Noninvasive estimation of max (dP/dt) of the left ventricle based on maximum aortic flow acceleration as measured by pulsed Doppler echocardiography

To obtain an index of left ventricular contractility, cardiac catheterization is necessary. In the present study, we ascertained whether max(dP/dt) could be obtained noninvasively in vivo based on the theoretical equation, max(dP/dt) not equal to rho cmax(du/dt), where rho is the density of blood, c is the pulse wave velocity of the aorta and max(du/dt) is the maximum acceleration of the aortic blood flow. This equation is based on the theory of pulse wave propagation, and was established in animal experiments. We further attempted to clarify the clinical usefulness of rho cmax(du/dt) by examining the effects of afterload and preload on rho cmax(du/dt). Twenty-seven patients without stenosis of their aortic valves and left ventricular outflow tracts were observed. During cardiac catheterization, we measured max(dP/dt) using a catheter-tip micromanometer, max (du/dt) using pulsed Doppler echocardiography and pulse wave velocity by simultaneously recording the femoral pulse wave and the carotid pulse wave. The measurements were performed at rest, before and after an increase in contractility with dobutamine administration, an increase in afterload with methoxamine administration and an increase in preload by leg elevation. There was good linear correlation (Y = 0.95X + 7.51, r = 0.84, p less than 0.0005) between max(dP/dt)[X] and rho cmax(du/dt)[Y] at rest. When the contractility was changed, rho cmax(du/dt) reflected changing of max(dP/dt). Moreover, when the afterload and preload were increased, the changing pattern of rho cmax(du/dt) was similar to that of max(dP/dt). Max(du/dt), index of cardiac performance previously proposed, showed a different changing pattern than max(dP/dt), indicating that max(du/dt) was influenced substantially by loading conditions. These results indicated that we can obtain max(dP/dt) noninvasively and reliably by measuring rho cmax(du/dt).     

Noninvasive estimation of left ventricular Max(dP/dt) from aortic flow acceleration and pulse wave velocity

The Doppler method of obtaining left ventricular Max(dP/dt) proposed recently was based on the measurement of mitral regurgitation velocity. Since Max(dP/dt) is an isovolumic phase index, its use in cases of mitral regurgitation may be open to argument. However, we had proposed a noninvasive method of estimating left ventricular Max(dP/dt) based on different principles. In our method, Max(dP/dt) had been given by Max(dP/dt) = (rho)cMax (du/dt), where rho is the blood density, c is the pulse wave velocity, and u is the flow velocity in the aorta. We had derived the above equation theoretically, and confirmed its validity by animal experiments. In our previous study, we also applied our method in the clinical setting. The aortic flow velocity was measured by Doppler echocardiography, and the pulse wave velocity by mechanocardiography or Doppler echocardiography. (Rho)cMax(du/dt) obtained noninvasively was compared with Max(dP/dt) measured with a catheter-tip micromanometer. We found an excellent correlation between (rho)cMax(du/dt) and Max(dp/dt), and concluded that (rho)Max(du/dt) is useful in assessing noninvasively the contractile state of the left ventricle. Here, we summarize our method, review previous results, and report new results of the clinical application of our method.     

A New Noninvasive Device for Measuring Central Ejection dP/dt Mathematical Foundation of Cardiac dP/dt Measurement Using a Model for a Collapsible Artery

We have developed a novel non-invasive device for the measurement of one of the most sensitive indices of myocardial contractility as represented by the rate of increase of intraventricular pressure (left ventricular dP/dt and arterial dP/dt performance index (dP/dt^ejc). Up till now, these parameters could be obtained only by invasive catheterization methods. The new technique is based on the concept of applying multiple successive occlusive pressures on the brachial artery from peak systole to diastole using a inflatable cuff and plotting the values against time intervals that leads to the reconstruction of the central aortic pressure noninvasively. The following describes the computer simulator developed for providing a mathematical foundation of the new sensor. At the core of the simulator lies a hemodynamic model of the blood flow on an artery under externally applied pressure. The purpose of the model is to reproduce the experimental results obtained in studies on patients (Gorenberg et al. in Cardiovasc Eng: 305–311, 2004; Gorenberg et al. in Emerg med J 22 (7): 486–489, 2005) and a animal model where ischemia resulted from balloon inflation during coronary catheterization (Gorenberg and Marmor in J Med Eng Technol, 2006) and to describe correlations between the dP/dt^ejc and other hemodynamic variables. The model has successfully reproduced the trends observed experimentally, providing a solid in-depth understanding of the hemodynamics involved in the new measurement. A high correlation between the dP/dt^ejc and the rate of pressure rise in the aorta during the ejection phase was observed. dP/dt^ejc dependence on other hemodynamic parameters was also investigated.     

