Stiffness index derived from digital volume pulse as a marker of target organ damage in untreated hypertension

OBJECTIVE: An index of large artery stiffness (SIDVP) simply derived from the digital volume pulse (DVP) was developed recently. However, the role of the SIDVP in untreated hypertensive patients was not well elucidated. METHODS: We enrolled 124 untreated hypertensive patients (mean age 55.4+/-13.1 years, 57 men). The DVP was measured in right index finger by a photoplethysmography. The SIDVP was formulated as body height divided by transition time from early systolic peak to the inflection point of reflection wave. Two functional indices of aortic compliance, stiffness index (SI) and distensibility (DI), were also used for measurement of aortic stiffness. RESULTS: The SIDVP was significantly correlated with blood urea nitrogen (BUN), and left ventricular mass index (LVMI). Patients with vascular diseases had higher level of SIDVP (10.12+/-2.97 vs 8.45+/-1.78, p<0.001), SI (13.76+/-7.63 vs 10.87+/-8.88, p=0.116), BUN (28.4+/-24.7 vs 14.5+/-4.6, p<0.001) and lower level of DI (1.34+/-0.88 vs 1.93+/-1.12, p=0.010) than those without vascular diseases. By multivariate analysis, only the SIDVP was significantly associated with vascular diseases (OR 1.39, 95% CI 1.06-1.82, p=0.016). CONCLUSIONS: SIDVP, SI and DI were significantly correlated with target organ damage in untreated hypertension. However, only the SIDVP was independently associated with presence of vascular diseases. SIDVP simply derived from the DVP can be used as a marker for risk stratification in untreated hypertensive patients.     

The vascular impact of aging and vasoactive drugs: comparison of two digital volume pulse measurements

BACKGROUND: Indices of pressure wave reflection (RI(DVP)) and large artery stiffness (SI(DVP)) can be derived from the digital volume pulse (DVP). Indices obtained from the second derivative of the DVP have also been proposed to characterize vascular aging and effects of vasoactive drugs. METHODS: We compared RI(DVP) and SI(DVP) with the indices a/b, a/c, a/d, and a/e calculated from sequential peaks of the second derivative of the DVP in 124 healthy men. The DVP was obtained by measuring infrared light transmission through the finger. In 10 men measurements were obtained at baseline and during intravenous infusion of glyceryl trinitrate (GTN, 3 to 300 microg/min) and, on separate occasions, angiotensin II (AII, 75 to 300 microg/min) and saline vehicle. RESULTS: SI(DVP) was strongly associated with age (R = 0.63, P <.001) but little influenced by AII or GTN. RI(DVP) was weakly associated with age but showed a consistent dose-dependent increase during AII and a decrease during GTN. d/a was strongly associated with age (R = -0.66, P <.001), influenced by vasoactive drugs but did not change in a dose-dependent manner during GTN. Other second derivative indices were less strongly correlated with age and showed an inconsistent response to vasoactive drugs. Within subject standard deviations of SI(DVP) and d/a for measurements on different occasions were 2.1 and 5.4 "years of vascular aging" respectively. CONCLUSIONS: In healthy men, RI(DVP) may be a more reliable index of the effects of vasoactive drugs than d/a. SI(DVP) is similarly associated with age as is d/a, but less variable and may thus be a better index of vascular aging.     

Circulating endothelial cells, arterial stiffness, and cardiovascular risk stratification in hypertension

BACKGROUND: Given the growing burden of cardiovascular disease, there is increasing interest in strategies to help predict future cardiovascular risk. Aims: To investigate the relationship between endothelial damage/dysfunction, arterial stiffness, and their association with predicted risk of future cardiovascular death among patients with hypertension. METHODS: We studied three patient groups 35 to 74 years old: healthy control subjects (n=63), subjects with high-risk hypertension (HHT) [n=65], and patients with treated, previously diagnosed, malignant-phase hypertension (MHT) [n=43]. We measured comparative indexes of arterial stiffness (stiffness index [SI] using digital volume photoplethysmography), endothelial damage/dysfunction (venous circulating endothelial cells [CECs], immunobead technique), and 5-year predictive risk of future cardiovascular death (Pocock scoring system). RESULTS: CEC counts, SI, and 5-year prediction of cardiovascular death were significantly higher in both hypertension groups (HHT and MHT), compared with healthy control subjects. CEC counts were significantly higher in the MHT group (p<0.05). There was a significant correlation between CECs and SI in the HHT group (r=0.61; p<0.0001) and the MHT group (r=0.59, p<0.0001) and between CEC, SI, and predicted 5-year risk of cardiovascular death in the two hypertension groups. On multiple linear regression analysis, arterial SI and CECs remained as significant predictors of the calculated 5-year risk of cardiovascular death (R2=0.37; p<0.0001). CONCLUSION: There is a consistent association between CECs, arterial stiffness, and the predictive risk of cardiovascular death among a group of patients with HHT or previously treated MHT. Registration number 05/Q2709/1.     

