Role of left atrial booster pump function in a worsening course of congestive heart failure.

We evaluated changes in left ventricular (LV) preload and the Doppler-derived transmitral late to early diastolic peak velocity ratio (A/E ratio) during the exercise in 27 patients with ischemic heart disease. After the exercise, A/E ratio decreased in 16 patients with a remarkable elevation in LV preload, and increased in 11 with a mild elevation. Further, Doppler transmitral flow in conjunction with pulmonary venous flow and hemodynamic parameters were analyzed in 11 dogs during a worsening course of heart failure induced by dextran infusion. The relationship of A/E ratio to LV end-diastolic pressure showed a quadratic curve concave to the pressure axis. A/E ratio, an index expressing left atrial (LA) contribution to LV filling, returned to that seen before volume loading under the condition of cardiac dysfunction. Pulmonary venous reflux fraction determined as the ratio of peak velocity of pulmonary venous reflux during LA systole to the sum of systolic and diastolic peak velocities of pulmonary venous antegrade flow, did not increase here. In this situation, blood could not be ejected from the left atrium into the left ventricle and even into the pulmonary veins during LA contraction. Finally, LV filling was not compensated by the left atrium, and LA booster pump function itself was deteriorated.     

Contributors of characteristic mitral flow velocity pattern in congestive heart failure--from clinical observations back to experimental validations.

Mitral flow velocity pattern in patients with left ventricular (LV) diastolic dysfunction usually includes decreased peak early diastolic filling velocity (E), slowed deceleration of the early diastolic filling wave and increased peak filling velocity at atrial contraction (A). However, the abnormal mitral flow velocity pattern can be normalized in the presence of concomitant congestive heart failure. In such cases E can be equal to or even higher than normal, its deceleration is normal or faster than normal value, and A can be normal or lower than normal value. Clinical observations in patients with severe heart failure showed that the mitral flow velocity pattern changes with vasodilating therapy, reflecting the changes in the left atrial (LA) to LV pressure difference rather than those in the absolute LA pressure or LV pressure alone. This was validated in the canine study in which levels of LV dysfunction were made by the injection of microspheres into the left coronary artery to study the interrelation among the mitral flow velocity pattern and LA and LV pressures. In this experiment, the changes in the mitral flow velocity pattern could not be explained by the changes in LA or LV pressure alone but was better explained by the changes in the LA to LV pressure difference. Not only LA-LV crossover pressure but also LA compliance seem to be important as determinants of LA pressure level in diastole. In addition to LV relaxation rate, incompleteness of relaxation, elastic recoil and LV passive elastic properties, extracardiac constraint is also considered to be an important determinant of the level of the LV diastolic pressure and hence of the mitral flow velocity pattern at least in the presence of congestive heart failure. Thus, mitral flow velocity pattern is determined by the interaction of LA and LV pressures, both of which are affected by chamber properties as well as loading conditions.     

Hemodynamic Determinants of Doppler Pulmonary Venous Flow Velocity Components: New Insights From Studies in Lightly Sedated Normal Dogs

Objectives. We sought to define the hemodynamic determinants of pulmonary venous (PV) flow velocities to assess how these are affected by respiration, heart rate and loading conditions.Background. Pulmonary venous flow velocity (PVFV) recorded with pulsed wave Doppler technique is currently used in the noninvasive evaluation of left ventricular (LV) diastolic function and filling pressures. Although previous studies in both animals and humans have shown that PV flow is pulsatile, the hemodynamic determinants of the individual components of this flow remain controversial. Understanding the physiologic mechanisms should help to better define the clinical utility of these Doppler techniques.Methods. PV flow velocities obtained with transesophageal pulsed wave Doppler imaging were recorded together with PV, left atrial (LA) and LV pressures in 10 sedated, spontaneously breathing normal dogs. PVFV and hemodynamic data were analyzed during apnea, inspiration and expiration, at atrial paced heart rates of 60, 80, 100 and 120 beats/min and mean LA pressures of 6, 12, 18 and 24 mm Hg.Results. The data showed that 1) PV pressure varied depending on recording site, resembling pulmonary artery pressure closer to the pulmonary capillary bed and LA pressure closer to the venoatrial junction; 2) PVFV qualitatively followed changes in the PV–LA pressure gradient; 3) four PVFV components exist under normal conditions—three of which follow phasic changes in LA pressure and one of which (the late systolic component) is more influenced by RV stroke volume and the compliance of the pulmonary veins and left atrium; 4) normal respiration and changes in heart rate significantly alter PVFV variables—in particular, reverse flow velocity at atrial contraction; and 5) increasing LA pressure results in larger PV A wave and PV early systolic flow velocities, as well as an earlier peak in PV late systolic flow velocity and a more prominent velocity minimum before PV diastolic flow.Conclusions. Using transesophageal pulsed wave Doppler technique, four PVFV components are identifiable and determined by PV–LA hemodynamic pressure gradients. These gradients appear to be influenced by a combination of physiologic events that include RV stroke volume, the compliance of the pulmonary vasculature and left atrium and phasic changes in LA pressure. PV flow velocity components are significantly influenced by heart rate, respiration and LA pressure. These findings have implications for the interpretation of LV diastolic function and filling pressures by current Doppler echocardiographic techniques but require further clinical investigation.     

