Evaluation of elastic structural change in coronary atherosclerosis using scanning acoustic microscopy.

Coronary atherosclerotic lesions were observed by scanning acoustic microscopy (SAM), a technique which can visualize regions of differing elasticity. Three regions, i.e., dark (dR), intermediate (iR) and bright (bR) demonstrating differences in acoustic reflection intensity and the velocity of surface acoustic waves, were seen in the lesions. Furthermore, lipid-positive areas were found to be dR and iR and fatty crystalline areas were observed only in iR regions by polarizing microscope. These phase transitions of fat affected the acoustic properties in each region. According to SAM images, intimal structural changes were classified into three types, minimum structural change (type I), the overcrowded net-like dR structure (type II) and markedly disturbed structure with a decrease of dR (type III). The medial structure change was also classified into three types paralleling the decrease of dR (types M1, M2 and M3). Intimal type II with a large degree of thickening and intimal type III with medial type M3 were highly prominent in the acute myocardial infarction (AMI) group (P less than 0.01). Therefore these results suggest that the anisotropic elasticity induced by micro-elastic changes in the arterial wall may be associated with functional disturbance of the vascular wall.     

Effect of intensive statin therapy on arterial elasticity in patients with coronary artery disease

OBJECTIVE: Reduced arterial compliance is an independent predictor of cardiovascular mortality and is commonly encountered in patients with coronary artery disease. Statins may produce cholesterol-independent effects which can result at least in part from direct improvement of the arterial function. In this study, we sought to determine the effect of intensive statin therapy according to the Adult Treatment Panel III guidelines on arterial compliance in dyslipidaemic patients with angiographically-proven CAD selected for medical treatment. METHODS: Patients (n = 33) received atorvastatin 40 mg/day for 6 months. Large arterial compliance and small arterial compliance were measured at baseline and after 6 months of atorvastatin treatment. RESULTS: After treatment, the large artery elasticity index (LAEI) increased from 11.85 +/- 3.46 to 13.80 +/- 3.95 ml/mm Hg x 100 (P < 0.001) and the small artery elasticity index (SAEI) increased from 3.84 +/- 1.97 to 4.97 +/- 1.98 ml/mm Hg (P = 0.03). There was no correlation between the change in either LAEI or SAEI and other baseline variables or changes in lipid levels. CONCLUSION: Our findings suggest that intensive statin therapy according to the Adult Treatment Panel III guidelines improves arterial elasticity in CAD patients selected for medical treatment. The beneficial vascular effect of atorvastatin on arterial elasticity was independent of lipid parameters.     

Relationship between arterial elasticity indices and carotid artery intima-media thickness

Functional and structural changes of the arterial wall appear to serve as early hallmarks of the hypertensive disease process. Structural vascular changes can be studied by the determination of the intima-media wall thickness (IMT) at the carotid artery. The elastic behavior of the proximal and distal parts of the arterial tree can be assessed from noninvasively recorded radial artery waveforms. The aim of the study was to compare large (proximal, C1) and small (distal, C2) artery elasticity indices in two age-matched study groups with high- and low-normal blood pressure (BP) and to assess the relation between elasticity indices and IMT. A total number of 22 subjects with high-normal BP (40 +/- 2 years; BP, 147 +/- 2.5/84 +/- 1.5 mm Hg) and 22 matched controls with low-normal BP (40 +/- 2 years; BP, 123 +/- 1.9/69 +/- 1.5 mm Hg) were enrolled. The IMT was echographically determined at the common carotid artery by the leading-edge technique. Large artery (C1) and small artery (C2) elasticity indices were calculated from a third-order, four-element model of the arterial circulation. In the group with high-normal BP large and small artery elasticity indices were significantly decreased versus controls with low-normal BP (C1: 1.63 +/- 0.08 v 1.99 +/- 0.09 mL/mm Hg, P < .01; C2: 0.059 +/- 0.005 v 0.076 +/- 0.007 mL/ mm Hg, P < .05) and IMT increased significantly (0.607 +/- 0.039 v 0.516 +/- 0.027 mm, P < .05). Moreover, there was an inverse relationship between IMT and small artery elasticity index (r = -0.60, P = .004). In subjects with a high-normal BP there is already a change in the IMT of the carotid artery versus normotension. The IMT is related to the small artery elasticity index (C2).     

