With stiffening of proximal elastic arteries with age, the ability of the arterial system to cushion flow pulsations is progressively lost. In consequence, pressure pulsations in the large arteries are increased, and flow pulsations extend more peripherally into small fragile arteries of organs with high resting blood flow, notably the brain and kidney. Ill effects on the heart include increased left ventricular (LV) pressure during systole with greater oxygen demand, and left ventricular hypertrophy (LVH) with predisposition to systolic and diastolic heart failure.
Decreased aortic pressure throughout diastole (and abbreviation of diastolic period in LVH) limits capacity for coronary perfusion and predisposes to myocardial ischaemia. Ill effects on large arteries include faster development of atherosclerotic plaques in coronary and cerebral arteries from increased pulsatile stress and altered endothelial shear stress, accelerated development of aneurysms at points of weakening (branching) in the cerebral circulation, atherosclerotic degeneration of the infra-renal aorta from increased pulsatile shear at the endothelium and radial stress in the media.
Ill effects on the microcirculation in brain and kidney are attributable to high pulsatile flow extending into these vessels, leading to medial disruption with micro-haemorrhage, and to endothelial damage and thrombosis with microinfarcts.
Despite the complexity of underlying mechanisms, and the importance of their consequences, clinical hemodynamic assessment of patients with disease, and evaluations of subjects without disease are made almost exclusively with the cuff sphygmomanometer, also known as the brachial cuff, applied to the upper arm. This process has not changed in the past century. Over one hundred years ago, before the brachial cuff was introduced, clinical information was sought from interpretation of pulse wave contours. This practice lapsed with introduction of the cuff, but has recently been revived with development of arterial tonometry.
Proponents of arterial tonometry have shown that features of the arterial pressure waveform do provide prognostic information which is incremental to that provided by cuff sphygmomanometric numbers of brachial systolic, diastolic, and pulse pressure. This has been shown for augmentation of the central (aortic or carotid) pressure pulse and for amplification of the pressure pulse between the aortic and upper limb arteries.
Advances in this field are limited by difficulties in analysis of the pressure waveforms. Measurement of late systolic augmentation is dependent on identification of the initial peak created by ventricular ejection, and its separation from the beginning of the reflected wave. Measurement of amplification is dependent on assessment of central and peripheral pressure waveforms, measured separately, or on the generation of the central waveform from the peripheral waveform, assuming a generalised transfer function or through assuming identity of mean and diastolic pressure in central and peripheral arteries.
A simplified method for pulse wave analysis, which is independent of such factors, is highly desirable, if this field is to advance. It is also desirable that such a method be independent of blood pressure cuff calibration. In major drug studies published to date, effects of pulsatile pressure change at the heart have been assessed from central systolic and pulse pressure, calibrated from brachial cuff pressure.
Errors in measurement of brachial systolic and diastolic pressure are well known, with the US standard (AAMI SP10) accepting mean offset and standard deviation respectively of ≦5 mmHg and ≦8 mmHg in equivalence comparisons. No such equivalence comparisons have been published for pulse pressure, but differences are likely to compound those for systolic and diastolic pressure. In comparisons of predictors of LV mass in treatment of hypertension, cuff pressures were of far less value than indices determined from the pressure waveform alone.