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The measurement of vena contracta is a promising method for quantification of mitral regurgitation (MR). No data exist regarding the ability of power Doppler echocardiography in the assessment of vena contracta in MR. We attempted to clarify the ability of power Doppler in the assessment of vena contracta in MR. The width of vena contracta was measured using power Doppler in 70 patients with chronic MR. Mean effective regurgitant orifice area (EROA) was calculated quantitatively by the spectral Doppler. The area of vena contracta was calculated by measuring the width of vena contracta from the following formula: Vena contracta area = π* (vena contracta width/2)2. The width of vena contracta ranged from 3.6 to 8.4 mm. The EROA varied from 0.10 to 0.56 cm2. Good correlations were found between EROA and vena contracta area obtained by power Doppler (r = .95, p < .0001, SEE = 0.04 cm2). Strong relationships were observed between the area of vena contracta and regurgitant volume (r = 0.93, p < .0001, SEE = 8.1 ml/beat), and regurgitant fraction (r = 0.95, SEE = 6.1%). Power Doppler may provide an additional method for assessing vena contracta in MR.

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.

We aimed to investigate whether the improvement of left ventricular (LV) diastolic function by cibenzoline, a class Ia antiarrhythmic drug, in hypertrophic obstructive cardiomyopathy (HOCM) is due to LV afterload reduction or a primary lusitropic effect on LV. Twenty-three patients with hypertrophic cardiomyopathy (11; HOCM, 12; non-obstructive HCM; HNCM) were examined. Pulsed-wave Doppler, color M-mode and tissue Doppler echocardiography were performed before and 90 minutes after oral administration of cibenzoline (300 mg), and were compared with a treatment of bisoprolol (5 mg/day, 10 days). Early (E) and late diastolic LV inflow velocity, E flow propagation velocity (FPV) and early diastolic mitral annulus velocity (Ea) were measured. E/FPV and E/Ea were calculated as indices of LV filling pressure. LV outflow pressure gradients estimated using continuous-wave Doppler in HOCM markedly decreased after cibenzoline (83 ± 42 to 40 ± 33 mmHg, p < 0.005) and bisoprolol (44 ± 40 mmHg, p < 0.005). Following cibenzoline, E/FPV and E/Ea were significantly decreased in both HOCM (1.75 ± 0.53 to 1.32 ± 0.28, p < 0.05, 18.9 ± 6.2 to 14.8 ± 5.0, p < 0.05, respectively) and HNCM (1.75 ± 0.58 to 1.41 ± 0.73, p < 0.05, 13.0 ± 4.3 to 9.7 ± 3.6, p < 0.01, respectively). Those in HNCM did not change by bisoprolol. Cibenzoline improved LV diastolic function in HCM, whereas bisoprolol did not affect it. Thus, the primary lusitropic effect of cibenzoline rather than LV after load reduction might have contributed to the improvement of diastolic function in HOCM.

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.

The aim of this study was to examine the influence of flow velocity, beam incident angle and a wall motion filter on the intensity of power Doppler image of steady flow in vitro. Power Doppler images of flow were recorded using a 7.5-MHz linear transducer with the fixed repetition frequency, gain and frame rate settings at the velocity levels of 15, 20, 35 and 65 cm/s with the beam incident angles of 30 degrees and 60 degrees. The power (P) of received Doppler signal was digitized to 25 gray values (G) for imaging using a wall motion filter with the transfer function: G = a x log P + b (a, b = constant values). Image intensity was measured at the center of the flow image off-line and compared with the flow velocity measured by conventional pulsed wave Doppler. Below the Nyquist limit, G increased as velocity increased, and G with the incident angle 30 degrees was lower than those with 60 degrees. Overall relationship between the Doppler shift frequency and the image intensity exhibited an excellent correlation when fit to the theoretical curve derived from the filter property (r = 0.97). The signal intensity of power Doppler image of flow depends upon the mean Doppler frequency shift or the flow velocity and was clearly affected by the wall motion filter.