Vascular compliance in women with polycystic ovary syndrome treated with spironolactone

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age in the United States and has been associated with several diseases including cardiovascular disease, obesity, and glucose intolerance. In this study, systolic blood pressure, diastolic blood pressure, pulse pressure (vascular compliance), large artery elasticity, systemic vascular resistance (SVR), total vascular impedance (TVI), and body mass index (BMI) were measured before and after treatment with spironolactone in 10 women with PCOS. Systolic BP, diastolic BP, and BMI were similar prior to treatment and after treatment. Pulse pressure decreased slightly post‐treatment compared to pretreatment but not to significance (P = 0.07). The results show that after treatment with spironolactone, there was a statistically significant increase in large artery elasticity (P = 0.047), while there was a statistically significant decrease in SVR and TVI (P = 0.0005 and P = 0.03). This study indicates that treatment with spironolactone improves large artery elasticity and reduces systemic vascular resistance without any change in small artery elasticity.     

Changes in Vascular Hemodynamics in Older Women Following 16 Weeks of Combined Aerobic and Resistance Training

The purpose of this study was to determine whether combined (aerobic and anaerobic) training decreases blood pressure (BP) and improves vascular properties. Seventy‐nine postmenopausal women were randomly assigned to 3 groups that trained at different frequencies. Maximum oxygen uptake, body composition, BP, and arterial elasticity were evaluated prior to training and after 16 weeks of training. There was a significant time effect (decrease) for resting systolic BP (SBP) and rate pressure product. Exercise SBP, diastolic BP (DBP), heart rate, and RPP also decreased. Changes in total vascular impedance were related to SBP and changes in systemic vascular resistance were related to changes in DBP independent of body composition changes. Our findings suggest that combined training reduces SBP and improves vascular properties and that combined training 1 d/wk decreases BP similar to more frequent combined training. Training‐induced changes in arterial resistance and impedance may be involved in inducing changes in BP. J Clin Hypertens (Greenwich). 2012;00:00–00 ©2012 Wiley Periodicals, Inc.     

The Global Burden of Cardiovascular Disease: The Role of Endothelial Function and Arterial Elasticity in Cardiovascular Disease as Novel and Emerging Biomarkers

Some consider the measurements of arterial elasticity and flow-mediated dilation to be an indirect “biomarker” of endothelial dysfunction. As such, we describe the various uses of these techniques in the evaluation of the natural history of vascular disease. These measures are potential markers of disease, as abnormalities reflect changes in the integrity of vascular structure but occur prior to the manifestation of symptomatic cardiovascular events. In this review, the natural history of arterial elasticity is discussed, and the effects of aging and inflammation are reviewed. The role that arterial elasticity and flow-mediated dilation have in predicting future cardiovascular disease, and the effects of pharmacologic agents on these measures, is also reviewed.     

Arterial stiffness/elasticity in the contribution to progression of heart failure

Arterial stiffness/elasticity plays a major role in the pathogenesis of heart failure beyond arterial blood pressure. Arterial wave reflections are generated from the periphery of the vascular system, especially at the level of the small arteries. The pattern change of the arterial wave reflections can alter the ventricular-vascular coupling in a pathologic manner, leading to heart failure. Several noninvasive techniques are used to estimate arterial stiffness/elasticity. Small artery elasticity has important predictive value for the diagnosis of heart failure. The beneficial effect of some cardiovascular therapy on arterial stiffness/elasticity has potential to prevent or delay the progression of heart failure.     

