Wave intensity (WI) is a new hemodynamic index that provides information about the dynamic behavior of the heart and the vascular system and their interaction. Carotid arterial wave intensity in normal subjects has two positive peaks. The first peak, W(1), occurs during early systole, the magnitude of which increases with increases in cardiac contractility. The second peak, W(2), which occurs towards the end of ejection, is related to the ability of the left ventricle to actively stop aortic blood flow. Between the two positive peaks, a negative area, NA, is often observed, which signifies reflections from the cerebral circulation. The time interval between the R-wave of ECG and the first peak (R - W(1)) corresponds to the pre-ejection period, and that between the first and second peaks (W(1) - W(2)) corresponds to ejection time. We developed a new ultrasonic on-line system for obtaining WI and arterial stiffness (beta). The purpose of this study was (1) to report normal values of various indices derived from WI and beta measured with this system, and (2) to evaluate the intraobserver and interobserver reproducibility of the measurements. The measurement system is composed of a computer, a WI unit, and an ultrasonic machine. The WI unit gives the instantaneous change in diameter of the artery and the instantaneous mean blood velocity through the sampling gate. Using these parameters and blood pressure measured with a cuff-type manometer, the computer gives WI and beta. We applied this method to the carotid artery in 135 normal subjects. The mean values of W(1), W(2), NA, R - W(1), and W(1) - W(2) were 8 940 +/- 3 790 mmHg m/s(3), 1 840 +/- 880 mmHg m/s(3), 27 +/- 13 mmHg m/s(2), 104 +/- 14 ms, and 270 +/- 19 ms, respectively. These values did not show a significant correlation with age. The mean value of beta was 10.4 +/- 4.8 and the values significantly correlated with age (men: r = 0.66, P < 0.0001; women: r= 0.81, P < 0.0001). The reproducibility was evaluated by intraobserver intrasession (IA), intraobserver intersession (IE), and interobserver intrasession variability (IO). The reproducibility of R - W(1) and W(1) - W(2) was high: the mean coefficient of variation (mCV) of IA was less than 3%; 95% confidence limits from the mean values (CL) were less than 8% for IE and less than 4% for IO. The reproducibility of W(1) and beta was good: mCV for IA was less than 10%; CL for IE and IO were less than 17%. W(2) and NA showed a higher variability than other indices: mCV for IA was less than 13%, and CL for IE and IO were less than 36%. However, two sessions by the same observer and two sessions by different observers were not biased. Wave intensity measurements with this system are clinically acceptable.

Wave intensity (WI) is a novel hemodynamic index, which is defined as (d P/d t) x (d U/d t) at any site of the circulation, where d P/d t and d U/d t are the derivatives of blood pressure and velocity with respect to time, respectively. However, the pathophysiological meanings of this index have not been fully elucidated in the clinical setting. Accordingly, we investigated this issue in 64 patients who underwent invasive evaluation of left ventricular (LV) function. WI was obtained at the right carotid artery using a color Doppler system for blood velocity measurement combined with an echo-tracking method for detecting vessel diameter changes. The vessel diameter changes were automatically converted to pressure waveforms by calibrating its peak and minimum values by systolic and diastolic brachial blood pressures. The WI of the patients showed two sharp positive peaks. The first peak was found at the very early phase of LV ejection, while the second peak was observed near end-ejection. The magnitude of the first peak of WI significantly correlated with the maximum rate of LV pressure rise (LV max. d P/d t) (r = 0.74, P << 0.001). The amplitude of the second peak of WI significantly correlated with the time constant of LV relaxation (r = -0.77, P << 0.001). The amplitude of the second peak was significantly greater in patients with the inertia force of late systolic aortic flow than in those without the inertia force (3,080 +/- 1,741 vs 1,890 +/- 1,291 mmHg m s(-3), P << 0.01). These findings demonstrate that the magnitude of the first peak of WI reflects LV contractile performance, and the amplitude of the second peak of WI is determined by LV behavior during the period from late systole to isovolumic relaxation. WI is a noninvasively obtained, clinically useful parameter for the evaluation of LV systolic and early diastolic performance at the same time.

Wave intensity (WI) is a hemodynamic index, which can evaluate the working condition of the heart interacting with the arterial system. It can be defined at any site in the circulatory system and provides a great deal of information. However, we need simultaneous measurements of blood pressure and velocity to obtain wave intensity, which has limited the clinical application of wave intensity, in spite of its potential. To expand the application of wave intensity in the clinical setting, we developed a real-time non-invasive measurement system for wave intensity based on a combined color Doppler and echo-tracking system. We measured carotid arterial WI in normal subjects and patients with various cardiovascular diseases. In the coronary artery disease group, the magnitude of the first peak of carotid arterial WI (W 1 ) increased with LV max. dP/dt (r = 0.74, P \ 0.001), and the amplitude of the second peak (W 2 ) decreased with an increase in the time constant of LV pressure decay (r = -0.77, P \ 0.001). In the dilated cardiomyopathy group, the values of W 1 were much lower than those in the normal group (P \ 0.0001). In the hypertrophic cardiomyopathy group, the values of W 2 were much smaller than those in the normal group (P \ 0.0001). In mitral regurgitation before surgery, W 2 decreased or disappeared, but after surgery W 2 appeared clearly. In the hypertension group, the magnitude of reflection from the head was considerably greater than that in the normal group (P \ 0.0001). We also evaluated hemodynamic effects of sublingual nitroglycerin in normal subjects. Nitroglycerin increased W 1 significantly (P \ 0.001). WI can be obtained non-invasively using an echo-Doppler system in the clinical setting. This method will increase the clinical usefulness of wave intensity.

Pulse wave velocity (PWV) is a basic parameter in the dynamics of pressure and flow waves traveling in arteries. Conventional on-line methods of measuring PWV have mainly been based on "two-point" measurements, i.e., measurements of the time of travel of the wave over a known distance. This paper describes two methods by which on-line "one-point" measurements can be made, and compares the results obtained by the two methods. The principle of one method is to measure blood pressure and velocity at a point, and use the water-hammer equation for forward traveling waves. The principle of the other method is to derive PWV from the stiffness parameter of the artery. Both methods were realized by using an ultrasonic system which we specially developed for noninvasive measurements of wave intensity. We applied the methods to the common carotid artery in 13 normal humans. The regression line of the PWV (m/s) obtained by the former method on the PWV (m/s) obtained by the latter method was y = 1.03x - 0.899 (R(2) = 0.83). Although regional PWV in the human carotid artery has not been reported so far, the correlation between the PWVs obtained by the present two methods was so high that we are convinced of the validity of these methods.

NTG increased W 1 and the mid-systolic expansion wave, which suggests enhanced cardiac power during the initial ejection and mid-systolic unloading. These results are new findings about the effects of NTG that can be added to the widely known late systolic unloading and preload reduction. NTG also increased arterial stiffness, which reduces the Windkessel function. By using an echo-Doppler system, WI can be obtained noninvasively. WI has the clinical potential to provide quantitative and detailed information about working conditions of the heart interacting with the arterial system.