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 examination conditions necessary for accurate measurement of regurgitant volume by the proximal flow convergence method applying a simple hemispheric equation remain uncertain. This study investigated the requirement for measuring regurgitant stroke volume from the combined continuous-wave and color Doppler proximal flow convergence approach. Twenty-five pulsatile flow rates were produced by driving five regurgitant stroke volumes ranging from 30 to 70 ml/beat through planar orifices with cross-sectional areas ranging from 0.10 to 1.0 cm 2 . Four different shaped orifices (circular, rectangular with a major/minor axis ratio 2:1, slitlike with a major/minor axis ratio of 8:1, and square) having identical orifice areas (0.5 cm 2 ) were examined. Regurgitant volume (RV) was estimated from the combined continuous-wave and color Doppler approach according to the previously described equation RV=2π × (r max) 2 × AV × (TVI/Vmax), where r max is maximal radial distance, AV is aliasing velocity, TVI is time velocity integral of regurgitant jet, and Vmax is peak velocity of regurgitant jet. Plotting the difference between actual and calculated RV versus radial distance of the proximal convergence shell for each flow rate from circular to rectangular orifices yielded curves conforming to a curvilinear function that crossed the point of zero difference at 1.0 cm. However, in the slitlike orifice, a more remote distance (1.6 cm) is required for the best agreement. Actual regurgitant stroke volume can be estimated well by the combined continuous-wave Doppler and proximal flow convergence method applying a simple hemispheric equation if an aliasing velocity is used that results in a radial distance of at least 1.0 cm. (Am Heart J 1997;133:19-28.)

Background It has been demonstrated that cyclic variation of ultrasonic integrated backscatter (CVIBS) may be useful in detecting altered physical conditions in the heart. However, no previous study has examined serial changes of CVIBS in the myocardium during the development of left ventricular dysfunction. Methods and Results We examined alterations of CVIBS in pacing-induced cardiac dysfunction. Eight pigs (36±2 kg) were studied before and sequentially during sustained rapid ventricular pacing (225±9 beats per minute). CVIBS was measured in the IVS and left ventricular PLW before pacing and daily for 4 days after onset of pacing. Five additional pigs (35±10 kg) were examined after 14 days of pacing. Regional function and CVIBS were assessed with pacemakers inactivated. A quantitative integrated backscatter imaging system (two-dimensional format) was used. Over 4 days of pacing, the magnitude of CVIBS progressively decreased in the PLW but was unchanged in the IVS, findings that persisted at 14 days. Percent wall thickening in the PLW progressively decreased to a greater degree than percent wall thickening in the IVS. A linear relation between the magnitude of CVIBS and percent wall thickening was found. At 14 days, blood flow to the two regions was similar but regional differences in CVIBS persisted. Conclusions Rapid left ventricular pacing produces abnormalities of regional myocardial function within 48 hours of pacing. Regional myocardial dysfunction is accompanied by a reduction in CVIBS in the same region.

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)

The migration as well as proliferation of coronary artery medial smooth muscle cells (SMC) into the intima is proposed to be an important process of intimal thickening in coronary atherosclerosis. In the current study, we examined the effects of the angiotensin type 1 receptor antagonist valsartan on angiotensin II (Ang II)-induced migration of cultured human coronary artery SMC using Boyden's chamber methods. Ang II significantly stimulated human coronary artery SMC migration in a concentration-dependent manner between 10(-6) and 10(-8) mol/l when cells of passage 4 to 6 were used. However, the migration response to Ang II was moderately decreased in cells of passage 10 to 12, and was markedly decreased in cells of passage 15 to 17, compared to that of passage 4 to 6. Ang II-induced migration was blocked by the Ang II type 1 (AT1) receptor antagonist valsartan in a concentration-dependent manner. By contrast, the Ang II type 2 (AT2) receptor antagonist PD 123319 did not affect Ang II-induced migration. Ang II modestly increased the cell number of human coronary artery SMC after a 24-h incubation. This increase in cell numbers was also clearly blocked by valsartan, but not by PD 123319. These results indicate that Ang II stimulates migration as well as proliferation via AT1 receptors in human coronary artery SMC when cells of passage 4 to 6 are used. Valsartan may prevent the progression of coronary atherosclerosis through an inhibition of Ang II-induced migration and proliferation in these cells, although in vivo evidence is lacking.

The purpose of our study has to determine the myocardial protective effects of the angiotensin-converting enzyme (ACE) inhibitor temocapril (TEM, 7 mg/kg/day) simultaneously administered with doxorubicin (Adriamycin). Twenty male Sprague-Dawley rats were intraperitoneally administered a cumulative dose of 15 mg/kg of doxorubicin (each dose of 1.0 mg/kg x 15) for 3 weeks, and divided into TEM-untreated and -treated rats. Seven control rats were injected with saline intraperitoneally. Body weight, hemodynamics, and echocardiographic measurements including quantitative analysis of ultrasonic integrated backscatter (IB) were obtained for 12 weeks after treatment. Finally, rats were killed for histopathologic study. At 6 weeks, end-diastolic left ventricular diameter (LVD) and percentage fractional shortening (%FS) were similar in TEM-treated and TEM-untreated rats, but cyclic variation of IB (dB) significantly decreased in TEM-untreated rats (7.3 +/- 1.2; control rats, 9.7 +/- 0.9; p < 0.01). At 12 weeks, %FS decreased in TEM-untreated rats (26.1 +/- 6.1%: TEM-treated rats, 34.2 +/- 6.2; p < 0.05), and calibrated IB (dB) in TEM-untreated rats (15.5 +/- 0.5) increased as compared with that in TEM-treated rats (12.1 +/- 0.7; p < 0.01). Interstitial collagen accumulation increased in TEM-untreated rats and was inhibited in treated rats. Simultaneous administration of TEM with doxorubicin was beneficial in preventing doxorubicin-induced myocardial damage, and myocardial tissue characterization was useful for the early detection of myocardial damage and the assessment of therapy.

