Arterial pressure waves were recorded noninvasively from the carotid, radial, femoral, or all three of these arteries of 1,005 normal subjects, aged 2-91 years, using a new transcutaneous tonometer containing a high fidelity Millar micromanometer. Waves were ensemble-averaged into age-decade groups. Characteristic changes were noted with increasing age. In all sites, pulse amplitude increased with advancing age (carotid, 91.3%; radial 67.5%; femoral, 50.1% from first to eighth decade), diastolic decay steepened, and diastolic waves became less prominent. In the carotid pulse, there was, in youth, a second peak on the downstroke of the waves in late systole. After the third decade, this second peak rose with age to merge with and dominate the initial rise. In the radial pulse, a late systolic wave was also apparent, but this occurred later; with age, this second peak rose but not above the initial rise in early systole, even at the eighth decade. In the femoral artery, there was a single systolic wave at all ages. Aging changes in the arterial pulse are explicable on the basis of both an increase in arterial stiffness with increased pulse-wave velocity and progressively earlier wave reflection. These two factors may be separated and effects of the latter measured from pressure wave-contour analysis using an "augmentation index," determined by a computer algorithm developed from invasive pressure and flow data. Changes in peak pressure in the central (carotid) artery show increasing cardiac afterload with increasing age in a normal population; this can account for the cardiac hypertrophy that occurs with advancing age (even as other organs atrophy) and the predisposition to cardiac failure in the elderly. Identification of mechanisms responsible offers a new approach to reduction of left ventricular afterload. (Circulation 1989;80:1652-1659

Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.

Amplification of the pressure pulse between central and peripheral arteries renders pressure values in the upper limb an inaccurate measure of ascending aortic (AA) pressure. Accuracy could be improved by allowance for such amplification. Transfer functions (TF) for pressures between AA and brachial artery (BA):(BATF) and between AA and radial artery (RA):(RATF) were derived from high-fidelity pressure recordings obtained at cardiac catheterization in 14 patients under control conditions, and after sublingual nitroglycerine 0.3 mg. There was no significant difference in BATF under control conditions and with nitroglycerine; hence results were pooled. Control and nitroglycerine results were also pooled to obtain a single RATF. BATF and RATF moduli peaked at 5 Hz and 4 Hz, reaching 2.5 and 2.8 times the value at zero frequency respectively. Frequency-dependent changes in modulus and phase of BATF and RATF were attributable to wave travel and reflection in the upper limb. BATF and RATF were compared to published transfer functions and those derived from analysis of aortic and brachial or radial pressure waves in previous publications. Results were similar. Our BATF and RATF were used to synthesize AA pressure waves from published peripheral pulses. Correspondence was close, especially for systolic pressure which differed by 2.4 +/- 1.0 (mean +/- SEM) mmHg, whereas recorded systolic pressure differed by 20.4 +/- 2.6 (mean +/- SEM) mmHg between central and peripheral sites. Results indicate that in adult humans a single generalized TF can be used with acceptable accuracy to determine central from peripheral pressure under different conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Spontaneous echo contrast is the cardiac factor most strongly associated with left atrial appendage thrombus and embolic events. Spontaneous echo contrast formation is promoted by reduced blood flow velocity and increased left atrial size but is diminished by mitral regurgitation.