Usefulness of negative dP/dt upstroke pattern for assessment of left ventricular relaxation in coronary artery disease

It has been reported that regional asynchrony due to acute ischemia disturbs the exponential nature of left ventricular (LV) pressure reduction and may alter the pattern of (-)dP/dt upstroke curve. If LV pressure decreases exponentially during the isovolumic relaxation period (P = Ae-t/T + B, where A and B = constants, t = time and T = time constant), the (-)dP/dt upstroke curve should also be exponential and upward-convex because dP/dt = A(-t/T)e-t/T. To test this theory in humans, the LV (-)dP/dt upstroke curve was analyzed in 9 normal subjects, 12 patients with effort angina pectoris (AP) and 15 with old myocardial infarction (MI) under the basal conditions. The (-)dP/dt upstroke was convex-upward in all normal subjects, but convex-downward in 9 of 12 patients with AP and in all patients with MI, which suggests nonexponential decrease in LV pressure in the groups with AP and MI. The dP/dt (20/60), which is the ratio of the (-)dP/dt value at 20 ms after peak (-)dP/dt to that at 60 ms after peak (-)dP/dt, was significantly lower in the group with AP (1.70 +/- 0.07) and in the group with MI (1.61 +/- 0.13) than in normal subjects (2.08 +/- 0.18) (p less than 0.005). This indicates that (-)dP/dt upstroke 20 to 60 ms after peak (-)dP/dt increases more slowly in the groups with AP and MI than in normal subjects. Theoretical consideration showed that such a slower increase of the upstroke resulted from impaired early to midrelaxation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transesophageal pulsed doppler echocardiographic evaluation of left atrial systolic performance in hypertrophic cardiomyopathy: combinEd analysis of transmitral and pulmonary venous flow velocities

Background: Hypertrophic cardiomyopathy (HC) is characterized by impaired left ventricular (LV) diastolic function due to an increase in LV wall thickness. The severity of this disease varies depending on the localization and extent of the hypertrophied myocardium and the presence and extent of myocardial disarray or fibrosis. Hypothesis: The purpose of this study was to examine the background of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole in patients with HC using pulsed Doppler echocardiography. Methods: Hemodynamic abnormalities between the left atrium and left ventricle during atrial systole were evaluated in patients with HC using transmitral flow (TMF) and pulmonary venous flow (PVF) velocities obtained by transesophageal pulsed Doppler echocardiography. The study population included 50 patients with HC, including 39 with asymmetric septal hypertrophy and 11 with apical hypertrophy, and showing fractional shortening of the left ventricle ≥ 30%. They were classified into three groups: (1) Group A (n = 11): the ratio of the late to early TMF velocity < 1, and peak atrial systolic PVF velocity (PVA) < 25 mm/s;(2) Group B (n = 13): their ratio < 1, and PVA ≥ 25 mm/s;and (3) Group C (n = 26): their ratio ≥ 1. The mean age of patients in Group A was lower than that in Groups B and C. Results: Left atrial dimension in Group B was significantly greater than that in the other HC groups and the control group. Furthermore, left atrial volume changes during atrial systole in Group B were significantly smaller than those in the other HC groups and the control group. Peak atrial systolic PVF velocity in Group B was significantly higher than that in the control group and in Group C. The duration of the atrial systolic waves of the TMF and PVF in Group B was significantly shorter and longer, respectively, than that in Group A. Left ventricular end-diastolic pressure (LVEDP) decreased in descending order with Group B > Group C > Group A. In all patients there was a significant positive correlation between the LVEDP and peak atrial systolic PVF velocity or the difference in duration between the atrial systolic waves of PVF and TMF. Plots of these values shifted toward the left and inferiorly in Group A, and toward the right and superiorly in Group B. Conclusion: Peak velocity and duration of TMF and PVF during atrial systole by transesophageal pulsed Doppler echocardiography are useful indices of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole, particularly a forceful atrial contraction mismatched to the left atrial afterload and severity of LV diastolic dysfunction, in HC.     

The pulmonary venous systolic flow pulse--its origin and relationship to left atrial pressure.

