l, P = 0.011) and baPWV (1562 +/- 354 vs. 1399 +/- 257 cm/s, P = 0.004) were significantly higher in the diabetic group than in the normal glucose group. Serum OPG levels in normal and diabetic patients correlated significantly with systolic blood pressure (r = 0.20, P = 0.035), FBG (r = 0.30, P = 0.002), right baPWV (r = 0.22, P = 0.021), left baPWV (r = 0.26, P = 0.006), homeostasis model assessment insulin resistance (HOMA-IR) (r = 0.19, P = 0.045), IL-6 (r = 0.32, P = 0.001) and hsCRP (r = 0.21, P = 0.027) after adjusting for age and sex. Multiple regression analysis showed that serum OPG level was significantly associated with age, FBG, IL-6, systolic blood pressure, triglyceride and hsCRP (R(2) = 0.299). CONCLUSIONS: In summary, serum OPG and baPWV levels are elevated in diabetic patients and serum OPG levels are significantly associated with inflammation and arterial stiffness.     

Prediction of cognitive function by arterial stiffness in the very elderly.

BACKGROUND: Cognitive function is impaired in elderly subjects, so the aim of the present study was to determine the role of arterial stiffness on cognitive function. METHODS AND RESULTS: Cognitive function and arterial stiffness were assessed by the Mini-Mental State Examination (MMSE) and measurement of the brachial-ankle pulse wave velocity (PWV), respectively. The cross-sectional association of the MMSE score and PWV was studied in 203 subjects (87 men, 116 women), all of whom were 85 years old. Sex distribution, systolic and diastolic blood pressures did not differ between the normal (MMSE score >or=24, n=128) and impaired MMSE groups (MMSE score <24, n=75). In contrast, the PWV was significantly increased in the impaired MMSE group than in the normal MMSE group (25.0+/-0.8 vs 22.9+/-0.5 m/s, p<0.05). In multiple regression analysis, the PWV was also independently and significantly associated with the MMSE score. CONCLUSIONS: These results suggest that cognitive function could be predicted by arterial stiffness, as assessed by the PWV, in the very old. Preventing atherosclerosis may play an important role in preserving normal cognitive function until very old age.     

Isolated systolic hypertension is characterized by increased aortic stiffness and endothelial dysfunction

Isolated systolic hypertension is associated with increased cardiovascular risk. It is thought to result from large artery stiffening, which is determined by structural components within the vasculature but also by functional factors including NO and endothelin-1. We hypothesized that endothelial dysfunction would account for increased arterial stiffness in patients with isolated systolic hypertension. The aim of this study was to investigate the relationship between endothelial function and arterial stiffness in these patients along with control subjects. We studied 113 subjects: 35 patients with isolated systolic hypertension (mean age+/-SD: 68+/-6 years), 30 age-matched control subjects (65+/-5 years), and 48 young control subjects (37+/-9 years). Aortic pulse wave velocity (PWV) was derived by sequential carotid/femoral waveform recordings. Conduit artery endothelial function was determined by flow-mediated dilatation. Aortic PWV was higher (9.65+/-2.56 m/s versus 8.26+/-0.85 m/s; P=0.009), and flow-mediated dilatation was lower (2.67+/-1.64% versus 4.79+/-3.1%; P=0.03) in patients with isolated systolic hypertension compared with age-matched control subjects. Similarly, aortic PWV was also higher, and flow-mediated dilatation lower, in older versus young control subjects (8.26+/-0.85 m/s versus 7.09+/-1.01 m/s and 4.79+/-3.1% versus 6.94+/-2.7%; P=0.004 for both). Overall, aortic PWV correlated inversely with flow-mediated dilatation (r=-0.3; P=0.001), which remained significant after adjustment for confounding factors (P=0.01). Patients with isolated systolic hypertension have higher aortic PWV and decreased endothelial function compared with age-matched control subjects. Our results suggest that endothelial function contributes significantly to increased arterial stiffness in patients with isolated systolic hypertension and with age.     