Association of increased arterial stiffness and inflammation with proteinuria and left ventricular hypertrophy in non-diabetic hypertensive patients

OBJECTIVE: Both arterial stiffness and proteinuria are important markers for organ damage in hypertension. This study was planed to investigate the association between arterial stiffness and inflammation and to define the influences of proteinuria on arterial stiffness and inflammation in non-diabetic hypertension. METHODS: We enrolled 205 patients (mean age 41 +/- 8 years, 66 women) with essential hypertension noted for less than 5 years in this study. They did not have diabetes mellitus or any overt cardiac, vascular, or renal complications. Stiffness index (SI) derived from digital volume pulse was used for assessment of arterial stiffness. High-sensitivity C-reactive protein (hsCRP) was measured in each patient during enrollment. Left ventricular hypertrophy (LVH) was documented by electrocardiography and proteinuria was assessed by measuring 24-h urine protein. RESULTS: SI was significantly correlated with hsCRP (r = 0.166, p = 0.017). LVH was noted in 34 patients (17%). SI was significantly higher in patients with LVH (8.03 +/- 1.74 vs 7.19 +/- 1.19 m/s, p = 0.001). Proteinuria was noted in three patients with LVH. SI was gradually increased among patients without LVH, with LVH but not proteinuria, and with LVH and proteinuria (7.19 +/- 1.19, 7.68 +/- 1.21, 11.75 +/- 2.51 m/s respectively; p<0.001). HsCRP was also gradually increased among patients without LVH, with LVH but not proteinuria, and with LVH and proteinuria (0.20 +/- 0.24, 0.30 +/- 0.59, 1.56 +/- 1.58 mg/dl respectively; p<0.001). CONCLUSIONS: SI was significantly correlated with hsCRP. Arterial stiffness and inflammation were increased in association with proteinuria in non-diabetic essential hypertension.     

Comparison of photoplethysmographic and arterial tonometry-derived indices of arterial stiffness

Arterial tonometry is a method to assess arterial stiffness and has become a valuable tool in the stratification of cardiovascular risk. The arterial tonometry-derived augmentation index (AIx) is a marker of arterial stiffness and an independent predictor of mortality. As the AIx is relatively cumbersome to obtain, simpler methods such as analysis of pulse waves obtained by digital photoplethysmography have been proposed to estimate arterial stiffness. The objective of this study is to compare the usefulness of the stiffness index (SI) derived from digital photoplethysmography and the AIx derived from radial tonometry for stratification of cardiovascular risk. We studied 83 subjects with a heterogeneous cardiovascular risk profile and determined the ability of the two devices to differentiate subjects with low from subjects with high cardiovascular risk estimated by the Europe (EU)-heart score. Failure rate in both devices was similar (3.6%). AIx and SI were modestly correlated (r=0.48, P<0.001) and both indexes correlated with the EU-score (r=0.54, P<0.001) and (r=0.56, P<0.001), respectively. Both devices discriminated accurately between subjects with high cardiovascular risk (upper tertile of the EU-score) and low cardiovascular risk (lower tertile). However, only the SI differentiated significantly between subjects with intermediate risk (middle tertile) and high risk (upper tertile). Compared with the AIx, assessment of the SI derived by digital photoplethysmography is simple and possibly yields an advantage in risk stratification of subjects with intermediate and high cardiovascular risk. Therefore, digital pulse wave analysis may be a valuable tool to estimate arterial stiffness in large clinical studies.     