Echocardiographic evaluation of left ventricular diastolic function: correlation between echocardiographic and hemodynamic parameters

AIM: The aim of this study was to assess the correlation between non invasive echo-Doppler parameters of diastolic function and invasively measured end-diastolic left ventricular (LV) filling pressures in patients with normal or depressed LV function. METHODS: The patient population was composed of 44 subjects, (34 men and 10 women) 52% with normal ventricular function, who underwent echo-Doppler and hemodynamic evaluation within 24 hours between the two exams. RESULTS: LV end-diastolic pressure was statistically different (P=0.022) in the 4 subgroups divided on the basis of the mitral flow pattern in the overall population and in the patients with depressed LV function, but not in those with normal LV function. In the overall population LV end-diastolic pressure was significantly correlated with: 1) E/A ratio of mitral flow (r=0.45, P=0.002); 2) mitral E wave peak velocity (r=0.39, P=0.017); 3) isovolumic relaxation time (r=-0.34, P=0.01); 4) left atrial diameter (r=0.33, P=0.037); 5) duration of retrograde A wave of pulmonary venous flow (r=0.33, P=0.03); 6) Pulmonary vein D wave peak velocity (r=0.29, P=0,05). Multivariate analysis showed that the correlation between the echo-Doppler variables and LV end-diastolic pressure was statistically significant only in patients with depressed LV function, but not in those with normal function. CONCLUSION: Among the echo-Doppler variables examined, those derived from transmitral flow and pulmonary vein flow show the best correlation with left ventricular end-diastolic pressure; however, the correlation is statistically significant only in patients with depressed LV function. Thus, the echo-Doppler evaluation of LV diastolic function should take into account this limitation and should be based on a multiparametric approach.     

Pulmonary vein blood flow velocity waveform--with special reference to pulmonary "systolic runoff" in patients with atrial septal defect

In order to evaluate the magnitude of pulmonary "systolic runoff", we studied the pulmonary vein blood flow velocity waveform by positioning a catheter-tip velocity-pressure transducer into the extraparenchymal pulmonary vein just distal to the left atrium. We recorded blood flow velocity and pressure simultaneously, and subsequently identified the zero blood flow velocity with blood flow velocity level of the pulmonary artery in diastole. Patients with atrial septal defect were used as subjects because of the technical ease although the altered hemodynamics were present. Two kinds of flow velocity waveforms were consistently demonstrated. One was a waveform of two peaks with the first peak in late systole and the second peak in early diastole (n = 9). The other was a waveform of one peak with a summit near the end of systole (n = 5). On the assumption that the blood flow velocity waveform obtained with this method is roughly equivalent to the flow volume waveform, we initiated the second study. The area encompassed between the actual flow velocity waveform and the line of zero flow velocity was divided into two compartments, i.e., ventricular systole (S) and diastole (D). The ratios of the area in systole to the sum of the areas in systole and diastole, i.e., (S)/[S) + (D], which are analogous to the pulmonary "systolic runoff", were 0.45 +/- 0.07 (mean +/- SD, n = 13). This suggests that about 40% of the right ventricular stroke volume flows into the pulmonary veins, the left atrium and a portion of the right atrium through the atrial septal defect during ventricular systole.     

