The most common method of clinical measurement of arterial blood pressure is by means of the cuff sphygmomanometer. This instrument has provided fundamental quantitative information on arterial pressure in individual subjects and in populations and facilitated estimation of cardiovascular risk related to levels of blood pressure obtained from the brachial cuff. Although the measurement is taken in a peripheral limb, the values are generally assumed to reflect the pressure throughout the arterial tree in large conduit arteries. Since the arterial pressure pulse becomes modified as it travels away from the heart towards the periphery, this is generally true for mean and diastolic pressure, but not for systolic pressure, and so pulse pressure. The relationship between central and peripheral pulse pressure depends on propagation characteristics of arteries. Hence, while the sphygmomanometer gives values of two single points on the pressure wave (systolic and diastolic pressure), there is additional information that can be obtained from the time-varying pulse waveform that enables an improved quantification of the systolic load on the heart and other central organs. This topical review will assess techniques of pressure measurement that relate to the use of the cuff sphygmomanometer and to the non-invasive registration and analysis of the peripheral and central arterial pressure waveform. Improved assessment of cardiovascular function in relation to treatment and management of high blood pressure will result from future developments in the indirect measurement of arterial blood pressure that involve the conventional cuff sphygmomanometer with the addition of information derived from the peripheral arterial pulse.

Large artery stiffness assessment has been an integral part of the SphygmoCor technology since 1998. Aortic stiffness is approximated with non-invasive measurement of carotid-femoral pulse wave velocity, with improvements made with time to make the assessment procedure quicker and more user independent. Also standard in the devices is the ability to reliably calculate the central aortic waveform shape from a peripheral pressure waveform from either the brachial or radial artery. This waveform contains much information beyond peak and trough (systolic and diastolic pressure). Relative waveform features such as the augmentation index, wave reflection magnitude, reflection time index, and subendocardial viability ratio are parameters that are influenced by the stiffness of systemic arteries. This article briefly describes these parameters related to large artery stiffness and provides reference to validation and repeatability studies relative to the clinical use of the SphygmoCor devices. It is beyond the scope to review here the 424 original research articles that have employed SphygmoCor devices in measuring arterial stiffness. Instead, the method of measurement across the devices is described, including tonometry, volumetric displacement through cuff placement around limbs, and ambulatory monitoring. Key population and subpopulation studies are cited where the average stiffness parameter progression with age and gender, as measured by SphygmoCor devices, is quantified in the healthy and general population. Finally, with reference to guidelines from working groups on arterial stiffness and hypertension, the clinical utility of large artery stiffness measurement is discussed in the context of the arterial stiffness parameters provided by the SphygmoCor systems.

Arterial stiffness index β and cardio-ankle vascular index (CAVI) are widely accepted to quantify the intrinsic exponent (β0) of the blood pressure (BP)-diameter relationship. CAVI and β assume an exponential relationship between pressure (P) and diameter (d). We aim to demonstrate that, under this assumption, β and CAVI as currently implemented are inherently BP-dependent and to provide corrected, BP-independent forms of CAVI and β. In P = Prefeβ0[(d/dref)-1], usually reference pressure (Pref) and reference diameter (dref) are substituted with DBP and diastolic diameter to accommodate measurements. Consequently, the resulting exponent is not equal to the pressure-independent β0. CAVI does not only suffer from this ‘reference pressure’ effect, but also from the linear approximation of (dP/dd). For example, assuming β0 = 7, an increase of SBP/DBP from 110/70 to 170/120 mmHg increased β by 8.1% and CAVI by 14.3%. We derived corrected forms of β and of CAVI (CAVI0) that indeed did not change with BP and represent the pressure-independent β0. To substantiate the BP effect on CAVI in a typical follow-up study, we realistically simulated patients (n = 161) before and following BP-lowering ‘treatment’ (assuming no follow-up change in intrinsic β0 and therefore in actual P–d relationship). Lowering BP from 160 ± 14/111 ± 11 to 120 ± 15/79 ± 11 mmHg (p < 0.001) resulted in a significant CAVI decrease (from 8.1 ± 2.0 to 7.7 ± 2.1, p = 0.008); CAVI0 did not change (9.8 ± 2.4 and 9.9 ± 2.6, p = 0.499). β and CAVI as currently implemented are inherently BP-dependent, potentially leading to erroneous conclusions in arterial stiffness trials. BP-independent forms are presented to readily overcome this problem.

We demonstrated previously that endogenous NO influences large-artery distensibility in the ovine hindlimb. However, the role of basal NO in larger human conduit arteries is controversial. The aim of this study was to investigate whether basal production of NO, acting locally, influences iliac artery distensibility in humans. Distensibility was assessed by intra-arterial measurement of the pulse wave velocity. Eighteen subjects, free of significant coronary or iliac artery disease, were studied after diagnostic cardiac catheterization. Simultaneous pressure waveforms were recorded with a high-fidelity dual-pressure sensing catheter, placed in the common iliac artery during intra-arterial infusion of saline (baseline), glyceryl trinitrate (4 nmol/min), or N ^G -monomethyl- l -arginine (8 and 16 μmol/min). Drugs were infused proximally, via the catheter to perfuse the segment of artery under study, or distally, via the sheath, to control for any reflex changes in flow or sympathetic activation. Velocity was calculated using the foot-to-foot methodology. Six subjects received glyceryl trinitrate and 12 N ^G -monomethyl- l -arginine. There was no change in velocity after infusion of glyceryl trinitrate or N ^G -monomethyl- l -arginine via the sheath. However, infusion of glyceryl trinitrate via the catheter significantly reduced velocity by 31.43±5.80% (mean±SEM; P <0.01; P =0.02 for comparison). Likewise, infusion of the highest dose of N ^G -monomethyl- l -arginine via the catheter significantly increased velocity by 27.25±8.20% ( P =0.001; P =0.02 for comparison). Importantly, there was no change in mean arterial blood pressure throughout the studies. These data indicate that under resting conditions, local NO production modulates human iliac artery distensibility and that exogenous NO increases arterial distensibility.