Effects of atorvastatin on aortic pulse wave velocity in patients with hypertension and hypercholesterolaemia: a preliminary study

As statins may contribute to plaque stabilisation, it is important to evaluate whether these drugs may modify arterial stiffness. In 23 patients, aged 32-70 years, with hypertension and hypercholesterolaemia, a double-blind randomised study vs placebo was performed to evaluate whether atorvastatin was able to modify aortic stiffness, measured from aortic pulse wave velocity (PWV), after a 12-week treatment. The results revealed that atorvastatin did not change blood pressure, significantly lowered (P<0.003; <0.002) plasma total and LDL cholesterol, and increased aortic PWV by +8% (vs -2% under placebo) (P相似文献   

Reduced arterial elasticity is associated with endothelial dysfunction in persons of advancing age: comparative study of noninvasive pulse wave analysis and laser Doppler blood flow measurement

BACKGROUND: Endothelial dysfunction is the earliest marker for age-related abnormalities in vascular function, and examination of endothelial function has important clinical relevance. The present study was performed to evaluate effects of aging on arterial elasticity by using pulse waveform analysis and to investigate whether the changes in arterial elasticity might be used as a noninvasive measure for endothelial dysfunction. METHODS: A total of 24 healthy male volunteers were divided into young (n = 12) and elderly (n = 12) groups. Endothelial function was evaluated by delivering acetylcholine (Ach) and sodium nitroprusside (SNP) to the forearm vessels using iontophoresis, respectively, and measured blood flow using laser Doppler fluximetry. Large and small artery elasticity indices were noninvasively assessed using pulse wave analysis. RESULTS: Basal blood flow was similar between the young and elderly groups (14.58 +/- 3.4 v 13.52 +/- 3.41 PU, P = NS). Peak blood flow induced by Ach was significantly reduced in the elderly group compared with the young group (83.4 +/- 11.9 v 93.75 +/- 10.87 PU, P < .05). However, peak blood flow induced by SNP was similar in the two groups (119.17 +/- 16.76 v 128.33 +/- 21.29 PU, P = NS). In parallel, C1 large artery elasticity and C2 small artery elasticity indices were significantly reduced in the elderly group compared with the young group (11.42 +/- 1.67 v 16.75 +/- 2.09 mL/mm Hg x 10, P < .001; and 7.67 +/- 1.56 v 10.75 +/- 1.86 mL/mm Hg x 100, P < .001, respectively). The Ach-induced peak blood flow correlated with C1 large and C2 small artery elasticity indices. CONCLUSIONS: Advancing age is associated with endothelial dysfunction and reduced arterial elasticity. Reduced arterial elasticity parallels changes in impaired endothelium dependent vasodilation. It appears that reduced arterial elasticity may be used as a noninvasive measure for the determination of endothelial function.     

Arterial compliance: is it reduced in antiphospholipid syndrome?

To assess vascular compliance in patients with antiphospholipid syndrome (APS), or antiphospholipid antibodies (aPLs) positivity in comparison to healthy people and diabetes mellitus patients. Twenty-five patients with APS or aPLs, 33 healthy people (HP), 28 patients with diabetes mellitus (DM) underwent pulse wave analysis. Data calculated included the small artery elasticity (SAE), large artery elasticity (LAE) and systemic vascular resistance (SVR). Statistical analysis was performed as appropriate. The patient group was divided into two subgroups: APS-1 with warfarin treatment, and APS-2 without warfarin treatment. All patients and healthy subjects were matched by gender, body mass index and lipid profiles. Patients in APS-1 group were significantly younger in comparison to three other groups. After the adjustment for age, we found that SAE in APS-1 group did not differ from SAE in the HP group (6.4+/-1.8 ml/mmHg x 100 and 5.54+/-3.4 ml/mmHg x 100, respectively, P>0.05). In contrast, SAE in the group APS-2 was significantly lower (3.41+/-1.2 ml/mmHg x 100) than in the APS-1 and was almost equal to SAE in the DM group (4.2+/-2.37 ml/mmHg x 100). The SAE in the APS-2, DM and HP groups was inversely correlated with age, whereas in the APS-1 group we did not find such correlation. This pilot study showed abnormal small vascular elasticity in the patients with positive aPL, relative to the healthy subjects. The APS patients, treated with warfarin had the normal vascular function. This data support the hypothesis that APS may be associated with diffuse changes in the arterial wall, and may be a risk factor for atherosclerotic disease.     

