Experimental pericardial effusion: relation of abnormal respiratory variation in mitral flow velocity to hemodynamics and diastolic right heart collapse

Pericardial effusion is associated with an abnormal increase in respiratory variation in mitral flow velocity. However, the relation of the changes in flow velocity to pericardial pressure, hemodynamics and two-dimensional echocardiographic findings is not established. Therefore, 11 sedated dogs with extensive hemodynamic instrumentation were studied with two-dimensional and Doppler echocardiography during four stages of progressively larger pericardial effusion. During all stages of effusion, respiratory variation in peak mitral flow velocity in early diastole and left ventricular isovolumetric relaxation time was increased compared with baseline (p less than 0.05). This increase was seen at the earliest stage of effusion (mean pericardial pressure 4.2 +/- 1.4 versus -0.8 +/- 0.9 mm Hg at baseline, p less than 0.05), and preceded the appearance of unequivocal diastolic right heart collapse in every dog. Maximal respiratory variation coincided with the appearance of right atrial collapse (mean pericardial pressure 7.1 +/- 2.4 mm Hg; mean inspiratory decrease in aortic pressure 9.5 +/- 2.6 mm Hg; mean aortic pressure 88.2 +/- 15.2 versus 102.2 +/- 11.2 mm Hg at baseline, p less than 0.05; and cardiac output 3.8 +/- 1.2 versus 5.5 +/- 1.3 liters/min at baseline, p less than 0.05), but did not increase at stages associated with more severe hemodynamic compromise. In addition, the respiratory changes in peak mitral flow velocity in early diastole were associated with simultaneous changes in the diastolic transmitral pressure gradient. It is concluded that in this model of acute pericardial effusion 1) increased respiratory variation in early diastolic mitral flow velocity, peak mitral flow velocity in early diastole and left ventricular isovolumetric relaxation time occurs almost immediately as pericardial pressure increases and persists at all stages of increasing pericardial effusion; 2) the abnormal respiratory variation occurs before equalization of intracardiac pressures and before the onset of unequivocal right heart collapse; 3) the respiratory variation occurs as a result of changes in the diastolic transmitral pressure gradient; and 4) the magnitude of the respiratory change is not necessarily predictive of pericardial pressure or severity of hemodynamic compromise, especially at the more severe stages of pericardial effusion.     

Experimental cardiac tamponade: a hemodynamic and Doppler echocardiographic reexamination of the relation of right and left heart ejection dynamics to the phase of respiration

A hallmark of cardiac tamponade is pulsus paradoxus. However, the exact mechanism of pulsus paradoxus and the relation of left and right ventricular ejection dynamics remain controversial, with some studies suggesting an inverse relation in ventricular filling and ejection and others citing a more important role for the effects of right heart ejection dynamics delayed by transit through the pulmonary artery bed. To specifically reexamine this issue, six sedated but spontaneously breathing dogs were studied during experimental cardiac tamponade with use of extensive hemodynamic instrumentation and Doppler methods. During cardiac tamponade, left ventricular systolic pressure decreased from 125.8 +/- 12.1 to 81.7 +/- 26.7 mm Hg (p less than 0.01) and cardiac output from 5.86 +/- 1.48 to 2.34 +/- 0.98 liters/min (p less than 0.001); mean pericardial pressure increased from -1.2 +/- 0.8 to 10.5 +/- 3 mm Hg (p less than 0.001) and pulsus paradoxus from 4.3 +/- 1.6 to 10.7 +/- 1.2 mm Hg (p less than 0.001) compared with baseline values. An inverse relation in left and right ventricular ejection dynamics that was very close to 180 degrees out of phase was seen throughout the respiratory cycle in multiple hemodynamic and Doppler variables including peak systolic pressures, aortic and pulmonary flow velocities and ventricular ejection times. Simultaneous recording of the transmitral pressure gradient provided indirect evidence that the ventricular ejection dynamics were directly related to changes in ventricular filling. However, the magnitude of ventricular pressure or output flow velocity for each respiratory cycle was variable, depending on the exact timing of filling and ejection in relation to the phase of respiration. Variation in left ventricular output due to changes in right ventricular output delayed by transit through the pulmonary vasculature was not recognized in any animal. It is concluded that in spontaneously breathing dogs with acute cardiac tamponade, peak ventricular pressures, ventricular ejection times and pulmonary and aortic flow velocities have an inverse relation that is very close to 180 degrees out of phase.     