OBJECTIVES: The purpose of this study was to determine the origin of the pulmonary venous systolic flow pulse using wave-intensity analysis to separate forward- and backward-going waves. BACKGROUND: The mechanism of the pulmonary venous systolic flow pulse is unclear and could be a "suction effect" due to a fall in atrial pressure (backward-going wave) or a "pushing effect" due to forward-propagation of right ventricular (RV) pressure (forward-going wave). METHODS: In eight patients during coronary surgery, pulmonary venous flow (flow probe), velocity (microsensor) and pressure (micromanometer) were recorded. We calculated wave intensity (dP x dU) as change in pulmonary venous pressure (dP) times change in velocity (dU) at 5 ms intervals. When dP x dU > 0 there is a net forward-going wave and when dP x dU < 0 there is a net backward-going wave. RESULTS: Systolic pulmonary venous flow was biphasic. When flow accelerated in early systole (S1), pulmonary venous pressure was falling, and, therefore, dP x dU was negative, -0.6 +/- 0.2 (x +/- SE) W/m2, indicating a net backward-going wave. When flow accelerated in late systole (S2), pressure was rising, and, therefore, dP x dU was positive, 0.3 +/- 0.1 W/m2, indicating a net forward-going wave. CONCLUSIONS: Pulmonary venous flow acceleration in S1 was attributed to a net backward-going wave secondary to a fall in atrial pressure. However, flow acceleration in S2 was attributed to a net forward-going wave, consistent with propagation of the RV systolic pressure pulse across the lungs. Pulmonary vein systolic flow pattern, therefore, appears to be determined by right- as well as left-sided cardiac events.     

Beat-to-beat modulation of right and left ventricular positive dP/dt by afterload. Implications for the evaluation of inotropy

OBJECTIVES: The rate of pressure rise (dP/dtmax) has mainly been studied in the left ventricle (LV), where it was demonstrated to be highly dependent of preload, but independent of afterload. Load dependence of right ventricular (RV) dP/dtmax is assumed to be similar to (LV)dP/dtmax, although this issue has not yet been investigated in detail. In the current study, we evaluated acute afterload dependence of dP/dtmax in both ventricles in rats. METHODS AND RESULTS: Adult Wistar rats (n = 8) were instrumented to record RV and LV pressures and septal-free wall diameters. RV and LV afterload elevations were performed by beat-to-beat graded constrictions of the pulmonary trunk or aortic root, respectively. Control cycles and low, moderate and high (isovolumetric) afterload levels were analysed. In both ventricles, afterload modulation of dP/dt was assessed by dP/dtmax normalized for end-diastolic dimensions (dP/dtmax/EDD) and by peak and mean accelerations of pressure rise. RV afterload elevation increased dP/dtmax, dP/dtmax/EDD, peak and mean acceleration of RV pressure rise, without changing the time from end-diastole to dP/dtmax. LV afterload elevations did not significantly change the corresponding left-sided parameters. CONCLUSIONS: In this study we demonstrated that, in contrast to the left ventricle, right ventricular dP/dtmax and dP/dtmax/EDD relation are significantly afterload sensitive. This should be taken into account for its application in the haemodynamic evaluation of cardiac function in experimental and clinical settings.     

Evaluation of left ventricular relaxation using the continuous-wave doppler velocity profile of aortic regurgitation: Noninvasive measurement of left ventricular negative dP/dt and time constant

Background: The maximal negative dP/dt [max (-)dP/dt] and time constant (T) are useful indices for evaluating left ventricular (LV) relaxation, but they require invasive procedures. Hypothesis: The purpose of this study was to obtain max (-)dP/dt and T using the continuous-wave Doppler aortic regurgitation velocity curve (AR-CW) noninvasively. Using the Bernoulli equation, the AR-CW allows accurate determination of the pressure gradients (PG) between the aorta and the left ventricle. Methods: In 10 patients with trivial to mild AR, the rising segment of the AR-CW reflecting LV pressure decrease was digitized with the cardiac image analysis system. Transpulmonary contrast-enhanced Doppler echocardiography was used in three patients to obtain intense velocity envelope. The PG curve and the first derivative curve were reconstructed and the maximal point of the first derivative curve, which is consistent with max (-)dP/dt, was termed as maximal rate of pressure fall (maxRPF). As T (calculated according to the method of Weiss) can be obtained from T=Pm/max (-)dP/dt [Pm: LV pressure at the phase of max (-)dP/dt], we calculated T from Pm/maxRPF (Pm=dicrotic notch pressure - 4Vm²) (Vm: AR velocity at the phase of maxRPF). Results: The Doppler-derived maxRPF and T (T_d) approximated the catheter-derived max (-;)dP/dt and T (y=0.85x+ 245, r=0.97, p<0.001, y=0.79x+4, r=0.87, p<0.001). In addition, dobutamine echocardiography was performed in nine patients showing increased maxRPF and decreased T_d, indicating improvement of LV relaxation. Conclusion: These Doppler-derived new indices are sufficiently useful to evaluate LV relaxation noninvasively.     