Combined effects of brachial pulse pressure and sialic acid for risk of cardiovascular events during 40 years of follow-up in 37 843 individuals

OBJECTIVE:: Pulse pressure (PP) is a risk marker for cardiovascular disease (CVD) in individuals 50 years and older. Inflammation is suggested to influence atherosclerosis, but could also increase PP. We aimed to examine the combined effects of PP and the inflammatory marker sialic acid, and their independent roles on CVD risk. METHODS:: From a population-based study in Sweden between 1962 and 1965, 18?429 men and 19?414 women at the age of 50 or older were selected and followed for first CVD event until 2005. We investigated the biological interactions between sialic acid and PP. The associations of PP and sialic acid with risk of CVD were calculated by using Cox proportional hazards model. Adjustments were made for conventional risk factors, mean arterial pressure (MAP) and socioeconomic status. RESULTS:: The mean age was 59.5 (SD 6.5) years and the number of incident CVD events in men and women were 3641 and 3227, respectively. No biological interaction was seen between PP and sialic acid. In men, the adjusted hazard ratio for PP was 0.92 [95% confidence interval (CI) 0.88-0.96, P?相似文献   

Abnormal soluble CD40 ligand and C-reactive protein concentrations in hypertension: relationship to indices of angiogenesis

BACKGROUND: Abnormal inflammation, platelets and angiogenesis are involved in the pathophysiology of cardiovascular disease (CVD). OBJECTIVE: To test the hypothesis that concentrations of high sensitive C-reactive protein (CRP, an index of inflammation) and soluble CD40 ligand (sCD40L, an index of platelet activation) would be abnormal in hypertension, and in turn, be related to plasma indices of angiogenesis, the angiopoietins-1 and -2, and vascular endothelial growth factor (VEGF), in addition to the presence or absence of CVD. METHODS: Using a cross-sectional approach, we measured plasma concentrations of CRP, sCD40L, VEGF, and angiopoietins-1 and -2 in 147 patients with hypertension (85 with a history of CVD event/s, 62 CVD event-free) and 68 age- and sex-matched healthy controls. RESULTS: Concentrations of sCD40L (P = 0.039), CRP (P < 0.001), angiopoietin-1 (P < 0.001), angiopoietin-2 (P = 0.003) and VEGF (P < 0.001) were all greater amongst hypertensive patients than in controls. There were no significant differences in sCD40L and VEGF concentrations between hypertensive individuals with and without CVD events, but CRP and angiopoietin-1 concentrations were significantly greater amongst those with CVD events. On multiple regression analysis, sCD40L was associated with angiopoietin-2 (P = 0.01) and VEGF (P = 0.007) in hypertensive individuals, but no such associations were found within the healthy control group. CONCLUSION: In patients with hypertension, sCD40L was associated with increased circulating markers of abnormal angiogenesis (angiopoietin-2, VEGF). The interaction between sCD40L and angiogenesis may contribute to the pathophysiology of CVD in hypertension.     

Aortic diameter, wall stiffness, and wave reflection in systolic hypertension

Systolic hypertension is associated with increased pulse pressure (PP) and increased risk for adverse cardiovascular outcomes. However the pathogenesis of increased PP remains controversial. One hypothesis suggests that aortic dilatation, wall stiffening and increased pulse wave velocity result from elastin fragmentation, leading to a premature reflected pressure wave that contributes to elevated PP. An alternative hypothesis suggests that increased proximal aortic stiffness and reduced aortic diameter leads to mismatch between pressure and flow, giving rise to an increased forward pressure wave and increased PP. To evaluate these two hypotheses, we measured pulsatile hemodynamics and proximal aortic diameter directly using tonometry, ultrasound imaging, and Doppler in 167 individuals with systolic hypertension. Antihypertensive medications were withdrawn for at least 1 week before study. Patients with PP above the median (75 mm Hg) had lower aortic diameter (2.94+/-0.36 versus 3.13+/-0.28 cm, P<0.001) and higher aortic wall stiffness (elastance-wall stiffness product: 16.1+/-0.7 versus 15.7+/-0.7 ln[dyne/cm], P<0.001) with no difference in augmentation index (19.9+/-10.4 versus 17.5+/-10.0%, P=0.12). Aortic diameter and wall stiffness both increased with advancing age (P<0.001). However, an inverse relation between PP and aortic diameter remained significant (P<0.001) in models that adjusted for age, sex, height, and weight and then further adjusted for aortic wall stiffness, augmentation index, and mean arterial pressure. Among individuals with systolic hypertension, increased PP is primarily attributable to increased wall stiffness and reduced aortic diameter rather than premature wave reflection.     