Echocardiographic estimation of left ventricular filling pressures in patients with mitral valve stenosis

Mitral stenosis (MS) is prevalent in developing countries. By improving healthcare systems, it could be expected that the incidence of new cases would decrease and therefore the mean age of mitral stenosis patients would increase. This increase in age of MS patients is accompanied by the occurrence of other diseases, such as coronary artery disease, hypertension, diabetes mellitus and chronic obstructive pulmonary disease.In a number of patients with MS, the question arises of the impact of mitral valve disease (MVD) on the presenting symptom. For example, in patients presenting with dyspnea, with both significant MS and hypertension, increased left ventricular (LV) filling pressure due to hypertension could influence assessment of the severity of MS. In these patients, severity of MS could be underestimated because the increased diastolic pressure reduces the mitral valve gradient, and the increased LV stiffness shortens pressure half-time (PHT).Similarly, patients with both pulmonary disease and MS may have dyspnoea because of pulmonary rather than cardiac cause. It is therefore advantageous to assess LV filling pressure in these cases in an attempt to prove or refute a cardiac cause for dyspnoea.Using Doppler measurements to estimate LV filling pressures is desirable. However, conventional Doppler measurements have limitations in the prediction of left ventricular end-diastolic pressure (LVEDP) in this group of patients. For example, in patients with MS, the left atrium (LA) is enlarged to compensate for the increase in LA pressure. Similarly, mitral inflow peak early diastolic velocity (E) is highly dependent on LA pressure1 and also preload.2 Pulmonary venous (PV) flow also has a blunted pattern in most patients with MS.3 Therefore, in MS patients, LA size, mitral inflow pattern and pulmonary venous pattern are all altered, making these measurements unreliable for the estimation of LVEDPHowever, other Doppler and tissue Doppler echocardiographic indices and time intervals, such as peak early diastolic velocity of mitral annulus (Ea), E/Ea ratio, mitral inflow propagation velocity (VP), E/VP, pulmonary vein velocities, Tei index and the ratio of isovolumic relaxation time (IVRT) to interval between the onset of mitral E and annular Ea (TE–Ea), which have shown promising values in the prediction of LV filling pressure in a variety of diseases,4-11 have not been assessed in the setting of mitral stenosis.The aim of this study was to analyse the components of mitral and pulmonary waves in patients with mitral stenosis and to construct a Doppler-derived LVEDP prediction model based on the combined analysis of transmitral and pulmonary venous flow velocity curves.     

Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocardiography. Effect of different loading conditions

It has previously been demonstrated that predictable changes occur in mitral flow velocities under different loading conditions. The purpose of this study was to relate changes in pulmonary venous and mitral flow velocities during different loading conditions as assessed by transesophageal echocardiography in the operating room. Nineteen patients had measurements of hemodynamics, that is, mitral and pulmonary vein flow velocities during the control situation, a decrease in preload by administration of nitroglycerin, an increase in preload by administration of fluids, and an increase in afterload by infusion of phenylephrine. There was a direct correlation between the changes in the mitral E velocity and the early peak diastolic velocity in the pulmonary vein curves (r = 0.61) as well as a direct correlation between the deceleration time of the mitral and pulmonary venous flow velocities in early diastole (r = 0.84). This indicates that diastolic flow velocity in the pulmonary vein is determined by the same factors that influence the mitral flow velocity curves. A decrease in preload caused a significant reduction in the initial E velocity and prolongation of deceleration time, and an increase in preload caused an increase in E velocity and shortening of deceleration time. An increase in afterload produced a variable effect on the initial E velocity and deceleration time and was dependent on the left ventricular filling pressure. The change in systolic forward flow velocity in the pulmonary vein was directly proportional to the change in cardiac output (r = 0.60). The pulmonary capillary wedge pressure correlated best with the flow velocity reversal in the pulmonary vein at atrial contraction (r = 0.81). Use of pulmonary vein velocities in conjunction with mitral flow velocities can help in understanding left ventricular filling.     

What is the most appropriate variable for estimation of mean pulmonary capillary wedge pressure by transesophageal pulsed Doppler echocardiography?