Doppler echocardiographic measurement of pulmonary artery pressure from ductal Doppler velocities in the newborn

The ductal flow velocities in 37 newborns (group 1: persistent pulmonary hypertension [n = 16], transient tachypnea [n = 3], other [n = 2]; group 2: respiratory distress syndrome [n = 16]) were prospectively evaluated by Doppler ultrasound for the purpose of deriving systolic pulmonary artery pressures. Maximal tricuspid regurgitant Doppler velocity in 21 of these patients was used to validate the pulmonary artery pressures derived from ductal flow velocities. There was a significant linear correlation between tricuspid regurgitant Doppler velocity and pulmonary artery systolic pressure derived from ductal Doppler velocities in patients with unidirectional (pure left to right or pure right to left) ductal shunting (p less than 0.001, r = 0.95, SEE 8) and in those with bidirectional shunting (p less than 0.001, r = 0.95, SEE 4.5). Systolic pulmonary artery pressure in group 1 (67 +/- 13 mm Hg) was significantly higher than that in group 2 (39 +/- 10 mm Hg) (p less than 0.001). In those with bidirectional shunting, duration of right to left shunting less than 60% of systole was found when pulmonary artery pressure was systemic or less, whereas duration greater than or equal to 60% was associated with suprasystemic pulmonary artery pressures. Serial changes in pulmonary artery systolic pressure, reflected by changes in ductal Doppler velocities, correlated with clinical status in persistent pulmonary hypertension of the newborn. Persistently suprasystemic pulmonary artery pressure was associated with death in five group 1 patients. It is concluded that ductal Doppler velocities can be reliably utilized to monitor the course of pulmonary artery systolic pressures in newborns.     

Hemodynamics of the Mueller maneuver in man: right and left heart micromanometry and Doppler echocardiography

Ten subjects with normal hemodynamics were studied during elective cardiac catheterization with right and left heart multisensor micromanometry to assess hemodynamic responses to the Mueller maneuver. Simultaneous right and left circulatory hemodynamics and left ventricular, pulmonary arterial, and aortic pressures were recorded, in addition to pulmonary arterial and aortic flow velocities. Steady-state cardiac outputs were determined by thermal dilution. Aortic systolic and mean pressures were not significantly changed during the Mueller maneuver, in contrast to a lower diastolic (p = .019) and higher pulse pressure (p = .016). Mean right atrial pressure (+/- SE) decreased from 7 +/- 1 to -17 +/- 4 mm Hg (p = .0002) and the right atrial "x" descent was markedly accentuated. Left ventricular end-diastolic pressure decreased from 12 +/- 4 to -3 +/- 13 mm Hg (p = .0025). Systemic vascular resistance and left ventricular peak positive dP/dt were increased during the Mueller maneuver (p less than .02), cardiac output and stroke volume were reduced (p less than .05), and there was no significant change in heart rate. Right and left peak flow velocities showed a trend toward a bilateral decrease (right, p = .054; left, p greater than .1), and times to peak flow velocity were increased in the pulmonary artery (p = .007) and reduced in the aortic root (p = .03). Normal subjects were studied separately by pulsed Doppler echocardiography. During the sustained Mueller maneuver, the internal jugular and right ventricular dimensions decreased, and superior vena cava Doppler flow was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)     

Doppler echocardiographic evaluation of tilting-disc prosthetic heart valves in children