Characterization of transmitral flow using color-coded Doppler in a case of left atrial myxoma

The authors describe the transmitral flow pattern by color flow imaging in a patient with left atrial myxoma. The usefulness of color Doppler relays in the identification of the eccentric direction of transmitral flow, possibly present in such situation.     

Transoesophageal Doppler pulmonary venous flow pattern and left atrial spontaneous contrast in mitral stenosis.

The relationship between transoesophageal Doppler pulmonary venous flow pattern and spontaneous left atrial contrast was studied in 23 patients with isolated severe mitral stenosis (mitral valve area = 0.8 +/- 0.2 cm2). The patients with none or minimal (1+) spontaneous contrast (n = 15, group I) were compared with those with significant spontaneous contrast (grade 2+, n = 8, group II) with regard to peak systolic velocity (33 +/- 14 cm/s vs 28 +/- 12 cm/s, p = NS), peak diastolic velocity (36 +/- 14 cm/s vs 28 +/- 8 cm/s, p = NS) and peak atrial reversal velocity (19 +/- 4 cm/s vs 19 +/- 8 cm/s, p = NS), systolic forward flow velocity time integral (3.37 +/- 1.73 cm vs 2.78 +/- 0.9 cm, p = NS), diastolic forward flow velocity time integral (2.85 +/- 1.2 cm vs 2.65 +/- 1.87 cm, p = NS), ratios of peak systolic and diastolic velocity (0.91 +/- 0.21 vs 0.95 +/- 0.29, p = NS) and duration of diastolic deceleration (117 +/- 59 ms vs 132 +/- 106 ms, p = NS). The results show that the occurrence of spontaneous contrast in the left atrium in patients with mitral stenosis is not related to the Doppler-estimated pulmonary venous flow.     

Interrelationship of mid-diastolic mitral valve motion, pulmonary venous flow, and transmitral flow

This study offers a unifying mechanism of left ventricular filling dynamics to link the unexplained mid-diastolic motion of the mitral valve with an associated increase in transmitral flow, with the phasic character of pulmonary vein flow, and with changes in the atrioventricular pressure difference. M mode echograms of mitral valve motion and Doppler echocardiograms of mitral and pulmonary vein flow velocities were recorded in 12 healthy volunteers (heart rate = 60 +/- 9 beats/min). All echocardiograms showed an undulation in the mitral valve (L motion) at a relatively constant delay from the peak of the diastolic phase of pulmonary vein flow (K phase). In six subjects, the L motion was also associated with a distinct wave of mitral flow (L wave). Measured from the onset of the QRS complex, Q-K was 577 +/- 39 msec; Q-L was 703 +/- 42 msec, and K-L was 125 +/- 16 msec. Multiple measurements within each subject during respiratory variations in RR interval indicated exceptionally small differences in the temporal relationships (mean coefficient of variation 2%). Early rapid flow deceleration is caused by a reversal of the atrioventricular pressure gradient, and the L wave arises from the subsequent reestablishment of a positive gradient due to left atrial filling via the pulmonary veins. The mitral valve moves passively in response to the flowing blood and the associated pressure difference. This interpretation is confirmed by (1) a computational model, and (2) a retrospective analysis of data from patients with mitral stenosis and from conscious dogs instrumented to measure transmitral pressure-flow relationships.     

Left atrial function in congestive heart failure: assessment by transmitral and pulmonary vein Doppler

