Age-Related Abnormalities in Arterial Compliance Identified by Pressure Pulse Contour Analysis

McVeigh, Gary E.; Bratteli, Christopher W.; Morgan, Dennis; Alinder, C.; Glasser, Stephen P.; Finkelstein, Stanley M.; Cohn, Jay N.

doi:10.1161/01.hyp.33.6.1392

Cited by 331 publications

(234 citation statements)

References 49 publications

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“…28 Ageing produces a progressive decline in both large artery and small artery elasticity consistent with the well-recognized relationship between age and the risk for cardiovascular events. 29 In contrast, CRP did not increase with age and did not correlate with small artery elasticity, a marker for endothelial dysfunction, or with the biochemical markers for atherosclerosis risk. Thus CRP appears to serve as an accelerator of atherosclerosis in individuals who exhibit early disease, not as an initiator of the process (Table 5).…”

Section: Discussionmentioning

confidence: 84%

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

et al. 2005

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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 (0.2970.40 mg/dl) and C1 (16.775.8 ml/mmHg), r ¼ À0.133, P ¼ 0.01; there was no significant correlation between hsCRP and C2 (6.673.2 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.

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Section: Discussionmentioning

confidence: 84%

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

et al. 2005

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“…4 A wrist stabilizer was positioned on the right wrist using two hook and loop straps in order to gently immobilize the wrist and stabilize the radial artery, making it readily accessible for placement of the Arterial pulsewavet Sensor. The Sensor electronically adjusts itself automatically in order to obtain an acceptable waveform.…”

Section: -10mentioning

confidence: 99%

“…Reduced arterial elasticity is a hallmark of ageing that precedes apparently obstructive atherosclerosis and cardiovascular events. [1][2][3][4] Our recent studies demonstrated that decreased arterial elasticity is associated with endothelial dysfunction in humans with ageing and measurement of arterial elasticity may be used as a novel index for the determination of endothelial function. 5 The mechanisms responsible for the age-related reduction in arterial elasticity and endothelium-dependent vasodilatation, however, have not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Circulating endothelial progenitor cell deficiency contributes to impaired arterial elasticity in persons of advancing age

et al. 2006

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Reduced arterial elasticity is a hallmark of ageing in healthy humans and appears to occur independently of coexisting disease processes. Endothelial-cell injury and dysfunction may be responsible for this fall in arterial elasticity. We hypothesized that circulating endothelial progenitor cells (EPCs) are involved in endothelial repair and that lack of EPCs contributes to impaired arterial elasticity. A total of 56 healthy male volunteers were divided into young (n ¼ 26) and elderly (n ¼ 30) groups. Large and small artery elasticity indices were noninvasively assessed using pulse wave analysis. The number of circulating EPCs was measured by using flow cytometry. Cells demonstrating DiI-acLDL and FITC-ulex lectin double-positive fluorescence were identified as EPCs. C1 large artery elasticity and C2 small artery elasticity indices were significantly reduced in the elderly group compared with the young group (11.7371.45 vs 16.8871.69 ml/mm Hg Â 10, Po0.001; 8.4071.45 vs 10.5871.18 ml/mm Hg Â 100, Po0.001, respectively). In parallel, the number of circulating EPCs was significantly reduced in the elderly group compared with the young group (0.1370.02 vs 0.1770.04%, Po0.05). The number of circulating EPCs correlated with C1 large and C2 small artery elasticity indices (r ¼ 0.47, Po0.01; r ¼ 0.4, Po0.01). The present findings suggest that the fall in circulating EPCs with subsequently impaired endothelial-cell repair and function contributes to reduced arterial elasticity in humans with ageing. The decrease in circulating EPCs may serve as a surrogate biologic measure of vascular function and human age.

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“…A computer-based third-order, 4-element modified Windkessel model of the circulation is used to match the diastolic pressure decay of the tonometrically obtained waveforms and to quantify changes in arterial waveform morphology in terms of SVR, C1, C2, and L. The values of C1, C2, and L given in the report are weighted averages of the values obtained on individual waveforms during a 30-second recording period. 26,27,39 SVR is calculated as mean arterial pressure (MAP) divided by cardiac output (CO). MAP is derived from the waveform analysis (after calibration with the oscillometrically obtained blood pressure) by integrating the area under each beat and then calculating the average of all beats included in the analysis.…”

Section: Hdi/pulsewave Research Cardiovascular Profiling Instrumentmentioning

confidence: 99%

A Comparison Between Systolic and Diastolic Pulse Contour Analysis in the Evaluation of Arterial Stiffness

et al. 2001

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Abstract-Several methodologically independent measures of arterial stiffness derived from either the systolic or diastolic segments of the arterial pulse have been proposed. The exact nature of the large and small artery elasticity indices (C1 and C2, respectively) derived from diastolic pulse contour analysis remains largely unexplored, although C2 has controversially been termed to be "oscillatory" and "reflective." We investigated the relation between C2 and, respectively, a prototype of arterial reflectivity (ie, the augmentation index, AIx) and a covariate of arterial reflectivity (body height). A validated transfer function is used to transform a tonometrically obtained radial pressure wave into an ascending aortic pressure wave, from which AIx is derived using systolic pulse contour analysis. Diastolic pulse contour analysis using a modified Windkessel model is used to derive C1 and C2. H emodynamics research has shifted away from a steadyflow approach toward a pulsatile flow approach, because the former was less predictive in relation to cardiovascular morbidity and mortality. [1][2][3][4][5] The growing importance of pulsatile pressure indices (systolic blood pressure [SBP] and pulse pressure) paralleled the notion that not only increases in systemic vascular resistance (SVR) but also increases in arterial stiffness are important in the pathophysiology of hypertension. 6,7 This interest in the arterial cushioning function of pulsatile flow has given us a myriad of arterial stiffness indices generated by a wide array of methodologically varied noninvasive measurement techniques. 8 -10 Several working definitions of arterial stiffness have been introduced: parameters of compliance or distensibility, which essentially express changes in mono-dimensional, bidimensional, or tridimensional space for a given pressure difference; parameters quantifying speed of wave propagation along an arterial segment (pulse-wave velocity); and parameters of global vascular elastic behavior derived from the arterial pressure pulse waveform.Given the complexity of the latter approach, simplified mathematical models have been developed. 9 The arterial pressure pulse waveform can be regarded as the result of incident (anterograde) and reflected (retrograde) pressure waves. [11][12][13] Wave reflection occurs at sites of discontinuity in calibre (bifurcations, branching points, and arterioles) or discontinuity in elastic properties (atherosclerosis) along the arterial tree. 14 Changes in amplitude and timing of wave reflections play a key role in aortic hemodynamics and, on a broader level, give us information on how the arterial vasculature affects the heart. [15][16][17][18][19] The SphygmoCor BPAS-1/A device (model SPT-301, PWV Medical Pty Ltd) calculates a number of parameters of ventriculo-arterial coupling and wave reflectance, of which the augmentation index (AIx) is preeminent. 11,20,21 Another approach in analyzing the arterial pulse is to regard the waveform as a basic pattern of exponential decay on which damped oscil...

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Age-Related Abnormalities in Arterial Compliance Identified by Pressure Pulse Contour Analysis

Cited by 331 publications

References 49 publications

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

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

Circulating endothelial progenitor cell deficiency contributes to impaired arterial elasticity in persons of advancing age

A Comparison Between Systolic and Diastolic Pulse Contour Analysis in the Evaluation of Arterial Stiffness

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