Although left ventricular (LV) inflow and pulmonary venous (PV) flow variables estimated by transesophageal Doppler echocardiography (TEE) reflect pulmonary capillary wedge pressure (PCWP), they are also affected by changes in cardiac function. The purpose of the present study was to detect the most appropriate variable for the estimation of PCWP by TEE in patients (pts) with ischemic heart disease. Several variables of LV inflow and left upper PV flow were compared with PCWP in 36 pts (six with angina pectoris and 30 with old myocardial infarction). Early diastolic flow (E) and atrial contraction flow (A) were used as LV inflow, while systolic forward flow (X), diastolic forward flow (Y) and atrial contractile reversal flow (z) were used as PV flow. The peak velocity of each flow wave (Ep, Ap, Xp, Yp, and Zp) and the time-velocity integral (Ei, Ai, Xi, Yi, and Zi) were measured. The ratio of Ep to Ap (Ep/Ap), Ei to Ai (Ei/Ai), Xp to Yp (Xp/Yp), Xi to Yi (Xi/Yi), Zp to Ap (Zp/Ap), Zi to Ai (Zi/Ai) and the systolic fraction of PV forward flow were calculated. Among these variables, the Zi/Ai ratio was most strongly correlated with PCWP (R=0.80). The Zi/Ai ratio may not be influeced by atrial function because the augmentation of atrial pump function increases Zi as well as Ai, and this may be one reason why the ratio correlated well with PCWP.Conclusion: The Zi/Ai ratio is a new useful variable for estimating PCWP by TEE.Abbreviations Ap peak velocity of left ventricular inflow during atrial contraction - Ep peak velocity of left ventricular inflow during early diastole - Yp peak velocity of diastolic pulmonary venous forward flow - Xp peak velocity of systolic pulmonary venous forward flow - Zp peak velocity of pulmonary venous reversal flow during atrial contraction - Ai time-velocity integral of left ventricular inflow during atrial contraction - Ei timevelocity integral of left ventricular inflow during early diastole - Yi time-velocity integral of diastolic pulmonary venous forward flow - Zi time-velocity integral of pulmonary venous reversal flow during atrial contraction - Xi time-velocity integral of systolic pulmonary venous forward flow     

Elucidating the B bump on the mitral valve M-mode echogram in patients with severe left ventricular systolic dysfunction

BACKGROUND: The B bump on mitral valve M-mode echogram is predictive of significant elevation of left ventricular end-diastolic pressure (LVEDP). However, its pathophysiologic mechanism remains unclear. METHODS: We investigated, by means of Doppler echocardiography, the hemodynamic events that take place at late diastole in left atrium (LA) and left ventricle (LV). The study group consisted of 10 consecutive and strictly selected patients with severe dilated LV dysfunction. The noninvasive validated index used for definition of high LVEDP was the difference between the durations of atrial reverse (AR) wave in pulmonary venous flow (PVF) and atrial (A) wave in mitral flow (MF). Peak velocities of PVF and MF were measured. The time interval from ECG P wave to the end of B bump (P-B) and from P wave to the end of AR (P-AR) were measured and correlated. Mitral diastolic regurgitation (DR) was searched with M-mode color Doppler. RESULTS: All patients presented with restrictive diastolic signs on MF and PVF. The mean value of AR time minus A time was 61+/-12 ms. There was a strong linear correlation between P-B and P-AR (r=0.94, p<0.001). Only five patients had DR. No patient had LV inflow during B bump. CONCLUSIONS: (1) Mitral B bump is essentially a late diastolic phenomenon in which the leaflets keep a semi-open position without LV inflow effectiveness. (2) The resultant LA pressure which prolongates the duration of AR wave beyond A wave, analogously work over mitral leaflets, pushing them toward LV generating the bump. (3) DR is caused by LVEDP higher than LA pressure and coexists with B bump without a cause-effect relationship.     

Diastolic ventricular interaction in normal and dilated heart during head-up tilting

