Journal Article•
Pulse wave analysis and arterial stiffness.
01 Jan 1998-Journal of Cardiovascular Pharmacology (Lippincott Williams and Wilkins)-Vol. 32, Iss: 3
TL;DR: In clinical studies, it has been shown that PWA is a highly reproducible technique and easy to apply, and together with ECG-gated assessment of pulse wave velocity, also using PWA, these measures provide important information about arterial stiffness.
Abstract: Assessment of the pulse character is one of the earliest recorded medical skills, but objective recordings of the pulse waveform--sphygmography--emerged only in the nineteenth century. This technique fell into disuse with the advent of the sphygmomanometer, but interest has recently been rekindled with the introduction of computer technology and applanation tonometry. Pulse wave analysis (PWA) is a technique that allows the accurate recording of peripheral pressure waveforms and generation of the corresponding central waveform, from which the augmentation index and central pressure can be derived. In clinical studies, we have shown that PWA is a highly reproducible technique and easy to apply. Together with ECG-gated assessment of pulse wave velocity, also using PWA, these measures provide important information about arterial stiffness. Stiffness may be partly under the functional control of the endothelium, which releases a number of vasoactive mediators, as well as being structurally determined. Increased stiffness is associated with most cardiovascular risk factors and established atherosclerosis. However, increased stiffness may be more than a marker for occult atheroma. It may be involved in the pathogenesis of cardiovascular disease by a number of mechanisms. Assessment of stiffness, perhaps using PWA, may therefore provide better risk assessment and allow treatment to be targeted to those most in need.
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TL;DR: An inverse, linear relationship between AIx is demonstrated, likely due to alterations in the timing of the reflected pressure wave, produced by changes in the absolute duration of systole, which may explain the lack of rise in central systolic pressure during incremental pacing despite an increase in peripheral pressure.
Abstract: Arterial stiffness is an important determinant of cardiovascular risk. Augmentation index (AIx) is a measure of systemic arterial stiffness derived from the ascending aortic pressure waveform. The aim of the present study was to assess the effect of heart rate on AIx. We elected to use cardiac pacing rather than chronotropic drugs to minimize confounding effects on the systemic circulation and myocardial contractility. Twenty-two subjects (13 male) with a mean age of 63 years and permanent cardiac pacemakers in situ were studied. Pulse wave analysis was used to determine central arterial pressure waveforms, non-invasively, during incremental pacing (from 60 to 110 beats min-1), from which AIx and central blood pressure were calculated. Peripheral blood pressure was recorded non-invasively from the brachial artery. There was a significant, inverse, linear relationship between AIx and heart rate (r = -0.76; P < 0.001). For a 10 beats min-1 increment, AIx fell by around 4 %. Ejection duration and heart rate were also inversely related (r = -0. 51; P < 0.001). Peripheral systolic, diastolic and mean arterial pressure increased significantly during incremental pacing. Although central diastolic pressure increased significantly with pacing, central systolic pressure did not. There was a significant increase in the ratio of peripheral to central pulse pressure (P < 0.001), which was accounted for by the observed change in central pressure augmentation. These results demonstrate an inverse, linear relationship between AIx and heart rate. This is likely to be due to alterations in the timing of the reflected pressure wave, produced by changes in the absolute duration of systole. Consideration of wave reflection and aortic pressure augmentation may explain the lack of rise in central systolic pressure during incremental pacing despite an increase in peripheral pressure.
1,029 citations
Cites background from "Pulse wave analysis and arterial st..."
...Therefore, measurement of central aortic, rather that brachial artery, pressure may provide a better prediction of cardiovascular risk (Wilkinson et al. 1999)....
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TL;DR: Reversing or stabilising the increased arterial stiffness associated with age and disease by targeting any or all of its causes provides a number of promising new approaches to the treatment of systolic hypertension and its sequelae, the main causes of mortality and morbidity in the developed world.
Abstract: Conduit arteries become stiffer with age due to alterations in their morphology and the composition of the their major structural proteins, elastin and collagen. The elastic lamellae undergo fragmentation and thinning, leading to ectasia and a gradual transfer of mechanical load to collagen, which is 100–1000 times stiffer than elastin. Possible causes of this fragmentation are mechanical (fatigue failure) or enzymatic (driven by matrix metallo proteinases (MMP) activity), both of which may have genetic or environmental origins (fetal programming). Furthermore, the remaining elastin itself becomes stiffer, owing to calcification and the formation of cross-links due to advanced glycation end-products (AGEs), a process that affects collagen even more strongly. These changes are accelerated in the presence of disease such as hypertension, diabetes and uraemia and may be exacerbated locally by atherosclerosis. Raised MMP activity, calcification and impaired endothelial function are also associated with a high level of plasma homocysteine, which itself increases with age. Impaired endothelial function leads to increased resting vascular smooth muscle tone and further increases in vascular stiffness and mean and/or pulse pressure. The effect of increased stiffness, whatever its underlying causes, is to reduce the reservoir/buffering function of the conduit arteries near the heart and to increase pulse wave velocity, both of which increase systolic and pulse pressure. These determine the peak load on the heart and the vascular system as a whole, the breakdown of which, like that of any machine, depends more on the maximum loads they must bear than on their average. Reversing or stabilising the increased arterial stiffness associated with age and disease by targeting any or all of its causes provides a number of promising new approaches to the treatment of systolic hypertension and its sequelae, the main causes of mortality and morbidity in the developed world. Copyright 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
581 citations
Cites background from "Pulse wave analysis and arterial st..."