Association of pulse waveform characteristics with birth weight in young adults

OBJECTIVE: An association between birth weight and blood pressure has been reported in many studies, but the strength of this association has been disputed. Birth weight could, however, be associated with alterations in the proximal arterial tree that have little effect on blood pressure. The objective of this study was to examine the relationship between birth weight and characteristics of the proximal arterial tree determined by pulse wave analysis. METHODS: An optically derived digital volume pulse was used to obtain indices of pressure wave reflection (reflection index; RI) determined by characteristics of small/medium sized arteries and of large artery stiffness (stiffness index; SI) in healthy young adults (n = 220, 111 women, aged 16-26 years). Birth weight was obtained from maternal recall. RESULTS: Diastolic blood pressure was significantly correlated with birth weight (P < 0.001) but birth weight accounted for only 5% of the variance in diastolic blood pressure. RI was significantly correlated with birth weight in women (r = -0.33, P < 0.001) but not in men, and there was a significant interaction between birth weight and sex (P < 0.001). SI was significantly independently correlated with birth weight in both men and women (r = -0.41 and -0.49, each P < 0.0001) and birth weight accounted for 17% of the overall (men and women) variance in SI. CONCLUSIONS: These results suggest a close association between birth weight and characteristics of the arterial tree proximal to resistance vessels in young adults and a sex-specific association with characteristics influencing arterial pressure wave reflection.     

原发性高血压并发心脑血管疾病患者的危险因素分析

目的：研究原发性高血压（EH）伴冠心病和／或脑血管病患者的临床特点，分析其相关的危险因素。方法：对55例EH伴冠心病和／或脑血管病患者，进行动脉硬化指数（ASI）测定，并检测患者的血尿酸、血糖、血脂、肌酐、尿素氮等血液生化指标及一般情况。另选不伴有冠心病、脑血管病的高血压患者63例作为对照。结果：与单纯高血压对照组比较，EH伴冠心病和／或脑血管的年龄大、病史时间长，ASI、脉压、血尿素氮水平明显升高（均P〈0.01）；收缩压、血尿酸、总胆固醇、肌酐水平也升高（均P〈0．05）；而舒张压（P〈0．01），心率（P〈0．05）却较低。多因素logistic回归分析显示：EH并发心脑血管疾病的相关危险因素有脉压、血肌酐、年龄（OR=1．204，1．120，1．099,P=0．028，0．045，0．039）；而血尿酸是负相关因素（OR=0．974，P=0．022）。结论：脉压、血肌酐水平和年龄可能是高血压患者并发心脑血管疾病的危险因素；血尿酸可能是一种保护因素。     

Effects of glycaemic control on cardiovascular disease in diabetic American Indians: the Strong Heart Study.

AIMS: Diabetes increases the risk of cardiovascular disease (CVD). Only part of this excess risk is explained by diabetes-associated hypertension, obesity, and lipid disorders. Poor glycaemic control may help explain the residual CVD risk. The aim of this study was to determine whether variations in glycaemic control are associated with CVD risk in diabetic individuals. METHODS: We examined longitudinal data from the Strong Heart Study, a population-based study of CVD and its risk factors among American Indians (a population with a high prevalence of diabetes). Diabetes was defined using the 1998 World Health Organization criteria: fasting plasma glucose >/= 126 mg/dl or 2-h plasma glucose >/= 200 mg/dl. American Diabetes Association guidelines for glycaemic control were used: good, A(1c) < 7%; fair, 7-7.9%; and poor, >/= 8%. The analysis was based on data from diabetic individuals with no CVD at baseline. RESULTS: During 9 years of follow-up, 494 of the 2011 diabetic participants developed CVD. Although Cox multivariate regression modelling showed dose-response effects of glycaemic control on overall CVD and coronary heart disease (CHD) incidence, the relationships were weakened when adjusted for confounding variables. Kaplan-Meier analysis, however, showed that diabetic individuals with poor baseline glycaemic control had significantly increased proportions of overall CVD and CHD (P = 0.001) during the 9 years of follow-up, compared with those who had good or fair control. CONCLUSIONS: These findings highlight the importance of risk factors, such as high blood pressure and dyslipidaemia, in increasing CVD risk in those with diabetes.     