BACKGROUND: The normal human heart behaves as a single functional unit during preload reduction; adaptations of the left ventricle to head-up tilting is mediated through ventricular interdependence and biventricular-lung interaction. HYPOTHESIS: We hypothesized that reduction of venous return in dilated cardiomyopathy is likely to have a great effect on ventricular chamber geometry and filling. The aim of this study was to evaluate the effects of gradual head-up tilting in normal subjects and in patients with dilated cardiomyopathy, addressing special attention to right (RV) and left ventricular (LV) dimensions, geometry, and filling, and to biventricular-lung interaction. METHODS: Twenty normal subjects and 23 patients with moderate heart failure due to dilated cardiomyopathy were studied with two-dimensional and Doppler echocardiography in supine position and after 20 degrees, 40 degrees, and 60 degrees tilting. Right ventricular and LV dimensions, LV geometry, and tricuspid, mitral, and pulmonary venous flow patterns were recorded at each step of the study. Geometric changes of the LV were evaluated by measurements of volumes and diameters in the apical four-chamber view (which identifies the interventricular septum and lateral wall) and apical two-chamber view (which identifies the inferior and anterior wall of the LV). RESULTS: In the two groups, tilting was associated with reduction of RV area and LV diameter and volumes; percent variations in LV diameter and volumes recorded in four-chamber view were lower at each step of tilting than with those derived from the two-chamber view in controls and in patients. In normal subjects, mitral and tricuspid peak early flow velocities were decreased at any tilting level; peak late velocities were unchanged; peak velocity of systolic forward flow of the pulmonary vein was reduced, diastolic forward flow was unchanged, and the difference in duration between reverse pulmonary flow and forward mitral A wave was reduced. Doppler findings were qualitatively similar in patients, but tilting induced a more marked redistribution of LV filling to late diastole because of a significant increase in atrial contribution. CONCLUSIONS: Preload reduction by tilting induces profound effects on left and right dimensions, geometry, and filling in normal and dilated heart; reduction or RV dimensions are associated with changes in LV ventricular geometry (minimal reduction in septal-lateral diameter, marked reduction in anterior-posterior diameter), redistribution of right and left diastolic filling to late diastole, and redistribution of pulmonary venous flow to early diastole. These mechanisms are probably due to a favorable interaction between heart and lungs, which increases compliance within the pericardial space and facilitates redistribution of flow from the lungs. Even a minimal amount of preload reduction causes more marked effects in LV filling patterns in dilated cardiomyopathy than in normal hearts, confirming that ventricular interaction and pericardial constraint are increased when heart volume enlarges.     

Diastolic blood flow into the pulmonary artery in carcinoid heart disease

A patient with carcinoid heart disease manifested by mild pulmonary stenosis, severe tricuspid incompetence and mild tricuspid stenosis had unequivocal evidence of blood flow from the right ventricle into the pulmonary artery during ventricular diastole. Simultaneous right ventricular and pulmonary arterial pressure curves demonstrated that right ventricular diastolic pressure exceeded pulmonary arterial pressure during mid-diastole, indicating consistent mid-diastolic opening of the pulmonary valve. This was followed by a parallel increase in right ventricular and pulmonary arterial pressures throughout the rest of diastole. Right heart cineangiograms, obtained with right atrial dye injection, substantiated the pattern of flow from the right ventricle to the pulmonary artery during ventricular diastole. This previously unrecognized phenomenon is probably due to the combined effects of increased right atrial pressure, decreased right ventricular compliance and normal pulmonary arterial pressure.     

Left atrial physiology and pathophysiology: Role of deformation imaging

The left atrium (LA) acts as a modulator of left ventricular (LV) filling. Although there is considerable evidence to support the use of LA maximum and minimum volumes for disease prediction, theoretical considerations and a growing body of literature suggest to focus on the quantification of the three basic LA functions: (1) Reservoir function: collection of pulmonary venous return during LV systole; (2) Conduit function: passage of blood to the left ventricle during early LV diastole; and (3) Contractile booster pump function (augmentation of ventricular filling during late LV diastole. Tremendous advances in our ability to non-invasively characterize all three elements of atrial function include speckle tracking echocardiography (STE), and more recently cardiovascular magnetic resonance myocardial feature tracking (CMR-FT). Corresponding imaging biomarkers are increasingly recognized to have incremental roles in determining prognosis and risk stratification in cardiac dysfunction of different origins. The current editorial introduces the role of STE and CMR-FT for the functional assessment of LA deformation as determined by strain and strain rate imaging and provides an outlook of how this exciting field may develop in the future.     

