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This study was designed to examine whether the cross-sectional area of vena contracta measured by color Doppler flow mapping (CFM) could be used for assessing aortic regurgitation (AR) and developing an index for grading AR. The 75 study patients with AR were classified into quadrant grades according to New York Heart Association functional class, regurgitant fraction, left ventricular (LV) end-diastolic dimension and LV end-systolic dimension. Using CFM, the cross-sectional area of the vena contracta was measured and it could distinguish all grades without significant overlap. An area of less than 0.10 cm(2) corresponded to Grade 1, 0.10-0.19 cm(2) corresponded to Grade 2, 0.20-0.29 cm(2) corresponded to Grade 3 and an area of more than 0.30 cm(2) corresponded to Grade 4. An area of vena contracta of more than 0.30 cm(2) identified high-scoring AR (Grade 4) in 11 of 11 (sensitivity 100%) and correctly predicted the absence of high-scoring AR in 60 of 64 (specificity 94%). Conversely, there was considerable overlap between the jet distances with the clinical grades. The cross-sectional area of the vena contracta measured by CFM can provide a simple quantitative assessment of AR that correlates well with the clinical grade of AR.

Recent technological advances in transthoracic Doppler echocardiography (TTDE) have provided noninvasive measurement of coronary flow velocity reserve (CFVR). We aimed to quantitate a correlation between endothelial dysfunction and fat distribution. In 36 patients with obesity, 16 with noninsulin-dependent diabetes mellitus (DM) and 12 healthy volunteers, coronary flow velocity was measured at the distal site of the left anterior descending branch. CFVR was defined as the ratio of hyperemic (IV infusion of 0.15 mg/kg/min adenosine) to basal peak diastolic flow velocity. Abdominal wall fat index (AWFI) was estimated by ultrasonography. Insulin resistance was quantified by the euglycemic hyperinsulinemic clump method. AWFI was significantly related to CFVR (r = -0.46, p = 0.011) and insulin resistance (r = -0.71, p < 0.0001). CFVR could be noninvasively evaluated using TTDE. Coronary endothelial dysfunction indicated as CFVR, body fat distribution and insulin resistance was quantitatively correlated in obesity.

Color M-mode Doppler echocardiography (CMD) has been utilized in assessing left ventricular (LV) filling dynamics. We tested a novel CMD index, the depth of the spatiotemporal maximum of early diastolic inflow (D-maxV) in the left ventricle, to clarify its significance in assessing LV diastolic function. In 26 normal subjects and 32 patients with ischemic heart disease, D-maxV was determined with CMD as the distance from the mitral valve opening point to the center of the aliasing area in early diastole. Transmitral flow velocity was measured with pulsed Doppler. During routine catheterization, high-fidelity LV pressure measurements yielded diastolic variables in patients. D-maxV was significantly lower in the patients than the normals (13.0 ± 7.0 vs 23.4 ± 6.8 mm, P < 0.0001). D-maxV exhibited significant linear correlations with the minimal first derivative of LV pressure (r = 0.72, P < 0.01), the time constant of isovolumic relaxation (r = −0.67, P < 0.01), and LV minimal pressure (r = −0.53, P < 0.02) in the patients with wide ranges of peak early to late inflow velocity ratio (0.43–3.9) and deceleration time of early filling (79–293 ms). D-maxV showed an inverse correlation with LV end-diastolic pressure (r = −0.53, P < 0.02) and no significant correlation with mean pulmonary capillary wedge pressure. Moreover, Kaplan-Meier analysis focusing on the patients with myocardial infarction revealed that the group with D-maxV < 10.4 mm (n = 13) exhibited a lower cumulative cardiac event-free rate than that with D-maxV ≥ 10.4 mm (n = 14) (49.4% vs 92.9% at 5 years, P < 0.05). The depth of the spatiotemporal maximum of early diastolic LV inflow velocity reflects LV relaxation and is free of pseudonormalization. Evaluation of the LV relaxation separately from preload may have a prognostic value for myocardial infarction.