Relationship between low-grade inflammation and arterial stiffness in patients with essential hypertension

BACKGROUND: Arterial stiffness is an independent cardiovascular risk factor in hypertensive individuals. Inflammation is associated with increased arterial stiffness and is implicated in the pathogenesis of hypertension. OBJECTIVES: To examine whether low-grade inflammation contributes to arterial stiffness and wave reflections independently of blood pressure, in patients with essential hypertension and in controls. METHODS: We studied 235 consecutive patients with uncomplicated, never-treated essential hypertension and 103 sex- and age-matched controls. The level of inflammation was evaluated with high-sensitivity C-reactive protein (hsCRP) and serum amyloid A (SAA). Arterial stiffness was assessed with carotid-femoral (c-f) and carotid-radial (c-r) pulse wave velocity (PWV), and wave reflections with augmentation index (AIx). RESULTS: In the hypertensive group, in multiple regression analysis, both PWVc-f and PWVc-r were independently correlated with log hsCRP (beta = 0.56, P = 0.006 and beta = 0.45, P = 0.016, respectively), whereas no correlation was found between PWV and log SAA (P = NS). No significant correlation was observed between heart-rate-corrected AIx and log hsCRP (P = NS) and log SAA (P = 0.07) in the same group. Similarly, in the control group, an independent association was observed between PWVc-f and PWVc-r with log hsCRP (beta = 0.68, P = 0.05 and beta = 0.74, P = 0.05 respectively), but not with log SAA (P = NS). Furthermore, no significant association was shown between heart-rate-corrected AIx and log hsCRP or log SAA (P = NS) in the control group. CONCLUSIONS: In hypertensive individuals, hsCRP is related to PWV, a direct marker of arterial stiffness, but not to AIx, a measure of wave reflections. Whether inflammation might act as a pathogenetic or modulating factor in arterial stiffening in chronic hypertension has to be confirmed.     

Decreased flow-mediated dilatation with increased arterial stiffness and thickness as early signs of atherosclerosis in polymyositis and dermatomyositis patients

Several autoimmune rheumatic diseases have been associated with accelerated atherosclerosis or other different types of vasculopathy depending on the underlying disease, leading to increased cardio- and cerebrovascular disease risk. Polymyositis (PM) and dermatomyositis (DM), members of idiopathic inflammatory myopathies (IIMs), a group of systemic autoimmune diseases are also associated with elevated risk of cardiovascular diseases (CVD). Up until now, no specific data is known on the mechanisms, risk factors, or possible vasculopathy leading to increased CVD risk. The aims of the present study were to assess the flow-mediated dilatation of the brachial artery by a TensioClinic arteriograph and to measure the thickness of carotid artery intima–media, the augmentation index, and the pulse wave velocity using high-resolution ultrasonography in a cohort of PM and DM patients. We also investigated the correlation of these parameters with the traditional risk factors of atherosclerosis and overall cardiovascular status within PM and DM patients. Twenty-seven patients (21 females, six males) with IIMs were enrolled in this study, and 38 healthy individuals matched for sex and age served as controls. We found a decreased flow-mediated dilatation in the brachial artery (6.36 vs. 8.39 %) with increased arterial stiffness and carotid artery thickness in our patients compared to healthy controls. We found significantly decreased flow-mediated dilatation of the brachial artery (5.57 vs. 8.39 %) in DM patients. We also detected a correlation between these parameters and the traditional cardiovascular risk factors, as well as hypertriglyceridemy, hypertension, and peripheral arterial disease. In DM, overall, more vascular abnormalities were found than in PM. Our findings suggest that flow-mediated dilatation of the brachial artery, arterial stiffness, and carotid artery thickness measurements could be beneficial for predicting the CVD risk in myositis patients. Further investigations need to find the potential differences and role of inflammation and immune mechanisms in atherosclerotic processes in DM and PM.     

Clinical utility of digital volume pulse analysis in prediction of cardiovascular risk and the presence of angiographic coronary artery disease