The relation of transmitral flow patterns and pulmonary venous velocities was analyzed from 50 heart failure patients (28 men, 22 women; mean [±SD] age 61 ± 9 years) with a left ventricular ejection fraction < 40%. Doppler echocardiography was performed in all patients. Transmitral flow measurements included early (E) and atrial (A) velocities and deceleration time of E wave (DT). Patients were assigned to two groups according to E/A ratio, DT, or both: 20 patients in the restrictive group, and 30 patients in the nonrestrictive group. Pulmonary venous flow was obtained by the transthoracic approach. Systolic (S), diastolic (D) and atrial reversal (Ar) velocities were measured. Of the study population, 13 patients had simultaneously determined pulmonary capillary wedge pressure (PCWP).The results showed a lower S (28 ± 11 vs. 51 ± 10 cm/sec, p < 0.01), a higher D (66 ± 13 vs. 44 ± 10 cm/sec, p < 0.01) and a smaller Ar (12 ± 10 vs. 24 ± 9 cm/sec, p < 0.01) in the restrictive group compared with those in nonrestrictive group. In the subgroup of patients undergoing invasive hemodynamic studies, there was no relationship between PCWP and atrial reversal velocity. However, a significant correlation was observed for pulmonary systolic (r = -0.70, p < 0.01) and diastolic (r = 0.76, p < 0.01) velocities to PCWP. These findings suggest a reduction in left atrial compliance and atrial systolic function and both play important roles in heart failure patients with the restrictive transmitral flow pattern.     

A new method for estimating left ventricular dP/dt by continuous wave Doppler-echocardiography. Validation studies at cardiac catheterization

In this study, we explored the use of continuous wave Doppler-echocardiography guided by color Doppler flow-mapping as a method for noninvasively calculating the rate of pressure rise (RPR) in the left ventricle. Continuous wave Doppler determination of the velocities in mitral regurgitant jets allows calculation of instantaneous pressure gradients between the left ventricle and the left atrium. Left atrial pressure variations in early systole can be considered negligible; therefore, the rising segment of the mitral regurgitation velocity curve should reflect left ventricular pressure increase. We studied 50 patients (mean age, 51 years; range, 25-66 years) in normal sinus rhythm with color Doppler-proven mitral regurgitation and compared the Doppler-derived left ventricular RPR with peak dP/dt obtained at cardiac catheterization. Doppler studies were performed simultaneously with cardiac catheterization in 11 patients and immediately before in the remaining cases. Two points were arbitrarily selected on the steepest rising segment of the continuous wave mitral regurgitation velocity curve (point A, 1 m/sec, point B, 3 m/sec), and the time interval (t) between them was measured. Following the Bernoulli relation, the pressure rise between points A and B is 32 mm Hg (4vB2-4vA2) and the RPR is 32 mm Hg/t. Results showed a linear correlation between the Doppler RPR and peak dP/dt (r = 0.87, SEE = 316 mm Hg/sec). The RPR in the left ventricle can be derived from the continuous wave Doppler mitral regurgitation velocity curve.     

Assessment of abnormal left atrial relaxation by transesophageal pulsed doppler echocardiography of pulmonary venous flow velocity

Background: Several studies on left ventricular relaxation have been undertaken in the past: however, left atrial (LA) relaxation has not been fully evaluated. Hypothesis: The purpose of this study was to assess abnormalities in LA relaxation by evaluating pulmonary venous flow velocity and interatrial septal motion using transesophageal echocardiography. Methods: The subjects were 56 untreated patients in sinus rhythm, including 25 with previous myocardial infarction, 9 with hypertrophic cardiomyopathy, 11 with dilated cardiomyopathy, as well as 11 with chest pain syndrome as controls. Peak first systolic velocity (PVS₁), peak atrial systolic velocity (PVA), and their time-velocity integrals (PVS₁-I and PVA-I, respectively) were calculated from the pulmonary venous flow velocity. Results: The PVS₁ and PVS₁-I correlated negatively with the maximum LA dimension and mean pulmonary capillary wedge pressure, and correlated positively with the amplitude of the interatrial septal motion during LA relaxation and percent fractional LA relaxation. The PVA and PVA-I did not correlate with the mean pulmonary capillary wedge pressure. There was a weak positive correlation between PVA and PVS₁, and a close positive correlation between the ratio of PVA to PVS₁ and mean pulmonary capillary wedge pressure. Multiple regression analysis indicated that the PVS₁ was most closely related to percent fractional LA relaxation, followed by mean pulmonary capillary wedge pressure. Conclusion: The PVS₁ determined from the pulmonary venous flow velocity is closely related to parameters of LA relaxation which may be determined by transesophageal M-mode echocardiography, and the ratio of PVA to PVS₁ is useful for noninvasive evaluation of LA pressure..     