Reduced arterial elasticity in rheumatoid arthritis and the relationship to vascular disease risk factors and inflammation

OBJECTIVE: Rheumatoid arthritis (RA) is associated with increased rates of cardiovascular disease. Reduced small artery elasticity (SAE) and large artery elasticity (LAE) and increased systemic vascular resistance (SVR) have been found in other high-risk groups. In the present study, we sought to determine whether arterial elasticity was reduced and SVR was increased in RA patients compared with controls matched for coronary artery disease (CAD) status, and to relate the results to vascular disease risk factors, including measures of inflammation. METHODS: Arterial elasticity was assessed by pulse wave analysis in RA patients with (n = 15) and without (n = 38) CAD, and in controls matched 1:1 for age, sex, and CAD status. Vascular risk factors, including high-sensitivity C-reactive protein (hsCRP), soluble vascular cell adhesion molecule 1 (sVCAM-1), and serum amyloid A (SAA) levels, were assessed. RESULTS: SAE and LAE were significantly lower and SVR was significantly higher in RA patients than in controls. RA patients also had higher levels of hsCRP, SAA, and sVCAM-1. SAE and LAE values were inversely correlated with markers of inflammation. Associations of SAE and LAE with RA were independent of conventional risk factors, but were dependent on markers of inflammation. CONCLUSION: Vascular function is abnormal in RA, with reduced SAE and LAE and increased SVR relative to controls. Arterial elasticity is inversely associated with measures of inflammation. These measures may be clinically useful in the detection and monitoring of vascular disease in RA.     

Age-related changes in aortic elasticity determined by gated radionuclide angiography in patients with systemic hypertension or healed myocardial infarcts and in normal subjects

We estimated the aortic volume elasticity (Ve), an index of aortic stiffness, using gated radionuclide angiography, and investigated age-related changes in aortic elasticity in 22 normal control subjects, 30 hypertensive patients and 36 patients with old myocardial infarction. Ve elasticity was calculated noninvasively as a ratio of the pressure change (dP) and the percent volume change (dV/Vo) determined by radionuclide angiography [Ve = dP/(dV/Vo)]. dV/Vo was calculated from the maximal and minimal counts in the aortic arch [dV/Vo = (maximum - minimum)/minimum]. Ve increased significantly with age in normal control subjects (r = 0.62, p less than 0.001), hypertensive patients (r = 0.60, p less than 0.001) and patients with old infarcts (r = 0.59, p less than 0.001). The age-related increase in Ve was significantly greater in hypertensive patients, and that for patients with old myocardial infarcts tended to be greater than in control subjects. Thus, hypertension accelerates the decrease in aortic elasticity with aging. The greater decrease in aortic elasticity resulted in a significant age-related increase in pulse pressure in patients with hypertension and old myocardial infarction.     

高血压病患者颈-股动脉和颈-桡动脉脉搏波速度改变及其影响因素

目的探讨不同年龄和血压水平的高血压病患者颈-股动脉和颈-桡动脉脉搏波速度的改变及其影响因素。方法应用脉搏波速度(pulse wave velocity,PWV)自动测量系统测定颈-股动脉PWV(CFPWV)和颈-桡动脉PWV(CRPWV)分别作为反映中央弹性大动脉和外周中等肌性动脉弹性功能的指标,对517例高血压患者[其中男272例,女245例,年龄17~82岁,平均(52.0±13.0)岁]和118例健康人[其中男52例,女66例,年龄19~82岁,平均(54.2±13.8)岁]进行PWV检测。结果健康人和高血压病患者颈-股动脉PWV均随年龄增大而增加(P<0.001),而颈-桡动脉PWV无此变化趋势;颈-股动脉PWV和颈-桡动脉PWV均随血压水平升高而增高(P<0.001)。多元逐步回归显示,年龄和收缩压是影响颈-股动脉PWV的独立因素;舒张压是影响颈-桡动脉PWV的独立因素(各标准化回归系数P<0.001)。结论年龄和血压组分对高血压患者中央弹性大动脉和外周中等肌性动脉弹性功能的影响不同。对大动脉弹性功能改变的检测较外周中等动脉有更重要的临床价值。     

The vascular smooth muscle of great arteries: local control site of arterial buffering function?