The stiffness of the aorta can be determined by measuring carotid-femoral pulse wave velocity (PWV(cf)). PWV may also influence the contour of the peripheral pulse, suggesting that contour analysis might be used to assess large artery stiffness. An index of large artery stiffness (SI(DVP)) derived from the digital volume pulse (DVP) measured by transmission of IR light (photoplethysmography) was examined. SI(DVP) was obtained from subject height and from the time delay between direct and reflected waves in the DVP. The timing of these components of the DVP is determined by PWV in the aorta and large arteries. SI(DVP) was, therefore, expected to provide a measure of stiffness similar to PWV. SI(DVP) was compared with PWV(cf) obtained by applanation tonometry in 87 asymptomatic subjects (21-68 years; 29 women). The reproducibility of SI(DVP) and PWV(cf) and the response of SI(DVP) to glyceryl trinitrate were assessed in subsets of subjects. The mean within-subject coefficient of variation of SI(DVP), for measurements at weekly intervals, was 9.6%. SI(DVP) was correlated with PWV(cf) ( r =0.65, P <0.0001). SI(DVP) and PWV(cf) were each independently correlated with age and mean arterial blood pressure (MAP) with similar regression coefficients: SI(DVP)=0.63+0.086 x age+0.042 x MAP ( r =0.69, P <0.0001); PWV(cf)=0.76+0.080 x age+0.053 x MAP ( r =0.71, P <0.0001). Administration of glyceryl trinitrate (3, 30 and 300 microg/min intravenous; each dose for 15 min) in nine healthy men produced similar changes in SI(DVP) and PWV(cf). Thus contour analysis of the DVP provides a simple, reproducible, non-invasive measure of large artery stiffness.

Abstract-Aortic augmentation index, a measure of central systolic blood pressure augmentation arising mainly from pressure-wave reflection, increases with vascular aging. The augmentation index is influenced by aortic pulse-wave velocity (related to aortic stiffness) and by the site and extent of wave reflection. To clarify the relative influence of pulse-wave velocity and wave reflection on the augmentation index, we studied the association between augmentation index, pulse-wave velocity, and age and examined the effects of vasoactive drugs to determine whether altering vascular tone has differential effects on pulse-wave velocity and the augmentation index. We made simultaneous measurements of the augmentation index and carotid-to-femoral pulse-wave velocity in 50 asymptomatic men aged 19 to 74 years at baseline and, in a subset, during the administration of nitroglycerin, angiotensin II, and saline vehicle. The aortic augmentation index was obtained by radial tonometry (Sphygmocor device, PWV Medical) with the use of an inbuilt radial to aortic transfer function. In multiple regression analysis, the aortic augmentation index was independently correlated only with age (Rϭ0.58, PϽ0.0001). Nitroglycerin (3 to 300 g/min IV) reduced the aortic augmentation index from 4.8Ϯ2.3% to Ϫ11.9Ϯ5.3% (nϭ10, PϽ0.002). Angiotensin II (75 to 300 ng/min IV) increased the aortic augmentation index from 9.3Ϯ2.4% to 18.3Ϯ2.9% (nϭ12, PϽ0.001). These drugs had small effects on aortic pulse-wave velocity, producing mean changes from baseline of Ͻ1 m/s (each PϽ0.05). In healthy men, vasoactive drugs may change aortic augmentation index independently from aortic pulse-wave velocity. Key Words: antihypertensive agents Ⅲ aorta Ⅲ arteries Ⅲ hemodynamics Ⅲ pulse S ystolic blood pressure is augmented by the reflection of pressure from the periphery of the circulation to the aortic root. 1 The aortic augmentation index (AIx) is defined as the increment in pressure from the first systolic shoulder (inflection point) to the peak pressure of the aortic pressure waveform expressed as a percentage of the peak pressure. 2 This index has been used to measure the additional load imposed on the left ventricle as a result of wave reflection and correlates with left ventricular mass. 3,4 AIx depends, at least in part, on aortic and large-artery pulse-wave velocity (PWV). A higher PWV results in earlier arrival of reflected waves and, hence, increased augmentation during early systole. 1,5 PWV is inversely related to arterial distensibility. 6 Therefore, AIx has been proposed as an index of "arterial stiffness" 7,8 and has been used as a measure of this. 9 -12 However, in addition to PWV, AIx may depend on the pattern of ventricular ejection and on arterial properties determining the amount and site of wave reflection. 1 These latter factors may be influenced by the vascular tone of the small muscular arteries/arterioles rather than by the elastic properties of the aorta. To clarify the relationship between AIx and PWV, we made simultaneous measurement...

Measurement of noninvasive impedance by this technique provides an accurate and repeatable assessment of mean and pulsatile cardiac load.

These new data may help to explain previous findings in women of an age-related increase in LV mass and excess symptomatic heart failure that are not explained by differences in brachial BP.