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

Although the hemodynamic responses to isotonic and isometric exercise are different, few data exist comparing the response to left ventricular (LV) diastolic filling dynamics with these two forms of exertion. Therefore we performed Doppler examination before and at the end of isotonic and isometric exercise in 20 normal volunteers to define the differential responses of LV filling to these two forms of exertion. Transmitral inflow velocity signals from the apical view and phonocardiography were recorded before and at the termination of treadmill exercise (TRD) to 11 METs and handgrip (HG) 50% maximal for 2 minutes). Mean blood pressure (mBP), heart rate (HR), early diastolic (E) and late atrial (A) inflow velocities, mean acceleration rate (ACC) of E wave, time velocity integral of inflow (Ti), and isovolumic relaxation time (IRT) from second heart sound to onset mitral inflow were measured. Absolute changes from baseline were significantly different for the two forms of exertion: TRD versus HG: BP = 11 +/- 9 versus 36 +/- 10 mm Hg, HR = 37 +/- 16 versus 16 +/- 9 beats/min, E = 11.6 +/- 11.3 versus -7.0 +/- 9.4 cm/sec, A = 29.9 +/- 14.5 versus 14 +/- 12 cm/sec, ACC = 164 +/- 151 versus -56 +/- 135 cm/sec2, Ti = 1.9 +/- 3.0 versus -1.7 +/- 1.7 cm, and IRT = -12 +/- 9 versus 9 +/- 10 msec, all p < 0.0001 except for A, p < 0.001). Isotonic treadmill exercise resulted in enhanced early diastolic filling manifested by increases in E and ACC and a decreased in IRT. Conversely, isometric handgrip exercise produced evidence of reduced early filling including decreased E and ACC and slightly increased IRT. Thus the response of LV filling dynamics recorded by Doppler differs for isotonic and isometric exertion and likely reflects the variable pressure and flow alterations induced by these two forms of exertion.

Sustained rapid left ventricular (LV) pacing has been used to induce congestive heart failure, but whether regional myocardial perfusion contributes to the development of myocardial dysfunction is unknown. Therefore, we examined 4 pigs before and sequentially during sustained rapid LV pacing (225 bpm) from the at posterolateral epicardium. We performed myocardial contrast echocardiography (MCE) with left atrial injection of an investigational galactose contrast agent prior to pacing and daily for 4 days after onset of pacing. Pacemakers were inactivated for 60 min prior to data acquisition. The ratio of peak intensity after injection and baseline intensity of region of interest (peak intensity ratio) was measured at 8 segments (Fig) in the short axis view at the tip of papillary muscle using video intensitometry. Percent wall thickening (%WTh) in the interventricular septum (IVS) and posterolateral wall (PLW) were assessed by M-mode echo. Over the 4 days of pacing, the peak intensity ratio progressively decreased in the PLW [region 4 (p l 0.01), 5 (p l 0.001),6 (p l 0.05)] but did not decrease in other regions. Significant regional-specific changes were observed between region 4 vs 8 (p l 0.0002). and region 5 vs 8 (p l 0.0001). Similarly, %WTh in the PLW progressively decreased (p l 0.0001) but was unchanged in the IVS. Conclusion These data suggest that sustained rapid LV pacing produces regional myocardial dysfunction in the initial development of LV failure. Myocardial contrast echocardiography suggests that relative hypoperfusion may contribute to regional myocardial dysfunction in this model. Download : Download high-res image (107KB) Download : Download full-size image