Assessment of left atrial appendage function and its relationship to pulmonary venous flow pattern by transesophageal echocardiography

We evaluated left atrial appendage function and its relationship to pulmonary venous flow in 53 patients divided into four groups. Group 1 consisted of 10 normal subjects. Group 2 included 15 patients with significant pure mitral stenosis in sinus rhythm. In group 3, there were 13 patients with pure significant mitral stenosis and atrial fibrillation. Group 4 consisted of 15 patients with normal mitral valve and atrial fibrilltion. We found significant decrease in left atrial appendage ejection fraction and maximum emptying flow velocity, velocity time integral of systolic pulmonary venous flow in Groups 2, 3 and 4 in comparison with normal subjects. Systolic pulmonary venous flow velocity was significantly decreased in Groups 3 and 4. There was significant correlation between left atrial appendage ejection fraction and peak emptying flow velocity (r = 0.62, P < 0,001). Systolic peak pulmonary venous flow velocity was significantly correlated with left atrial appendage ejection fraction and maximum emptying flow velocity (r = 0.67, P = 0,01; r = 0.58, P < 0,001, respectively). There was also significant correlation between systolic pulmonary venous flow velocity time integral and left atrial appendage ejection fraction (r = 0.66, P = 0.001). When normals were excluded from analysis, all the correlations were still significant. We concluded that left atrial appendage is a contractile structure, and that systolic pulmonary venous flow velocity is influenced by left atrial appendage dysfunction. Therefore left atrial appendage function needs to be considered when interpreting Doppler transmitral and systolic pulmonary venous flow patterns.     

Doppler transmitral and pulmonary venous flow in young orienteers and sedentary young adults

Doppler filling indices may provide important information on left ventricular diastole and possibly diastolic adaptation in endurance athletes. We therefore undertook a comparative study to obtain reference values for transmitral and pulmonary venous Doppler flow velocities and to characterize differences between young orienteers and young sedentary adults. Seventy-six elite orienteers (42 female and 34 male; 17-30 years old) and 61 sedentary young subjects (32 female and 29 male; 17-33 years old) underwent echocardiography. No significant differences between the athletes and sedentary controls regarding peak transmitral flow were found, although the athletes had significantly higher peak pulmonary flow velocity during diastole than the sedentary controls (0.69+/-0.13, 0.61+/-0.10, 0.78+/-0.12, and 0.57+/-0.09 m/sec for female athletes, female sedentary controls, male athletes, and male sedentary controls, respectively). Because no significant differences were revealed in the transmitral flow velocities between the athletes and the sedentary subjects, the relative force between the left atrium and the left ventricle should not diverge during early filling. An increase in pulmonary venous pressure or a decrease in left atrial pressure can augment the force between the pulmonary veins and the left atrium. A rise in pulmonary venous pressure is a hemodynamically unlikely adaptation in endurance athletes; therefore, to maintain the same transmitral pressure with an assumed lower left atrial pressure, the data suggest a more rapid relaxation and an improved left ventricular elastic recoil, which would enable the athletes to achieve a more rapid negative left ventricular pressure change during early filling.     

Noninvasive assessment of left ventricular end-diastolic pressure by the response of the transmitral a-wave velocity to a standardized Valsalva maneuver

Impaired relaxation is frequently masked by elevated filling pressures, resulting in a pseudonormal flow pattern (E/A >1.0). Because the E/A wave ratio increases as filling pressures rise, it is generally assumed that patients with an E/A ratio of <1.0 (impaired relaxation pattern) have relatively low filling pressures. Nevertheless, patients with an E/A ratio of <1.0 can have as profoundly elevated filling pressures as patients with a pseudonormal or restrictive filling pattern. Because left ventricular (LV) pressure during end-diastole essentially determines atrial afterload, the response of the A-wave velocity to a reduction of atrial afterload by a standardized Valsalva maneuver should allow estimation of LV end-diastolic pressure (LVEDP) regardless of the baseline Doppler flow pattern. This was tested in 20 consecutive patients who were studied by pulse-wave Doppler echocardiography during cardiac catheterization. There was a close correlation between LVEDP and the change in A-wave velocity during the Valsalva maneuver (r = 0.85, SEE 6.7 mm Hg) regardless of the baseline E/A ratio. In patients with a LVEDP of <15 mm Hg the A wave decreased by 21 +/- 15 cm/s. In patients with a LVEDP of >25 mm Hg the A wave increased by 18 +/- 13 cm/s. The change in the E/A ratio during Valsalva correlated fairly with LVEDP (r = -0.72, SEE 8.8 mm Hg), the baseline E/A ratio correlated poorly, and scatter was substantial (r = 0.46, SEE 11.2 mm Hg). Just as elevated filling pressures can mask impaired relaxation, the impaired relaxation pattern can mask the presence of elevated filling pressures. This can be revealed by testing the response of the A wave to the Valsalva maneuver, allowing estimation of LVEDP independent of the baseline E/A ratio.