INTRODUCTION AND OBJECTIVES: To characterize the viscoelastic properties of the aorta and pulmonary arteries and the effects of vascular smooth muscle activation on arterial buffering function. MATERIAL AND METHOD: Aortic and pulmonary artery pressure and diameter were measured in six anesthetized sheep under baseline conditions, and during arterial hypertension induced by mechanical vascular occlusion (passive), and i.v. phenylephrine (active). Arterial wall elasticity and viscosity were calculated, and buffering function was characterized: a) locally as the viscosity/elasticity ratio, and b) globally for each circuit, as the time-constant of ventricular relaxation. RESULTS: Viscoelasticity was higher in the aorta than in the pulmonary artery (p < 0.05), however, parietal buffering function was similar in both. Global buffering function was highest in the systemic circuit (p < 0.05). During passive hypertension, elasticity was significantly increased with no change in viscosity; this led to a significant reduction in local buffering function, and in global buffering function in each circuit. During active hypertension, viscosity increased (p < 0.05), while local and global buffering functions returned to baseline values. CONCLUSIONS: The viscosity/elasticity ratio was higher in the aorta than in the pulmonary artery, and arterial wall buffering function was similar in both vessels. Systemic global buffering function was higher than pulmonary circuit buffering function. Elasticity depends on intravascular pressure, whereas viscosity is a marker of the degree of smooth muscle activation. Smooth muscle activation may benefit the cardiovascular system by maintaining local and global buffering functions.     

Is Isolated Systolic Hypertension Worse Than Combined Systolic/Diastolic Hypertension?

J Clin Hypertens (Greenwich). 2012;14:808–809. ©2012 Wiley Periodicals, Inc. New developments in cardiovascular translational sciences have significantly advanced our understanding of the endovascular biology of blood pressure. Reductions in vascular elasticity and vessel compliance of conduit arteries are key components of both ISH and SDH. Vascular changes from the matrix metalloproteinase family of enzymes are involved in arterial wall remodeling and vascular stiffness. This new translational information helps further our understanding of both ISH and SDH.     

Relationship between C-reactive protein and arterial stiffness in an asymptomatic population

Plasma concentration of high sensitive C-reactive protein (hsCRP) is used as a marker for inflammatory states and is directly correlated with the risk for coronary heart disease. Evidence concerning the role of inflammation in atheroma formation has been derived from several models of atherosclerosis. Inflammation should exert its adverse vascular effects by structural changes in the artery wall and consequently alterations in arterial elasticity, which could be detected already in asymptomatic early vascular disease. We hypothesized that CRP is related to large artery elasticity, but not to small artery elasticity in early vascular disease. Therefore, we examined the association between arterial stiffness of large and small arteries and inflammation in an asymptomatic population referred for primary prevention cardiovascular screening. Studies were performed in 391 subjects (age 21-82 years; 254 men, 137 women) who underwent screening at the Cardiovascular Disease Prevention Center. Large artery (C1) and small artery (C2) elasticity indices were obtained by the CVProfiler 2000 (HDI, Eagan, MN, USA). After overnight fasting, venous samples were taken for measurement of hsCRP, lipids, glucose. There was a significant inverse correlation between hsCRP (0.29 +/- 0.40 mg/dl) and C1 (16.7 +/- 5.8 ml/mmHg), r = -0.133, P = 0.01; there was no significant correlation between hsCRP and C2 (6.6 +/- 3.2 ml/mmHg). C2, but not hsCRP, was inversely correlated with age, abnormal lipids and glucose, whereas C1, but not hsCRP, was inversely correlated with age and systolic blood pressure (SBP). In multiple regression analysis, the relationship between hsCRP and C1 was not affected by age, body mass index, SBP, serum glucose or lipids. In conclusion, these findings support the hypothesis that hsCRP, a marker for acute and low-grade inflammation, is associated with large artery but not with small artery elasticity in asymptomatic individuals undergoing primary prevention cardiovascular screening.     