Beta-blockers reduce aortic stiffness in hypertension but nebivolol, not atenolol, reduces wave reflection

BACKGROUND: There is conflicting information with regard to the effect of beta-blockers on arterial stiffness and wave reflection. We compared a vasodilating beta-blocker, nebivolol, with atenolol. METHODS: We randomized 40 subjects with untreated hypertension (mean +/- s.e.m. systolic/diastolic blood pressure (BP) of 160 +/- 3/98 +/- 1 mm Hg, age 49 +/- 1 years) 16 of whom were women, to atenolol 50 mg or nebivolol 5 mg daily for 4 weeks. Arterial stiffness was assessed in terms of carotid-femoral pulse wave velocity (PWV, Complior) and arterial wave reflection (augmentation index (AIx) by applanation tonometry, Sphygmocor). RESULTS: Both beta-blockers produced an equal reduction in brachial BP but aortic pulse pressure (PP) was reduced to a greater extent by nebivolol (P < 0.05). PWV was decreased significantly by both therapies (nebivolol: from 11.5 +/- 0.5 to 9.9 +/- 0.5 m/s; atenolol: from 11.1 +/- 0.4 to 9.8 +/- 0.4 m/s; P < 0.01) but only nebivolol significantly reduced AIx (from 35 +/- 5 to 28 +/- 2%, P < 0.05). In addition, whereas PP amplification (PP, mm Hg) decreased with atenolol therapy (from 10 +/- 1 to 7 +/- 1, P < 0.01), it increased with nebivolol therapy (from 8 +/- 1 to 14 +/- 3, P < 0.01). Atenolol reduced heart rate to a greater extent than nebivolol did (14 +/- 3/min reduction by atenolol vs. 8 +/- 2/min reduction by nebivolol, P < 0.05). There was no difference between the two treatments in respect of the effect on transit time. CONCLUSION: The beta-blockers, atenolol and nebivolol, have a similar effect in reducing arterial stiffness in the large elastic aorta, largely secondary to BP reduction. Nebivolol, in contrast to atenolol, has an effect on small muscular arteries, increasing PP amplification and reducing wave reflection, possibly because of increased levels of nitric oxide (NO). Such ancillary properties may impart important distinct hemodynamic effects, and therefore beta-blockers cannot be regarded as a homogeneous group.     

Early identification of vascular damage in patients with systemic sclerosis

Vascular involvement in systemic sclerosis (SSc) plays a key role in the pathogenesis of fibrosis. We assessed arterial stiffness using a new echo-tracking technique in patients with SSc asymptomatic for cardiovascular diseases. We enrolled 22 patients (21 female, 63 ± 14 years) and 20 controls (12 female, 62 ± 3 years). Carotid intima-media thickness (IMT) was comparable between the 2 groups (1.1 ± 0.3 vs 1.0 ± 0.4 mm, P = ns), whereas the stiffness parameters were significantly increased in patients (β: 9.5 ± 4.2 vs 5.8 ± 1.1, P = .001; pulse wave velocity [PWV]: 6.5 ± 1.5 vs 5.2 ± 0.6 m/sec, P = .003). A correlation between stiffness parameters, anti-Scl-70 antibodies (β: r = .46, P = .03; PWV: r = .50, P = .02), and anticentromere antibodies (β: r = -.54, P = .020; PWV: r = -.53, P = .023) was found. Echo-tracking technique may be valuable in early identification of vascular involvement in patients with SSc.     

Inverse relationship between ambulatory arterial stiffness index and glomerular filtration rate in arterial hypertension

BACKGROUND: Arterial stiffness and mild-to-moderate renal dysfunction are predictors of cardiovascular (CV) morbidity and mortality. Recently, the ambulatory arterial stiffness index (AASI) has been proposed as a surrogate index of arterial stiffness. It has been associated with an enhanced risk of stroke. The aim of our study was to assess the relationship between AASI and glomerular filtration rate (GFR) in a group of hypertensive patients with no CV complications. METHODS: A total of 143 untreated hypertensive subjects (mean age: 44 +/- 12 years; men 57%), with serum creatinine <1.5 mg/dl, were enrolled. AASI was calculated as one minus the regression slope of diastolic on systolic blood pressure (BP) obtained by individual 24-h BP recordings. GFR was computed from the scintigraphic determination of the technetium-99m diethylenetriaminepentaacetic acid uptake within the kidneys, by the Gates' method. RESULTS: Hypertensive patients with AASI above the median value (n = 71) had lower GFR than those with AASI below the median (n = 72) (98.3 +/- 31 vs. 122.4 +/- 32 ml/min/1.73 m(2); P < 0.001). This difference held even after adjustment for age and gender. The linear regression analysis disclosed a significant inverse correlation between GFR and AASI (r = -0.30; P < 0.001), that was replicated (beta = -0.19; P = 0.02) in a multiple regression model including, as independent variables (besides AASI), age, gender, high-density lipoprotein cholesterol, body mass index, 24-h pulse pressure (PP) and nocturnal reduction in BP. CONCLUSIONS: AASI is inversely related to GFR in arterial hypertension. This may help to explain the increased CV risk associated with mild-to-moderate renal dysfunction.