Triphasic mitral inflow documented by Doppler echocardiography and cardiac catheterization: a case study

An 85-year-old woman with hypertension was referred to our hospital for the management of chest pain. Echocardiography showed left ventricular (LV) hypertrophy with impaired systolic function (ejection fraction, 40%) and mitral regurgitation. Pulsed Doppler echocardiography for checking mitral inflow showed triphasic mitral inflow velocity. Simultaneous recording of the LV and pulmonary artery wedge (PAW) pressures showed a high mean PAW pressure with a prominent v wave. The LV pressure showed a temporary elevation in early diastole; it was unusually decreased in mid-diastole, and finally was elevated to such an extent that it exceeded PAW pressure. In this patient, the mid-diastolic decrease in LV pressure, despite the presence of simultaneous LV filling flow, cannot be explained by conventional pressure-volume relation; rather it can be attributed to the abrupt increase in the inflow volume due to the impaired diastolic function. This case shows the characteristics of triphasic mitral inflow in patients with diastolic dysfunction.     

Sound pressure correlates of the Austin Flint murmur. An intracardiac sound study.

Mitral valve motion and pressure correlates of the Austin Flint murmur (AFM) were investigated in nine patients with aortic regurgitation using high fidelity catheter tip micromanometers and the mitral valve echocardiogram (MVE). External phonocardiography demonstrated a mid-diastolic murmur (MDM) in eight subjects and a presystolic murmur (PSM) in five. Maximum intensity of both AFM components was found in the left ventricular (LV) inflow tract; the murmur was not recordable in the left atrium (LA). In two patients, an apparent AFM was recorded in the intracardiac phonocardiogram when absent externally. Only one subject had a significant late diastolic "reversed" or LV to LA gradient; in this patient, presystolic mitral regurgitation was shown angiographically but no PSM was present and MVE revealed absence of atriogenic mitral valve re-opening. In two subjects, a PSM disappeared from the external phono when a "reversed" gradient occurred during the diastolic pause following a ventricular premature systole; this LV to LA gradient was associated with diastolic mitral regurgitation recordable in the left atrial phono. In two patients, LV inflow phono showed the MDM to begin 80-120 msec after the aortic second sound and during the D to E phase of the MVE. The rate of early diastolic mitral valve closure in patients (152 +/- 24 mm/sec) was not significantly different from 13 normals (232 +/- 10 mm/sec). With regard to the genesis of the AFM, the present study concludes: 1) diastolic mitral regurgitation plays no role, and 2) antegrade mitral valve flow is required but simultaneous retrograde aortic flow may also be necessary.     

Determinants of forward pulmonary vein flow: an open pericardium pig model

OBJECTIVE

To elucidate determinants of pulmonary venous (PV) flow.

BACKGROUND

Right ventricular (RV) systolic pressure (vis a tergo), left atrial (LA) relaxation and left ventricular (LV) systole and relaxation (vis a fronte) have been suggested as determinants of the pulmonary venous (PV) anterograde Doppler flow velocities, but their relative contributions to those flow velocities have not been quantified.

METHODS

We analyzed, by multiple regression analysis, the determinants of PV anterograde velocities in an open-pericardium, paced (70 and 90 beats/min) pig model in which LA afterload was modified by creating LV regional ischemia (left anterior descending coronary artery constriction). We measured high fidelity LA, LV and RV pressures and Doppler flow velocities (epicardial echocardiography). We calculated LV tau, LA relaxation (a through x pressure difference divided by time, normalized by a pressure), LA peak v through x and RV systolic through LA peak v (RVSP-v) pressure differences, LV ejection fraction, long-axis shortening, stroke volume (LV outflow integral × outflow area) and LA four-chamber dimensions, Doppler transmitral and PV flow velocities and velocity-time integrals.

RESULTS

Left ventricular regional ischemia increased mildly LA y trough pressure (8 ± 1 vs. 6 ± 1 mm Hg, p = 0.001). Left ventricular stroke volume (coefficient: 0.5 cm/ml, SE: 0.2, p = 0.005) and LA peak v pressure (coefficient: −0.8 cm/mm Hg, SE: 0.3, p = 0.008) determined the PV total systolic integral. Left atrial relaxation determined both PV early systolic peak velocity and integral (coefficient: −0.8 cm/mm Hg, SE: 0.3, p = 0.04). Left atrial maximum area (coefficient: 2 cm⁻¹, SE: 0.7, p = 0.01) and RVSP-v (coefficient: 0.1 cm/mm Hg, SE: 0.05, p = 0.03) determined the late systolic integral. The PV total systolic integral determined both PV early diastolic peak velocity and integral (coefficient: 1.2, SE: 0.2, p = 0.001).

