Role of intra-ventricular vortex in left ventricular ejection elucidated by echo-dynamography.

PURPOSE: From the correlation between the blood flow dynamics and wall dynamics in the left ventriocle (LV) analyzed using echo-dynamography, the ejection mechanisms and role of the intra-ventricular vortex in the LV were elucidated in detail during the pre-ejection transitional period (pre-ETP), the very short period preceding LV ejection. METHODS: The study included 10 healthy volunteers. Flow structure was analyzed using echo-dynamography, and LV wall dynamics were measured using both high-frame-rate two-dimensional echocardiography and a phase difference tracking method we developed. RESULTS: A large accelerated vortex occurred at the central basal area of the LV during this period. The main flow axis velocity line of the LV showed a linearly increasing pattern. The slope of the velocity pattern reflected the deformity of the flow route induced by LV contraction during the pre-ETP. The centrifugal force of the vortex at its junction with the main outflow created a stepwise increase of about 50% of the ejection velocity. CONCLUSION: Ejection of blood from the LV was accomplished by the extruding action of the ventricular wall and the centrifugal force of the accelerated vortex during this period. During ejection, acceralated outflow was considered to create a spiral flow in the aorta with help from the spherical structure of the Valsalva sinus.

Deformability of the pulsating left ventricular wall: A new aspect elucidated by high resolution ultrasonic methods.

BACKGROUND: Although the deformability of the left ventricular (LV) wall appears to be important in maintaining effective cardiac performance, this has not been debated by anyone, probably owing to the difficulties of the investigation. OBJECTIVES: This study applies a new technology to demonstrate how the LV wall deforms so as to adjust for optimum cardiac performance. SUBJECTS AND METHODS: Ten healthy volunteers were the subjects. Using echo-dynamography, an analysis at the "microscopic" (muscle fiber) level was done by measuring the myocardial axial strain rate (aSR), while the "macroscopic" (muscle layer) level contraction-relaxation/extension (C-R/E) properties of the LV wall were analyzed using high frame rate 2D echocardiography. RESULTS: Deformability of the LV was classified into three types depending on the non-uniformity of both the C-R/E properties and the aSR distribution. "Basic" deformation (macroscopic): The apical posterior wall (PW) thickness change was concentric and monophasic, whereas it was eccentric and biphasic in the basal part. This deformation was large in the PW, but small in the interventricular septum (IVS). The elongation of the mitral ring diameter and the downward movement of its posterior part were shown to be concomitant with the anterior extrusion of the PW. "Combined" deformation (macroscopic and microscopic): This was observed when the basic deformation was coupled with the spatial aSR distribution. Three patterns were observed: (a) peristaltic; (b) bellows-like; and (c) pouch-like. "Integrated" deformation: This was the time serial aSR distribution coupled with the combined deformation, illustrating the rotary pump-like function. The deformability of the LV assigned to the apical part the control of pressure and to the basal part, flow volume. The IVS and the PW exhibited independent behavior. CONCLUSIONS: The non-uniformity of both the aSR distribution and the macroscopic C-R/E property were the basic determinants of LV deformation. The apical and basal deformability was shared in LV mechanical function.

Non-uniform distribution of the contraction/extension (C-E) in the left ventricular myocardium related to the myocardial function.

OBJECTIVE: We attempted to disclose the microscopic characteristics of the non-uniform distribution of the contraction and extension (C-E) of the left ventricular (LV) myocardium using a new methodology (echo-dynamography). METHODS: The distributions of the "axial strain rate" (aSR) and the intra-mural velocity in the local areas of the free wall including the posterior wall (PW) and interventricular septum (IVS) were microscopically obtained using echo-dynamography with a high accuracy of 821 µm in the spatial resolution. The results were shown by the color M-mode echocardiogram or curvilinear graph. Subjects were 10 presumably normal volunteers. RESULTS: (1) Both the C-E in the pulsating LV wall showed non-uniformity spatially and time-sequentially. (2) The C-E property was better evaluated by the aSR distribution method rather than the intra-mural velocity distribution method. (3) Two types of non-uniformity of the aSR distribution were observed: i.e. (i) the difference of its (+)SR (contraction: C) or (−)SR (extension: E) was solely the "magnitude"; (ii) the coexistence of both the (+) SR and (−)SR at the same time. (4) The aSR distribution during systole was either "spotted," or "multi-layered," or "toned" distribution, whereas "stratified," "toned," or "alternating" distributions were observed during diastole. (5) The aSR distribution in the longitudinal section plane was varied in the individual areas of the wall even during the same timing. (6) To the mechanical function of the LV, there was a different behavior between the IVS and PW. . CONCLUSIONS: The aSR and its distribution were the major determinants of the C-E property of the LV myocardium. Spatial as well as time-sequential uniformity of either contraction or extension did not exist. The myocardial function changed depending on the assemblage of the aSR distribution, and by the synergistic effect of (+)SR and (-)SR, the non-uniformity itself potentially served to hold the smooth LV mechanical function.