QW3600 (EG) is a new perflourocarbon (dodecaflouropentane) ultrasonic contrast agent capable of producing myocardial opacification by IV injection. However, the doses required for myocardial visualization have sometimes been associated with transient hemodynamic changes. Therefore, we evaluated the ability of pretreatment with: (1) antihistamines and corticosteroids to eliminate hypersensitivity and thus reduce hemodynamic changes; and (2) administration of coronary vasodilators to enhance myocardial intensity. We performed 2–D echo in the short axis parasternal view in 10 closed chest ventilated dogs in whom LV, Ao and pulmonary artery catheters enabled direct assessment of hemodynamics. All animals were given benadryl 1 mg/kg and Solu-Mediol 1 mg/kg approximately one hour prior to the study. Subsequently, a 0.5 cc/kg EchoGen®injection was repeated. Contrast intensity was quantified by a 0.3 cm2region of interest positioned in the midventricular wall and peak videointensity (PVI) was measured in gray levels. Results *= p l 0.01 for EG vs DIP + EG. HR FA (S) FA (D) LV PA PVI BASE 145 ± 23 172 ± 14 120 ± 7 165 ± 12 122 ± 6 23 ± 18 EG 150 ± 24 163 ± 13 114 ± 7 159 ± 13 28 ± 10 69 ± 50 DIP 142 ± 19 171 ± 14 114 ± 15 162 ± 23 24 ± 3 33 ± 21 DIP + EG 145 ± 23 156 ± 31 99 ± 21 145 ± 32 32 ± 4 110 ± 41 Thus, combination of antihistamine-steriod pretreatment and dipyridamole vasodilation enables enhanced visualization of myocardial perfusion by reduced doses of EG without significant hemodynamic effects. This approach may be of value in achieving myocardial opacification in patients with EG without incurring side effects.

Doppler approaches to the calculation of stenotic and regurgitant effective orifice area (EOA) have been based on the assumption of a constant contraction coefficient (Cc). However, it has been demonstrated that Doppler-derived EOA is underestimated with lower stroke volumes in mechanical valves, and debate continues whether this phenomenon is due to incomplete valve opening or to alteration of the Cc in restrictive orifices. Therefore, we studied the relationship between true orifice area (TEA) and EOA in an in vitro pulsatile flow model (Harvard model 1423). Pulsatile flow using a cornstarch solution adjusted to a physiological viscosity of 3.5 cP was driven through circular planar orifices of 0.24, 0.30, 0.50 and 0.75 cm 2. Stroke volume (SV) was varied from 20 to g0 ml/beat in increments of 10 m[/beat, pump rate was fixed at 40/min. Further, to explore the influence of orifice shape we used three different shaped orifices (circular, rectangular with a ratio 2:1, and square) of the same orifice area (0.5 cm2). "instantaneous peak orifice flow velocities were obtained by continuous-wave Doppler and the time velocity integral (TVl) of orifice flow was measured an average of five consecutive beats. EOA was calculated by dividing SV by the TVI of orifice velocity (EOA=SV/TVI) for each SV. We calculated contraction coefficient (Cc) as follows; Cc = EOA/TOA. RESULTS: Cc was decreased consistently at lower SV and plateaued at higher SV. This trend is unchanged by odfice shape. The Cc at which plateau occurred was dependent upon orifice size. Thus, these data indicate that, in 08 t ~ia BBme ~ the setting of pulsatile flow: a a a 9 9 9 (1) Cc is dependent upon SV

Few data exist directly documenting the ability of contrast echo (CE) to demonstrate the presence and development of coronary collaterals. Therefore, we performed serial CE in 5 closed chest awake pigs in whom an ameroid constrictor placed around the proximal LCx produced total occlusion and development of collateral flow gradually over 3 weeks. A second inflatable cuff constrictor was placed distal to the ameroid for acute occlusion. Short axis echos during left atrial injections of 1 gram of SHU 504 (Levovist) were performed with and without inflation of the acute occluder at baseline, 5, 10, 20, and 25 days. Ameroid occlusion produced only a transient contractile abnormality: posterolateral wall thickening was 71, 39, and 67% at BASE, 10, and 25 days. With the acute cuff occluder open. interventricular septum (IVS) opacification was dense during all studies. while posterolateral wall (PLW) intensity was dense at BASE, decreased markedly at 10 days, and increased again at 25 days as collaterals developed. Acute inflation of the cuff resulted in a clear PLW perfusion deficit during BASE to day 10, which improved significantly at day 25. We measured videointensity (gray levels) from a 0.3 cm2region of interest in the mid IVS and PLW. The ratio of IVS/PLW intensity increased on day 10 as the constrictor occluded, and then decreased on day 25 as collaterals developed, even with the acute cuff inflated (Figure). Thus, in a porcine model in which gradual coronary occlusion induces collaterals. CE demonstrates opacification of the involved myocardium. These data document the ability of CE to identify and track the development of coronary collateral flow. Download : Download high-res image (61KB) Download : Download full-size image