BackgroundStiffness Index (SI), assessed by finger photoplethysmography (digital volume pulse analysis), has been suggested as a simple and easy measure of arterial stiffness. However, its potential association with cardiovascular risk and coronary artery disease (CAD) has been little studied. The aims of the study were to investigate the relation of SI with classical risk factors and established arterial stiffness indices and its ability to predict cardiovascular risk and the presence of angiographic CAD.MethodsWe enrolled 126 consecutive patients (mean age 61 years, 74% males) with suspected stable CAD undergoing diagnostic coronary angiography. Cardiovascular risk was assessed using Framingham risk score (FRS) and the European Heart score. Carotid-femoral (PWVcf) and carotid-radial (PWVcr) pulse wave velocity and augmentation index, using applanation tonometry, and SI using finger photoplethysmography, were measured in all patients.ResultsSI was positively correlated with PWVcr (p = 0.017) but not with PWVcf. Increased SI (R² 0.19, p < 0.001) was independently associated with higher diastolic blood pressure and male gender. Increased SI and PWVcf were associated with higher FRS and Heart score (p < 0.05 for all), while only higher PWVcf was associated with the presence of angiographic CAD (p = 0.007).ConclusionsSI, easily derived using finger photoplethysmography, was related to classical risk factors and peripheral arterial rather than aortic stiffness. SI and PWVcf were the only vascular indices associated with cardiovascular risk, but only PWVcf was related to the presence of coronary atherosclerosis. Further research is needed to clarify the value of this useful index of arterial stiffness in risk stratification.     

Ambulatory arterial stiffness index, pulse wave velocity and augmentation index--interchangeable or mutually exclusive measures?

BACKGROUND: The ambulatory arterial stiffness index (AASI) has been proposed as a novel measure of arterial stiffness and has been prospectively shown to predict stroke and cardiovascular death, but not cardiac death. This index has prompted considerable controversy as to whether it is a true measure of arterial stiffness. OBJECTIVE AND METHODS: The present study aimed to examine three different measures of arterial stiffness - pulse wave velocity (PWV; Complior), wave reflection [augmentation index (AIx)] and AASI - in a large hypertensive population, comparing their determinants and intercorrelations, both unadjusted and adjusted for confounders, and using Bland-Altman analysis to determine 95% confidence intervals for the ability of the AASI to predict PWV, the proposed gold standard of arterial stiffness. RESULTS: The AASI correlated univariately with both PWV and the AIx in individuals overall (r = 0.28 for PWV and r = 0.24 for AIx; both P < 0.001) and in those with untreated or treated hypertension. Adjustment for age in the current study negated entirely the positive correlation between the AASI, PWV and AIx. Additional adjustment for confounders did not significantly alter these nonsignificant relationships. Furthermore, the 95% prediction limits for the AASI to predict PWV were +/- 4.18 m/s and for the AASI to predict AIx were +/- 25.4%, suggesting that the methods would not be interchangeable in a clinical setting. Direct comparative studies would be required to establish the relative predictive strength of each measure and whether combining measures can provide additional risk prediction. Until such data become available, we propose that the measures should not be considered interchangeable.     

Effects of Blood Pressure, Smoking, and Their Interaction on Carotid Artery Structure and Function

-In the present study, we examined the relationships among carotid blood pressure, arterial geometry, and wall stress and determined the impact of hypertension, smoking status, and their interaction on these relationships. The study involved 679 subjects aged 49 to 82 years: 372 smokers (190 men and 182 women) and 307 nonsmokers (110 men and 197 women). Blood samples were taken to determine total cholesterol levels. Central pulse pressure was derived from measured brachial artery pressure with a linear regression equation from data obtained in a subgroup of 276 subjects that related brachial and carotid pulse pressures; the latter was measured with applanation tonometry. Carotid intima-media thickness (IMT), lumen diameter (D), and stiffness index (SI) were determined with high-resolution B-mode ultrasound. Mean and pulsatile circumferential stress (final sigma(C)) was calculated according to the Laplace relationship. Indexes of arterial geometry and function were adjusted for age, height, and heart rate. Hypertension (treated and/or screening blood pressure of >140/90 mm Hg) was present in 71 nonsmokers and 186 smokers. Nonsmokers and smokers did not differ in blood pressure and cholesterol levels. Hypertension and smoking individually and interactively significantly increased adjusted IMT, D, and SI. The radius-to-wall thickness ratio (R/IMT) (where R=D/2) and final sigma(C) were increased in hypertensives. SI was correlated with IMT (r=0.56, P:<0.001); radius-to-wall thickness ratio was inversely correlated with central pulse pressure (r=-0.38, P:<0.001). Smoking did not influence these relationships. In conclusion, carotid artery wall remodeling appears to follow Laplace's law but is insufficient to prevent an increase in circumferential stress in hypertensive subjects. Unlike hypertension, smoking does not influence the lumen-to-wall ratio but has a significant effect on wall stiffness.     

