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Papers on Aortic AI

Validity of pulse pressure and augmentation index as surrogate measures of arterial stiffness during beta-adrenergic stimulation
Daniel Lemogoum, Gabriella Flores,Wouter Van den Abeele, Agnieszka Ciarkac, Marc Leeman, Jean Paul Degaute, Philippe van de Borne and Luc Van Bortel
Journal of Hypertension 2004, 22:511–517

Objective Increased arterial stiffness is a determinant of cardiovascular mortality. Pulse wave velocity (PWV) is a direct measure of arterial stiffness. Aortic augmentation index (AI) and pulse pressure (PP) are surrogate measures of arterial stiffness. Both PWV, AI and PP increase with cardiovascular risk factors. The aim of this study was to test the validity of AI and PP as surrogate measures of arterial stiffness compared with PWV, during betaadrenergic stimulation with Isoprenaline (Iso).


Pulse-Wave Analysis
Clinical Evaluation of a Noninvasive, Widely Applicable Method for Assessing Endothelial Function
Ian B. Wilkinson, Ian R. Hall, Helen MacCallum, Isla S. Mackenzie, Carmel M. McEniery, Bart J. van der Arend, Yae-Eun Shu, Laura S. MacKay, David J. Webb, John R. Cockcroft

ImageThe vascular endothelium releases a number of biologically active mediators, including nitric oxide (NO), that regulate vessel tone and prevent the development of atheroma. 1 Endothelial dysfunction is associated with a range of risk factors for cardiovascular disease, including hypercholesterolemia, 2,3 and some therapies that improve clinical outcome also reverse endothelial dysfunction.4 Vasomotor responses in the peripheral and coronary circulations are correlated,5 and coronary endothelial dysfunction is associated with cardiovascular risk.6 However, no direct link between improved endothelial function and reduced risk has been made, and the prognostic significance of endothelial dysfunction has not been assessed in a major observational study.



Prediction of aortic augmentation index using radial pulse transmission-wave analysis
Elizabeth O.Y. Lau, Hung-Fat Tse, Raymond H.W. Chana, Wai-Hong Chen, Pui-Yin Lee, Stephen W.L. Lee, Allen T. Chwang and Chu-Pak Lau
Journal of Hypertension 2006, 24:723–730

Objective Current arterial transfer functions have low capability in predicting aortic augmentation index (AIx) from radial pulse contour (RPC), because of the difficulty in accurately identifying the merging point (inflection point) in the derived aortic pulse contour (APC). We hypothesize that the formation time between each characteristic wave in APC is about one-third of ejection duration (ED/3). We sought to assess the accuracy of ED/3 in identifying the merging point in APC as compared to the conventional differential method. In addition, we sought to derive the AIx from RPC based on an arterial transfer function and the ED/3 method.


Peripheral or central augmentation index: an esoteric question or a non-invasive clue to central haemodynamics?
Marc L. De Buyzere and Patrick Segers
Journal of Hypertension 2007, 25:289–293

Historical perspective and definitions related to the augmentation index In the early 1980, when studying aorta input impedance in humans, Murgo et al. [1] introduced the concept of A- and C-type central pressure waveforms. In the C-type waveform (usually seen in the young and healthy adult), the amplitude of the reflected wave is small, arrives in late systole and the addition of the reflected wave onto the forward wave does not increase systolic pressure. On the other end of the spectrum, in A-type waveforms (usually seen in elderly subjects), the amplitude of the reflected wave is much higher and the addition of the reflected wave onto the forward wave in early systole leads to a pronounced ‘pressure augmentation’ (AP). The associated augmentation index (AI¼AP/PP) is the ratio of the ‘augmented pressure’ (augmentation of pressure after a characteristic point; AP) to the total pressure amplitude (pulse pressure; PP). AI is mostly expressed as a percentage and obviously is dimensionless. Physiological and mathematical principles underlying pressure augmentation are detailed in McDonald’s Blood Flow in Arteries [2]. In studies with sufficient numbers of subjects and variation of baseline characteristics, it has been clearly demonstrated that AI increases with age and peripheral blood pressure and decreases with increasing height and heart rate [3,4]. The interested reader will find greater detail on these factors affecting AI in a review article by Davies and Struthers [5]. Nevertheless, it has been shown that AI reaches a plateau from the age of 55– 60 years [6]. The magnitude and timing of the reflected wave and pulse wave velocity are also well-accepted determinants of AI. Physiologically speaking, AI appears to depend on the back-and-forth travel time of the pressure wave to the reflection sites relative to the timing of cardiac ejection.


Augmentation of the aortic and central arterial pressure waveform
Michael F. O’Rourkea and Alfredo L Paucab
Blood Pressure Monitoring 2004, 9:179–185

Late systolic augmentation of the ascending aortic and central arterial pressure wave is a characteristic feature of aging, and is attributable to stiffening of the aorta and major central arteries. It is caused by increased pulse wave velocity in these vessels with early return of wave reflection from peripheral sites, predominantly in the lower part of the body. Augmentation is measurable through identification of the shoulder or early systolic peak of pressure, which corresponds to peak flow in the aorta, and measurement from this point to the second peak, or shoulder of the wave in late systole. Difficulties in measurement of augmentation arise from problems in identification of the initial shoulder, especially when this is close to the foot of the reflected wave, to amplification of the pulse wave between ascending aorta and carotid artery, and to a Venturi effect in the aorta at the peak of aortic flow. Augmentation is systematically higher in the left ventricle than in the aorta, and systematically higher in the aorta than in more peripheral arteries such as the carotid or radial. Since properties of upper limb arteries are relatively constant with age, blood pressure, gender and drug therapy, a generalized transfer function can be used to synthesize the aortic from the radial pressure waveform. Comparison of measured directly and aortic pressure calculated with the Sphygmo- Cors process under control conditions and with nitroglycerine infusion gave values of augmentation with mean difference 0.9, SD 7.7 mmHg, which lie within AAMI criteria for equivalence, as do measures of end systolic pressure (difference 3.8, SD 3.6mmHg). Blood Press Monit 9:179–185 c 2004 Lippincott Williams & Wilkins.


Arterial Stiffness, Wave Reflections, and the Risk of Coronary Artery Disease
Thomas Weber, MD; Johann Auer, MD; Michael F. O’Rourke, MD; Erich Kvas, ScD; Elisabeth Lassnig, MD; Robert Berent, MD; Bernd Eber, MD
DOI: 10.1161/01.CIR.0000105767.94169.E3

Background-Increased arterial stiffness, determined invasively, has been shown to predict a higher risk of coronary atherosclerosis. However, invasive techniques are of limited value for screening and risk stratification in larger patient groups.


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