CONCLUSIONS

In an experimental model of LV acute ischemia of limited duration, the main independent predictors of PV systolic anterograde flow velocities are LA relaxation and compliance (LA peak v pressure) and LV systole—all vis a fronte factors. In the setting of mildly increased LA pressures, PV systolic flow (LA reservoir filling) is an independent predictor of PV early diastolic flow (LA early conduit).     

Doppler echocardiographic-determined changes in left ventricular diastolic filling flow velocity during the lower body positive and negative pressure method

Changes in parameters of left ventricular (LV) diastolic filling flow obtained with Doppler echocardiography during the lower body positive and negative pressure method were analyzed in 15 patients (12 with coronary artery disease and 3 with dilated cardiomyopathy). Lower body pressure was altered at 5 steps (+20, +10, 0, -20 and -40 mm Hg vs atmospheric pressure). Pulmonary capillary wedge pressure measured with a balloon-tipped catheter was changed proportionally with lower body pressure during the procedures (p less than 0.01). Mean systemic arterial pressure was changed slightly during lower body positive pressure and negative pressure of -40 mm Hg. Heart rate was almost unchanged except at lower body pressure of -40 mm Hg. The peak velocity of LV early diastolic filling flow was changed with pulmonary capillary wedge pressure in an almost parallel fashion during the procedures (p less than 0.01). The peak velocity of LV late diastolic filling flow showed smaller changes than that of early diastolic filling flow. Changes in pulmonary capillary wedge pressure correlated positively with changes in the peak velocity of LV early diastolic filling flow (r = 0.759, p less than 0.01), but not with changes in the peak velocity of LV late diastolic filling flow (r = 0.039, not significant) during lower body negative pressure of -20 mm Hg. These data suggest that left atrial pressure is one of the important determinants of LV early diastolic filling flow in this acute clinical setting and that LV late diastolic filling flow is less sensitive to changes in left atrial pressure than LV early diastolic filling flow.     

Evaluation of the hemodynamic relationship between the left atrium and left ventricle during atrial systole by pulsed tissue Doppler imaging in patients with left heart failure.

The objective of the present study was to evaluate the hemodynamic relationship between the left atrium (LA) and left ventricle (LV) during atrial systole in the presence of an elevated left ventricular end-diastolic pressure (LVEDP) and LV failure using pulsed tissue Doppler imaging (TDI). Fifty-three patients with LV systolic dysfunction and no regional LV asynergy were divided into 3 groups: relaxation failure group (RF, n=20) with a ratio of peak early diastolic to atrial systolic velocity of the transmitral flow (E/A) < or = 1; pseudonormalization group (PN, n=19) with 1 or =2. In addition, 20 normal patients (E/A > or = 1) were studied as a control group. The transmitral and pulmonary venous flow velocities were recorded by transesophageal pulsed Doppler echocardiography. The wall motion velocity patterns were recorded at the middle portion of the LV posterior wall (LVPW) and at the mitral annulus (MA) of the LVPW site in the apical LV long-axis view by transthoracic pulsed TDI. The LVEDP was significantly greater in the PN and RS groups than in the RF and control groups. The moan pulmonary capillary wedge pressure was greatest in the RS group. The percent fractional change of the LA area during atrial systole determined by 2-dimensional echocardiography was significantly lower in the RS group than in the PN group. The peak atrial systolic pulmonary venous flow velocity was significantly greater in the PN group than in the RS group. The peak atrial systolic motion velocity (Aw) at the LVPW was significantly lower in the PN and RS groups than in the RF and control groups. The Aw at the MA was significantly lower in the RS group than in the other groups. There was no significant difference in Aw between the LVPW and MA in the RS group, whereas Aw at the MA was significantly greater than that at the LVPW in the PN group. In conclusion, the measurements of Aw at the LVPW and MA can be used to noninvasively evaluate the hemodynamic relationship between the LA and LV during atrial systole in patients with LV failure.     