Regional body composition as a determinant of arterial stiffness in the elderly: The Hoorn Study

OBJECTIVE: To estimate the relation of precisely measured regional body composition with peripheral and central arterial stiffness in the elderly. METHODS: We investigated 648 participants (mean age 69.0 +/- 6.0 years) of the Hoorn Study, a population-based cohort study. Trunk fat, leg fat, trunk lean and leg lean mass were distinguished by dual-energy X-ray absorptiometry. We used ultrasound to measure the distensibility and compliance of the carotid, femoral and brachial arteries, and carotid Young's elastic modulus, as estimates of peripheral stiffness. As estimates of central stiffness we measured carotid-femoral transit time, aortic augmentation index and systemic arterial compliance. RESULTS: After adjustment for sex, age, height, mean arterial pressure, leg lean and leg fat mass, a larger trunk fat mass was consistently associated with higher peripheral arterial stiffness (standardized beta (beta) of mean Z-scores of all three large arteries -0.24, P < 0.001). In contrast, larger leg fat mass (beta = 0.15, P = 0.009) and leg lean mass (beta = 0.09, P = 0.20) were associated with lower peripheral arterial stiffness. Trunk or leg fat mass were not associated with central arterial stiffness. Leg lean mass, however, was consistently associated with lower central arterial stiffness (beta = 0.29, P < 0.001). CONCLUSIONS: Trunk fat mass may have adverse effects on peripheral, but not on central arterial stiffness, while leg fat was not harmful and may have a slight protective effect. Larger leg lean mass was the most important determinant of lower central arterial stiffness. These results provide a pathophysiological framework to explain not only the higher cardiovascular risk in individuals with larger trunk fat mass, but also the reduced cardiovascular risk in individuals with larger leg lean and fat mass.     

A New Two-Pulse Synthesis Model for Digital Volume Pulse Signal Analysis

Analysis of digital volume pulse (DVP) signal measured by photoplethysmograph (PPG) technique is a low cost non-invasive method of obtaining vital information related to arterial conditions. In this paper, we present a new two-pulse synthesis (TPS) model for deriving arterial parameters, useful for noninvasive assessment of human vascular health. The model is based on the use of Rayleigh function. Relevance of the proposed model is established by applying it on a sample set of 113 PPG signals, obtained form healthy and treated hypertensive subjects. The TPS model compares well with the conventional methods in determining parameters such as pulse transit time or foot-to-foot delay (D), reflection index (RI), stiffness index (SI) and pulse wave velocity (PWV). A new parameter, viz. differential pulse spread (DPS) has also been introduced for DVP signals using the model. The differential pulse spread provides a new dimension to estimate the process of arterial degeneration.     

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.     

Diabetes,pulse pressure and cardiovascular mortality: the Hoorn Study

OBJECTIVE: Type 2 diabetic patients have an increased arterial stiffness and a very high risk of cardiovascular death. The present study investigated the relationship between pulse pressure, an indicator of vascular stiffness, and risk of cardiovascular mortality among type 2 diabetic and non-diabetic individuals. Second, we determined the relationship between pulse pressure and its main determinant (i.e. age), and the influence of diabetes and mean arterial pressure on this relationship. DESIGN AND METHODS: We studied a cohort of 2484 individuals including 208 type 2 diabetic patients. Mean age and median follow-up for non-diabetic and diabetic individuals, respectively, were 61 and 66 years, and 8.8 and 8.6 years. One-hundred and sixteen non-diabetic and 34 diabetic individuals died of cardiovascular causes. Relative risks of cardiovascular mortality were estimated by Cox proportional hazards regression adjusted for age, gender and mean arterial pressure. RESULTS: Pulse pressure was associated with cardiovascular mortality among the diabetic, but not among the non-diabetic individuals [adjusted relative risk (95% confidence interval) per 10 mmHg increase, 1.27 (1.00-1.61) and 0.98 (0.85-1.13), P interaction = 0.07]. Further adjustment for other risk factors gave similar results. The association, at baseline, between age and pulse pressure was dependent on the presence of diabetes (P interaction = 0.03) and on the mean arterial pressure (P interaction< 0.001) (i.e. there was a stronger association when diabetes was present and when mean arterial pressure was higher). CONCLUSIONS: We conclude that, in type 2 diabetes, pulse pressure is positively associated with cardiovascular mortality. The association between age and pulse pressure is influenced by the presence of type 2 diabetes and by the height of the mean arterial pressure. These findings support the concept of accelerated vascular aging in type 2 diabetes.