Pulse waveform analysis and arterial wall properties.

Risk factors for cardiovascular disease mediate their effects by altering the structure, properties, and function of wall and endothelial components of arterial blood vessels.1 The ability to detect and monitor change in the physical properties of arteries, representative of the cumulative and integrated influence of hemodynamic, metabolic, and inflammatory stimuli in impairing arterial wall integrity, holds potential to intervene at a preclinical stage to prevent or attenuate disease progression. The importance of assessing arterial wall integrity has been highlighted by recent studies demonstrating that a decrease in the pulsatile function of large arteries represents an independent predictor for future cardiovascular events.2 Information about the interaction between the left ventricle and the physical properties of the arterial circulation can be derived by the descriptive and quantitative analysis of the arterial pressure pulse waveform.3 Consistent characteristic changes in the pressure pulse waveshape have been described with aging and disease states predisposing to an increase in vascular events. One such age-related change involves a steepening of the pressure decay in diastole, largely determined by impaired buffering function of the proximal aorta.3,4 Loss of the oscillatory waveform that distorts the proximal portion of diastole from a pure exponential represents a further early and consistent finding with aging and risk factors for cardiovascular disease including hypertension, smoking, and diabetes mellitus.3–7 This feature arises from reflection of the incident pressure wave generated by the left ventricle from peripheral reflecting sites with a major contribution originating from impedance mismatches in small arteries and arterioles. The progressive appearance of the reflected wave in systole and eventual summation with the forward incident wave results in augmentation of the systolic blood pressure. Given the proximity of the central aorta to the major peripheral reflecting sites in the lower limbs, augmentation of the systolic blood pressure occurs in this vessel before changes are recorded in the upper limb vessels. Recently, techniques based on the determination of a pressure transfer function between the radial artery and the aorta have been employed to provide an estimate of central pressure wave reflection.8 In this issue of Hypertension, Millasseau et al9 report on the accuracy of employing a generalized transfer function to the radial artery pressure pulse waveform to provide an estimate of the aortic augmentation index. The accuracy of the approach was assessed against data derived directly from the carotid pressure pulse waveform or after application of a transfer function to the waveform. The authors confirm prior observations that indicate the use of a general transfer function can show a considerable amount of bias and variation that limits the utility of this approach in accurately predicting the central augmentation index.10,11 Further support for this contention is provided by a recent study where simultaneous recordings of invasive central aortic and noninvasive radial blood pressure waveforms were made in 78 subjects.12 Values for the augmentation index, derived using transfer functions applied to the radial waveforms, were significantly different from directly measured values, and no correlation was evident between the 2 estimates. However, as the radial artery pressure pulse waveform contains all the information required to synthesize a central pressure waveform; similar information relating to pressure pulse wave reflection in the arterial circulation may be derived directly from the peripheral waveform without resorting to the use of a transfer function. Millasseau et al show a simple method for estimating the radial augmentation index to provide information about pressure pulse wave reflection in the arterial system. An important issue relates to how information provided by detecting and tracking this marker of wave reflection is interpreted in relation to the status of the arterial vasculature and the hemodynamic actions of drug interventions. The determinants influencing wave reflection in the arterial circulation comprise the pattern of left ventricular ejection in addition to the magnitude and timing of reflected waves from peripheral reflecting sites in the arterial vasculature.9 Assessing the effects of wave reflection in altering the pressure pulse waveshape has proven valuable in marking altered structure or tone in the vasculature and is a sensitive tool for studying the hemodynamic actions of drug interventions.3,13 For example, nitroglycerin administration produces marked changes in the pressure pulse waveshape, which can be dissociated from a change in total peripheral resistance or the pulse transit time measured by aortic pulse wave velocity.14,15 The effects are explained by changes in the mechanical properties of peripheral muscular arteries that result in improved impedance matching and attenuation of wave reflection in response to nitroglycerin. Direct ultrasonic techniques employed to assess local wall properties of peripheral muscular arteries indicate that arterial compliance (a property that depends on arterial geometry and intrinsic vessel wall properties) improves consistently, whereas distensibility (an intrinsic property of the arterial wall materials) does not necessarily change in response to nitroglycerin administration.16 The nature and magnitude of change in the derived measures are sensitive to various confounding influences, which can be independent of The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. From the Department of Therapeutics and Pharmacology, Queen’s University Belfast, Northern Ireland Correspondence to Gary E McVeigh, MD, PhD, Department of Therapeutics and Pharmacology, 97 Lisburn Road, Belfast BT9 7BL, Northern Ireland. E-mail [email protected] (Hypertension. 2003;41:1010-1011.) © 2003 American Heart Association, Inc.