多普勒组织成像与脉冲多普勒方法对比评价高血压患者舒张功能

目的应用脉冲多普勒组织成像测量二尖瓣环平均舒张速度,以鉴别高血压患者舒张功能假性正常。方法在健康者(正常组200例)与高血压患者(高血压组47例)中,应用脉冲多普勒技术分别测量二尖瓣口舒张早期峰值速度(E)、舒张晚期峰值速度(A),肺静脉收缩波(S)、舒张波(D)及心房收缩波(Ar)。应用脉冲多普勒组织成像测量二尖瓣环各点舒张早期峰值速率(Ea)、舒张晚期峰值速率(Aa)。结果正常组与对照组患者二尖瓣E、A、E/A差异无显著性意义,肺静脉S、S/D、Ar差异有显著性意义,二尖瓣环平均Ea间差异有显著性意义,Aa间差异无显著性意义。结论二尖瓣环舒张早期速率可用于鉴别高血压舒张功能假性正常。     

Improvement of afterload mismatch of left atrial booster pump function with positive inotropic agent

OBJECTIVES: The objective of this study was to examine the hypothesis that a positive inotropic agent improves left ventricular (LV) filling during left atrial (LA) contraction in the presence of markedly elevated LV filling pressure. BACKGROUND: In patients with old myocardial infarction (MI), an increase in the operational LV chamber stiffness reduces LV filling during the LA contraction, resulting from an "afterload mismatch" of the LA booster pump function. METHODS: We investigated the effect of dobutamine infusion (3 microg/kg/min) on the LA pump function in the presence of elevated LV filling pressure induced by aortic constriction (Aoc) during acute MI in 10 dogs. Transmitral flow velocity was determined by transesophageal echocardiography, LV pressure by a micromanometer and LV volume by a conductance catheter. We measured the early (E) and late (A) diastolic peak transmitral flow velocities (cm/s) and LV chamber stiffness (deltaP/deltaV: mm Hg/ml; where deltaP is developed pressure and deltaV is the absolute filling volume during LA contraction). RESULTS: When the deltaP/deltaV was increased by Aoc during MI (from 1.1 +/- 0.8 to 3.1 +/- 2.6 mm Hg/ml, p < 0.01), A decreased significantly (from 30 +/- 5 to 22 +/- 8 cm/s, p < 0.01), and the ratio of E to A increased (from 1.0 +/- 0.3 to 1.4 +/- 0.8, p < 0.05) compared with MI without Aoc, showing the pseudonormal transmitral flow pattern, the so called "LA afterload mismatch." Dobutamine under this condition significantly reduced the deltaP/deltaV (to 1.7 +/- 1.2 mm Hg/ml, p < 0.05), resulting in an increase in A (to 31 +/- 8 cm/s, p < 0.01) and a decrease in E/A (to 1.0 +/- 0.3, p < 0.05), and the transmitral flow became a prolonged relaxation pattern as in MI without Aoc in all dogs. There was an inverse correlation between the deltaP/deltaV and the time-velocity integral of A (r = -0.70, p < 0.01). CONCLUSIONS: Dobutamine improved the afterload mismatch of the LA booster pump function. This effect may have been due to the reduction in LV operational chamber stiffness, resulting in an increase in the LA forward ejection into the LV.     

尿毒症维持性血液透析患者左心室构型和功能的超声心动图研究

目的 评价尿毒症维持性血液透析患者的左心室形态学及舒张、收缩功能.方法 入选尿毒症维持性血液透析患者40例(尿毒症组),正常人45例(对照组).应用常规超声心动图、组织多普勒、实时三维超声心动图的多项指标对比分析尿毒症组左心室形态学改变、左心室重构类型;分析左心窒舒张和收缩功能变化,并对舒张功能异常进行分级;评价左心窜收缩及舒张的同步性.结果 尿毒症组的室壁厚度、左心室质量指数、左心室质量/容积比值显著性高于对照组(P<0.01),左心室构型以向心型肥厚为主(占50.0%),其次为向心型重构和偏心型肥厚(各占17.5%).尿毒症组的各项舒张功能指标与对照组差异有统计学意义(P<0.05),舒张功能异常以松弛功能受损类型居多(占85.0%),其中38.2%伴有左心室充盈压升高.尿毒症组的左心室射血分数、每搏量与对照组差异无统计学意义,但组织多普勒二尖瓣环收缩期运动速度显著低于对照组(P<0.05).左心室收缩不同步指标两组差异无统计学意义,舒张不同步指标尿毒症组显著高于对照组(P<0.05).结论 左心室肥厚、心肌质量增加和左心室舒张功能异常是尿毒症维持性血透患者心肌损害最突出的特征,舒张功能异常的出现早于收缩功能异常.