New concept of the contraction-extension property of the left ventricular myocardium.

OBJECTIVES: Using newly developed ultrasonic technology, we attempted to disclose the characteristics of the left ventricular (LV) contraction-extension (C-E) property, which has an important relationship to LV function. METHODS: Strain rate (SR) distribution within the posterior wall and interventricular septum was microscopically measured with a high accuracy of 821µm in spatial resolution by using the phase difference tracking method. The subjects were 10 healthy men (aged 30-50 years). RESULTS: The time course of the SR distribution disclosed the characteristic C-E property, i.e. the contraction started from the apex and propagated toward the base on one hand, and from the epicardial side toward the endocardial side on the other hand. Therefore, the contraction of one area and the extension of another area simultaneously appeared through nearly the whole cardiac cycle, with the contracting part positively extending the latter part and vice versa. The time course of these propagations gave rise to the peristalsis and the bellows action of the LV wall, and both contributed to effective LV function. The LV contraction started coinciding in time with the P wave of the electrocardiogram, and the cardiac cycle was composed of 4 phases, including 2 types of transitional phase, as well as the ejection phase and slow filling phase. The sum of the measurement time duration of either the contraction or the extension process occupied nearly equal duration in normal conditions. CONCLUSION: The newly developed ultrasonic technology revealed that the SR distribution was important in evaluating the C-E property of the LV myocardium. The harmonious succession of the 4 cardiac phases newly identified seemed to be helpful in understanding the mechanism to keep long-lasting pump function of the LV.

Physiological basis and clinical significance of left ventricular suction studied using echo-dynamography.

BACKGROUND: The existence as well as the exact genesis of left ventricular suction during rapid filling phase have been controversial. In the present study, we aimed at resolution of this problem using noninvasive and sophisticated ultrasonic methods. The clinical meaning was also documented. METHODS: Ten healthy male volunteers were examined by 2D echocardiography and echo-dynamography which enables us to obtain detailed instantaneous data of blood flow and wall motion simultaneously from the wide range of the left ventricle. The correlation of blood flow and wall motion was also studied. RESULTS: Rapid ventricular filling was divided into 2 phases which had different physiology. The early half (early rapid filling: ERF) showed the effect which was alike drawing a piston. This was proved by the shape of the velocity of inflow and the basal muscle contraction which actively assisted extension of the relaxed apical and central parts of the left ventricle, giving the negative pressure which causes the ventricular suction. The later half (late rapid filling: LRF) showed the turning of the fundamental flow and the squeezed basal part just like the sphincter in addition to the expansion of the apical and central portions of the left ventricle, and all of these cooperatively augmented the suction effect. CONCLUSION: Ventricular suction does exist to help ventricular filling. Simultaneous appearance of the contraction in the basal part and the relaxation or extension in the apical part during the post-ejection transitional period was made to occur the suction in the LV. And it can be said that the suction appeared in the late stage of systole as the one of the serial systolic phenomena.

Spiral systolic blood flow in the ascending aorta and aortic arch analyzed by echo-dynamography.