Impaired endothelial progenitor cell activity is associated with reduced arterial elasticity in patients with essential hypertension

Endothelial dysfunction is related to reduced arterial elasticity in patients with essential hypertension. Circulating endothelial progenitor cells (EPCs), an important endogenous repair approach for endothelial injury, is altered in hypertensive patients. However, the association between alteration in circulating EPCs and hypertension-related reduced arterial elasticity has not been reported. The purpose of this study is to investigate the association between alteration in circulating EPCs and hypertension-related reduced arterial elasticity. We measured the artery elasticity profiles including brachial-ankle PWV (baPWV) and C1 large and C2 small artery elasticity indices in patients with essential hypertension (n = 20) and age-matched normotensive subjects (n = 21). The number and activity of circulating EPCs isolated from peripheral blood were determined. Compared to normotensive subjects, the patients with hypertension exhibited decreased C1 large and C2 small artery elasticity indices, as well as increased baPWV. The number of circulating EPCs did not differ between the two groups. The migratory and proliferative activities of circulating EPCs in hypertensive patients were lower than those in normotensive subjects. Both proliferatory and migratory activities of circulating EPCs closely correlated with arterial elasticity profiles, including baPWV and C1 large and C2 small artery elasticity indices. Multivariate analysis identified both proliferative and migratory activities of circulating EPCs as independent predictors of the artery elasticity profiles. The present study demonstrates for the first time that impaired activity of circulating EPCs is associated with reduced arterial elasticity in patients with hypertension. The fall in endogenous repair capacity of vascular endothelium may be involved in the pathogenesis of hypertension-related vascular injury.     

Mitochondria and cardiovascular aging

Old age is a major risk factor for cardiovascular diseases. Several lines of evidence in experimental animal models have indicated the central role of mitochondria both in lifespan determination and in cardiovascular aging. In this article we review the evidence supporting the role of mitochondrial oxidative stress, mitochondrial damage and biogenesis as well as the crosstalk between mitochondria and cellular signaling in cardiac and vascular aging. Intrinsic cardiac aging in the murine model closely recapitulates age-related cardiac changes in humans (left ventricular hypertrophy, fibrosis and diastolic dysfunction), while the phenotype of vascular aging include endothelial dysfunction, reduced vascular elasticity, and chronic vascular inflammation. Both cardiac and vascular aging involve neurohormonal signaling (eg, renin-angiotensin, adrenergic, insulin-IGF1 signaling) and cell-autonomous mechanisms. The potential therapeutic strategies to improve mitochondrial function in aging and cardiovascular diseases are also discussed, with a focus on mitochondrial-targeted antioxidants, calorie restriction, calorie restriction mimetics, and exercise training.     

Arterial elasticity and erectile dysfunction in hypertensive men

Erectile dysfunction is a common symptom among hypertensive patients that impairs quality of life and adherence to antihypertensive pharmacologic therapy. It is also associated with cardiovascular risk factors and disease. The Sexual Health Inventory in Men (SHIM) was administered to 105 ambulatory hypertensive patients, and large and small artery elasticity indices were measured. Each variable was examined in a simple linear regression model or 1-way analysis of variance model to determine each variable's relationship with the SHIM score. Variables that were significantly associated with the SHIM score in the univariate models included age, duration of hypertension, peripheral vascular disease, and small artery elasticity. Large artery elasticity was not significantly associated with the SHIM score. In the multivariate model, age, hypertension duration, and peripheral vascular disease were associated with a lower SHIM score. This study demonstrates a relationship between erectile dysfunction and reduced artery elasticity.     

Aging-related skin changes: development and clinical meaning

The medical literature is replete with articles that discuss the spectrum of sun-induced changes in human skin. These extrinsic, actinically induced changes, more prevalent in the elderly, include wrinkling and loss of elasticity; dyspigmentation; vascular ectasias and hemorrhage; atrophy; and benign and malignant neoplasms. This article, however, focuses on the intrinsic changes behind geriatric skin problems, providing a non-specialist's illustrated guide to recognizing structural and functional changes due to normal, chronological aging and how they manifest clinically in elderly patients.