Cardiac amyloidosis has been documented to show mitral regurgitation (MR) and a thickened mitral valve (MV) due to amyloid deposits. However, the changes in the physical properties of the thickened MV tissue in cardiac amyloidosis, which may be a causative factor of the MR, have not been described. Physical properties of the tissue, which are expressed by the elastic bulk modulus, can be evaluated by tissue sound speed. If biological tissue is assumed to be fluid-like, the tissue sound speed may be given by c= square root of K/rho, where c is the tissue sound speed, K is the elastic bulk modulus, and rho is the density. A reduction in tissue sound speed indicates a reduction in the elastic bulk modulus of the tissue, assuming that there is little change in rho. This suggests that the tissue is less elastic. The purpose of this study was to assess the physical properties of MV tissue by evaluating the sound speed of the MV tissue in cardiac amyloidosis. MV specimens were obtained at autopsy from 20 control adults without cardiovascular diseases and from 20 patients with cardiac amyloidosis. An acoustic microscope operating at 450 MHz was used to measure the tissue sound speed in the tip and basal portions of the MV tissue. The density of MV tissue was measured by microgravimetry. The severity of the MR had been evaluated by Doppler echocardiography before death, and it was compared with the tissue sound speed measured after death. In cardiac amyloidosis showing mild MR, the tissue sound speed of the MV in the tip portion (1605 +/- 19 m/s) and in the basal portion (1791 +/- 64 m/s) were lower than the corresponding values in control subjects (1637 +/- 42 m/s and 1851 +/- 62 m/s). However, these differences were not statistically significant. In cardiac amyloidosis showing moderate MR, the tissue sound speed of MV in the tip portion (1563 +/- 17 m/s) and in the basal portion (1654 +/- 59 m/s) were significantly lower than the corresponding values in the control subjects (p < 0.001) and the patients with mild MR (p < 0.05). No significant differences were observed in the density of MV tissue among the three groups. Therefore, the low value of the MV tissue sound speed in patients with cardiac amyloidosis indicated a reduced elastic bulk modulus, suggesting the less elasticity of the MV tissue. Furthermore, the patients with moderate MR demonstrated the greater reduction in the tissue sound speed than the patients with mild MR. The data suggest that the changes in physical properties of the MV tissue may be one of the causes of MR in cardiac amyloidosis.

Background: Cibenzoline, a class la antiarrhythmic drug, can be used to relieve left ventricular (LV) outflow obstruction in hypertrophic obstructive cardiomyopathy (HOCM). However, the mechanism of this agent in HOCM has been controversial. Hypothesis: This study was designed to investigate the effect of cibenzoline on regional LV function and the acoustic properties in HOCM using ultrasonic integrated backscatter. Methods: Ten patients with HOCM and 16 healthy volunteers were examined. In patients with HOCM, wall thickening (%WT) and the magnitude of cyclic variation of integrated backscatter (mag-CVIBS) in the interventricular septum (IVS) and LV posterior wall were measured before and after oral administration of cibenzoline. To assess asynchrony of contractile elements, the phase difference between CVIBS and%WT were measured from the LV posterior wall. Pressure gradients at the LV outflow tract were estimated using continuous-wave Doppler echocardiography. Results: Although%WT decreased significantly in the LV posterior wall, %WT and mag-CVIBS remained unchanged in the IVS. The phase difference in the LV posterior wall was significantly greater in patients with HOCM than in healthy volunteers (HOCM:healthy volunteers, 1.57 ± 0.23:1.00 ± 0.03, p < 0.001) at baseline. After administration of cibenzoline, the phase difference shifted to normal value (from 1.57 ± 0.23 to 1.28 ± 0.27, p = 0.0382), and pressure gradients at the LV outflow tract decreased (from 109 ± 55 to 58 ± 48 mmHg, p = 0.0063). Changes in pressure gradients at the LV outflow tract and the phase difference were closely related. Conclusions: Regional function and the acoustic properties of myocardium in HOCM were altered by cibenzoline in the LV posterior wall but remained unchanged in the IVS. The normalization of the phase difference in the LV posterior wall was closely related to the decrease in pressure gradients at the LV outflow tract. These findings suggest that negative inotropic action and the improvement of asynchrony in the LV posterior wall rather than in the IVS may contribute to the reduction of pressure gradients at the LV outflow tract in HOCM.

The authors measured the aortic regurgitant orifice area (ROA) using Doppler echocar diography and attempted to clarify how important the ROA is in determining the regur gitant volume (RV) in 22 patients with chronic aortic regurgitation (AR). The RV was calculated from the difference between the left ventricular ejection flow volume and transmitral inflow volume as measured by Doppler echocardiography. The ROA was obtained by two methods: RV/time velocity integral of AR jet measured by continuous wave Doppler (calculation method) and manual tracing of minimum cross-sectional area of short-axis color Doppler. The RV ranged from 10 to 90 mL/beat and the ROA by calculation method was from 0.05 to 0.35 cm2, which showed a strong correlation ( r = 0.93, p < 0.001). The time velocity integral of aortic regurgitant jet showed a poor correlation with the RV (r = 0.45, p < 0.05). The values of ROA by the two methods showed a good correlation ( r = 0.93, p < 0.001). Thus, the authors conclude that the ROA is a basic determinant of the RV in AR and that color Doppler can be employed to precisely assess the ROA.