Using echo-dynamography, systolic blood flow structure in the ascending aorta and aortic arch was investigated in 10 healthy volunteers. The blood flow structure was analyzed based on the two-dimensional (2D) and 1D velocity vector distributions, changing acceleration of flow direction (CAFD), vorticity distribution, and Doppler pressure distribution. To justify the results obtained in humans, in vitro experiments were done using straight and curved tube models of 20mm diameter. The distribution of the CAFD showed a spiral staircase pattern along the flow axis line. In addition, the changes in the velocity profile in the short-axis direction, 2D distribution of the vorticity, and velocity vector distribution on the aortic cross-section plane, all confirmed the presence of systolic twisted spiral flow rotating clockwise toward the peripheral part of the ascending aorta. The rotation cycle of this spiral flow correlated inversely with the maximum velocity of the aortic flow, so that this cycle was shorter in early systole and longer in late systole. The model experiments showed similar results. The spiral flow seemed to be produced by several factors: (i) anterior shift of the direction of ejected blood flow due to the anterior displacement of the projection of the aorta; (ii) accelerated high pressure flow ejected antero-upward; (iii) inertia resistance at the peripheral boundary of the sinus of Valsalva; and (iv) reflection caused by the concave spherical structure of the inner surface of the basal part of the aorta. Because the main spiral flow axis line nearly coincided with the center line of the aorta, it is concluded that the occurrence of the spiral flow plays an important role in maintaining the blood flow direction passing through the cylindrical curved aortic arch and thus in keeping the most effective ejection as well as in dispersing the shear stress in the aortic wall.

Blood flow structure and dynamics, and ejection mechanism in the left ventricle: analysis using echo-dynamography.

Using our "echo-dynamography", blood flow structure and flow dynamics during ventricular systole were investigated in 10 normal volunteers. The velocity vector distribution demonstrated blood flow during ejection was laminar along the ventricular septum. The characteristic flow structure was observed in each cardiac phases, early, mid- and late systole and was generated depending on the wall dynamic events such as peristaltic squeezing, hinge-like movement of the mitral ring plane, bellows action of the ventricle and dimensional changes in the funnel shape of the basal part of the ventricle, which were disclosed macroscopically by using the new technology of high speed scanning echo-tomography and microscopically by the strain rate distribution measured by phase tracking method. The pump function was reflected on the changes in the flow structure represented by the flow axis line distribution and the acceleration along the flow axis line. The acceleration of the ejection had three modes, "A", "B" and "C", and generated by the wall dynamic events. "A" appeared from the apical to the outflow area along the main flow axis line, "B" along the anterior mitral leaflet and the branched flow axis line, and "C" generated by the high speed vortex behind the mitral valve. The magnitude of the acceleration was estimated quantitatively from the velocity gradient along the flow axis line. Macroscopic and microscopic asynchrony in the myocardial contraction and extension appeared systematically in the local part of the ventricular wall, which was helpful for making the flow structure and for performing the smooth pump function.

Effects of Dobutamine Infusion on Mitral Regurgitation.

Both intensity of mitral regurgitant murmur and color-coded Doppler regurgitant signal area have been reported to correlate with the degree of regurgitation. To evaluate the relationship between the intensity of regurgitant murmur and severity of mitral regurgitation, phonocardiography, echocardiography, and Doppler ultrasound were performed in 18 patients with mitral regurgitation before and during dobutamine infusion. Mitral regurgitation was due to mitral valve prolapse with ruptured chordae tendineae in 8 patients, rheumatic change in 5 patients, and dilated cardiomyopathy in 5 patients. With intravenous dobutamine infusion, heart rate (77-103 beats/min), systolic blood pressure (119-144 mmHg), peak mitral regurgitant jet velocity (4.5-5.4 m/sec), intensity of mitral regurgitant murmur (to 201% of that before infusion in early systole) increased, while left ventricular end-diastolic volume (124-102 mm), left ventricular end-systolic volume (57-42 mm), mitral anular diameter (33-28 mm), and color Doppler mitral regurgitant signal area (704-416 mm(2)) decreased (P < 0.05). Total (forward + backward) left ventricular stroke volume (66-61 mL/beat) showed no change. Dobutamine decreased mitral regurgitant flow/beat, regardless of etiology of mitral regurgitation, which was probably due to the decrease of left ventricular size and mitral annular diameter. Although total (forward + backward) left ventricular stroke volume was unchanged, dobutamine effectively increased forward left ventricular stroke volume by decreasing backward regurgitation. Mitral regurgitant murmur became louder despite the decrease of mitral regurgation, indicating the uselessness of auscultation in the grading of the severity of mitral regurgitation.