Myocardial stiffening may be attributed to progressive collagen accumulation, collagen phenotype shift and enhanced collagen cross-linking, but not to either compensatory LV hypertrophy or LV hypertrophy that progresses from the compensatory stage.
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.
The forces underlying left ventricular ejection were investigated by applying a wavefront analysis to blood pressure (P) and velocity (U) waveforms measured in the ascending aorta of anesthetized dogs (n = 13). Wavefronts travel forward (to the periphery) and/or backward (to the heart) after peripheral reflection. They are characterized by the rate of pressure change they cause, i.e., the time derivative of pressure (dP/dt): compression wavefronts have dP/dt > 0: expansion wavefronts have dP/dt < 0. Wave intensity is defined as (dP/dt)(dU/dt), where dU/dt is the time derivative of U. Forward wavefronts contribute positively to wave intensity and backward wavefronts contribute negatively. Therefore, wave intensity indicates whether the effects of forward wavefronts are predominant or whether those of backward wavefronts predominate in the formation of pressure and velocity waveforms. Under control conditions, wave intensity was positive in early and late systole, indicating that forward compression and expansion wavefronts dominate aortic acceleration and deceleration, respectively. Compression wave intensity was increased during inotropic stimulation by dobutamine (10-15 microg/kg per min i.v. infusion; +161% +/- 31% mean change in peak value +/- SEM (%), P < 0.05), and was reduced during beta-blockade by propranolol (1 mg/kg i.v. injection; -58% +/- 7%, P < 0.05). Expansion wave intensity was unchanged by dobutamine and propranolol (n = 6). In a separate group of animals (n = 7), expansion wave intensity was reduced during vasodilatation by nitroglycerin (0.5mg i.v. injection and 0.02 microg/kg per min infusion; -32% +/- 12%, P < 0.05), but was unchanged during vasoconstriction by methoxamine (2 mg i.v. injection). However, methoxamine reduced compression wave intensity (-46% +/- 14%, P < 0.05). These results indicate that (1) compression and expansion wavefronts generated by the left ventricle dominate acceleration and deceleration in the ascending aorta, (2) compression wave intensity is related to the inotropic state of the left ventricle, but is reduced during vasoconstriction, and (3) expansion wave intensity is reduced during vasodilatation. This time domain analysis of traveling wavefronts readily provides information concerning the dynamics of the ventriculoarterial interaction.
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