Although dobutamine stress echocardiography is important for assessing cardiac ischemia and viability, analysis of wall motion is qualitatively performed. We quantitatively evaluated left ventricular wall motion using a newly developed omnidirectional M-mode echocardiography that can depict the M-mode at the site of region of interest on the 2-dimensional image in real time, and established its usefulness for analyzing the myocardial response to dobutamine infusion. Dobutamine stress echocardiography with omnidirectional M-mode was performed in 57 patients with coronary lesions. In 38 of these patients, exercise stress single-photon emission computed tomographic thallium scintigraphy (Tl-201 SPECT) was performed. Endocardial excursion of 103 regions was measured from omnidirectional M-mode at baseline, low-dose (6 microg/kg/min), and at peak dose (30 microg/kg/min) dobutamine. A decrease and increase in wall excursion was scored (from -3 to 3) for a changes of every 2 mm, and a quantitative wall motion score (QWMS) was calculated as a summation of the scores from baseline to low dose and from low to peak doses. Quantitative coronary stenosis score (QCSS) was calculated as a summation of stenotic and collateral scores. The stenosis scores were graded as: 1 = 0% to 50%, 2 = 50% to 75%, 3 = 75% to 90%, 4 = 90% to 95%, 5 = 95% to 100%; collateral scores were graded as: -1 = poor collateral, -2 = good collateral. Based on the QWMS at each dose of dobutamine, the serial changes in wall motion were divided into 4 groups: augmented, biphasic, no change, and worsening. The QCSS was clearly different among these groups. QWMS was significantly correlated with QCSS (r = 0.657, p

The long-term effect of mexiletine on left ventricular (LV) contractility in patients with congestive heart failure is not clear. The authors therefore measured LV contractility before and after continuous oral administration of mexiletine in patients with congestive heart failure accompanied by mitral regurgitation (MR) using Doppler echocardiography. The study population consisted of 8 patients with congestive heart failure (6 due to dilated cardiomyopathy and 2 due to old myocardial infarction) accompanied by significant functional MR who had more than 1000 ventricular premature contractions (VPCs) per day or Class IV Lown classification arrhythmias before mexiletine administration. The LV contractility was evaluated by calculating a Doppler-derived index, the rate of increase in LV pressure during the isovolumic contraction time (ICT delta P/delta t), which has been confirmed to be nearly equal to LV Max dP/dt. The increase in LV pressure (delta P) between 1 and 3 m/sec of the MR flow velocity as measured by continuous-wave Doppler echocardiography was calculated using the simplified Bernoulli's equation, and ICT delta P/delta t was derived by dividing delta P by the time required for this change. The left ventricular ejection fraction and the left ventricular and left atrial dimensions also were measured by echocardiography. These parameters were obtained before and after 2 to 4 weeks of daily oral administration of mexiletine 300 mg. Values of ICT delta P/delta t were 640 +/- 202 mm Hg/sec and 650 +/- 210 mm Hg/sec before and after mexiletine administration, respectively, showing no change.(ABSTRACT TRUNCATED AT 250 WORDS)

Since acoustic properties of the myocardium are sensitive to the myocardial structure and the contractile conditions of myocyte, the authors evaluated cardiac dysfunction based on the integrated ultrasonic backscatter in 18 hemodialysis (HD) patients (duration: 102 +/- 84 months, mean age: 57.6 +/- 9.7 years) and 11 age-matched normals. The cyclic variation of integrated backscatter (CV-IB) at interventricular septum (IVS) and left ventricular posterior wall (PW) was measured and compared with percent fractional shortening (%FS) and percent wall thickening (%Th). The CV-IB of HD patients was smaller than that of control subjects (IVS: 6.2 +/- 1.1 dB vs 8.2 +/- 1.1 dB, p = 0.0003 and PW: 8.4 +/- 2.2 vs 10.3 +/- 1.3, p= 0.025). No significant difference was observed in %FS and %Th between HD patients and control subjects. In HD, the ratio of velocities of early diastolic inflow (E) to late atrial inflow was decreased (0.7 +/- 0.2 vs 1.1 +/- 0.7, p = 0.049) and deceleration time of E was prolonged significantly (200 +/- 28 msec vs 159 +/- 30 msec, p = 0.0082). In the absence of overt cardiac systolic dysfunction, myocardial damage indicated as a decrease in CV-IB and diastolic dysfunction identified on transmitral velocity waveform were detected, which may reflect from the myocardial fibrosis. As a mechanism, pressure overload, hyperparathyroidism, and anemia were neglected, and the other humoral factors may contribute to the myocardial damage in chronic renal failure.

Left atrial wall elasticity is one of the important factors regulating left atrial stiffness and functions. The authors evaluated left atrial wall elasticity by measuring the sound speed through the left atrial wall, based on the hypothesis that high elasticity tissues will yield larger sound speed values through the tissue, and examined age-associated changes in left atrial wall elasticity. Left atrium specimens were obtained from 30 normal subjects (age, 15-95 years) at autopsy. An acoustic microscope, operating at 450 MHz, was used to measure the sound speed in the endocardium and the myocardium of the left atrium. The sound speeds in endocardium and myocardium demonstrated significant correlation with age (r=0.74, p Katsufumi Mizushige, MD Second Department of Internal Medicine Kagawa Medical University 1750-1, Miki-cho, Kita-gun Kagawa 761-0793, Japan