...Both these parameters have been used as surrogates of conduit arterial stiffness [218], although their reliability when compared to PWV measurements has been questioned [219,220], as has their theoretical basis [4]...
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TL;DR: It is demonstrated, for the first time, that basal NO production influences large-artery distensibility and, in addition, exogenous acetylcholine and glyceryl trinitrate both increase arterial Distensibility, the former mainly through NO production.
Abstract: Background— Arterial stiffness is an important determinant of cardiovascular risk. Several lines of evidence support a role for the endothelium in regulating arterial stiffness by release of vasoactive mediators. We hypothesized that nitric oxide (NO) acting locally regulates arterial stiffness in vivo, and the aim of this experiment was to test this hypothesis in an ovine hind-limb preparation.
Methods and Results— All studies were conducted in anesthetized sheep. Pulse wave velocity (PWV) was calculated by the foot-to-foot methodology from 2 pressure waveforms recorded simultaneously with a high-fidelity dual pressure-sensing catheter placed in the common iliac artery. Intra-arterial infusion of NG-monomethyl-L-arginine (L-NMMA) increased iliac PWV significantly, by 3±2% (P<0.01). Infusion of acetylcholine and glyceryl trinitrate reduced PWV significantly, by 6±4% (P=0.03) and 5±2% (P<0.01), respectively. Only the effect of acetylcholine, however, was significantly inhibited during coinfusion of L-NMMA (P=0.03). There was no change in systemic arterial pressure throughout the studies. Importantly, infusion of L-NMMA or acetylcholine distal to the common iliac artery (via the sheath) did not affect PWV.
Conclusions— These results demonstrate, for the first time, that basal NO production influences large-artery distensibility. In addition, exogenous acetylcholine and glyceryl trinitrate both increase arterial distensibility, the former mainly through NO production. This may help explain why conditions that exhibit endothelial dysfunction are also associated with increased arterial stiffness. Therefore, reversal of endothelial dysfunction or drugs that are large-artery vasorelaxants may be effective in reducing large-artery stiffness in humans, and thus cardiovascular risk.
507 citations
TL;DR: The findings suggest that augmentation index may be a useful marker of cardiovascular risk in patients with cardiovascular disease and in subjects with atherosclerotic disease.
Abstract: Objectives Augmentation index is a parameter measured by pulse wave analysis (PWA) and is used as a surrogate measure of arterial stiffness. The aim of this study was to assess whether augmentation index is associated with cardiovascular risk, as well as to evaluate whether the determinants of augmentation index are different in patients with cardiovascular disease compared to healthy subjects. Design and methods We related augmentation index to risk scores in 216 subjects with or without a cardiovascular disease. Subjects without cardiovascular disease were classified according to the ‘coronary risk chart’ of the European Society of Cardiology (ESC), and those with cardiovascular disease were classified using the SMART (Second Manifestations of ARTerial disease) score and the EPOZ (Epidemiological Prevention study Of Zoetermeer) function. Augmentation index was derived by PWA using carotid applanation tonometry. Augmentation index was also correlated to age, blood pressure, heart rate, smoking history, cholesterol, height, body mass index and gender in subjects categorized as healthy or with cardiovascular disease. Results Augmentation index significantly increased with increasing risk scores (P < 0.0001) and was significantly correlated to cardiovascular risk (ESC: P < 0.0001; SMART: P < 0.0001; EPOZ: P < 0.0001). In subjects with and without cardiovascular disease, augmentation index was correlated with diastolic blood pressure, heart rate, height and gender. Age was found to be significantly correlated with augmentation index only in healthy subjects but not in those with atherosclerotic disease. Conclusions Our findings suggest that augmentation index may be a useful marker of cardiovascular risk. Further studies are required to investigate the relationship between age and augmentation index in subjects with
432 citations
TL;DR: Patients with hypercholesterolemia have a higher central pulse pressure and stiffer blood vessels than matched controls, despite similar peripheral blood pressures, and assessment may improve risk stratification.
431 citations
Cites background from "Pulse wave analysis and arterial st..."
...are currently ongoing (51), and these will serve not only to...
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