To determine the Doppler characteristics of tilting-disc prosthetic heart valves in children, 22 children with mitral prostheses were studied 8 +/- 2 months after surgery, and 10 children with aortic prostheses were studied 37 +/- 26 months after surgery. All valves were thought to be functioning normally by clinical examination. Valve competence was interrogated and peak and mean velocities were measured by standard pulsed wave, continuous wave and color Doppler techniques. Prosthetic valve area was calculated and compared to the known valve area. Mild prosthetic valve regurgitation was present in 8 of 22 mitral and 7 of 10 aortic prostheses. For mitral prostheses, peak velocity was 192 +/- 41 cm/s, mean velocity was 118 +/- 37 cm/s and mean gradient was 7 +/- 4 mm Hg. For aortic prostheses, peak velocity was 287 +/- 88 cm/s, mean velocity was 197 +/- 59 cm/s, peak gradient was 36 +/- 21 mm Hg and mean gradient was 19 +/- 11 mm Hg. Prosthetic mitral valve area, calculated by the pressure half-time and modified Gorlin methods, correlated well with the known valve area (r = 0.89, standard error of the estimate = 0.29 and r = 0.95, standard error of the estimate = 0.21, respectively). Prosthetic aortic valve area, calculated by the modified Gorlin method, correlated well with the known valve area (r = 0.89, standard error of the estimate = 0.18). Residual valvular abnormalities are common after prosthetic valve insertion in children. Doppler estimates of prosthetic valve area correlate well with the known valve area but have a large standard error of the estimate.     

Ventricular performance related to transmural filling pressure in clinical cardiac tamponade

In clinical cardiac tamponade, open-catheter intrapericardial pressure (IPP) may be used to estimate left ventricular transmural filling pressure (TMFP). However, it has been suggested recently that right atrial pressure (RAP) is superior to IPP in assessing true extracardiac pressure during pericardial drainage. In 10 patients with subacute cardiac tamponade, pulmonary wedge pressure (PWP), RAP, and IPP were measured along with indexes of systolic function. To test the relative merits of IPP and RAP in assessing true pericardial pressure, three TMFP estimates were analyzed: TMFP1 = (PWP - IPP); TMFP2 = (PWP - 1/3 RAP - 2/3 IPP); and TMFP3 = (PWP - RAP). An accurate TMFP presumably should increase during pericardiocentesis and correlate with left ventricular stroke work. In addition, to test the role of preload variation in pulsus paradoxus, respiratory variation in TMFP was analyzed. In the initial tamponade state, RAP and IPP were essentially equal, so all three TMFP estimates gave equivalent results. For instance, TMFP1 averaged 4 +/- 2 mm Hg but fell to 0.2 +/- 1.3 mm Hg during inspiration (p less than .001 vs expiration) and showed beat-by-beat correlation with pulse arterial pressure. After intermediate pericardiocentesis (280 +/- 160 ml), the IPP of 6 +/- 3 mm Hg fell significantly below the RAP of 10 +/- 3 mm Hg (p less than .001), but with a 570 +/- 320 ml residual effusion suggesting continued IPP measurement accuracy. By complete pericardiocentesis (810 +/- 430 ml) there was a significant increase in TMFP1 to 8 +/- 4 mm Hg (p less than .05 vs tamponade) but not in the TMFP3 of 1 +/- 3 mm Hg. Encompassing tamponade and pericardiocentesis data, left ventricular stroke work index showed positive correlation with TMFP1 (r = .59) and TMFP2 (r = .52) but not with TMFP3. Thus cardiac tamponade often may be diagnosed with a TMFP averaging well above zero, and diastolic equalization of PWP, RAP, and IPP may be a predominantly inspiratory finding ("inspiratory tracking"). This supports the role of preload variation in the genesis of pulsus paradoxus. On the other hand, true pericardial pressure may fall substantially below RAP in the course of pericardial drainage. This may be reconciled with the concept that normal pericardial pressure nearly equals RAP by hypothesizing an increased pericardial capacity in subacute tamponade so that pericardiocentesis produces a state analogous to removal of normal pericardial constraint.     

Validation of Doppler-derived pulmonary arterial pressure in patients with ductus arteriosus under different hemodynamic states

Twenty-nine patients with a patent ductus arteriosus (PDA) in isolation (n = 17) or in combination with other lesions (n = 12) underwent simultaneous hemodynamic assessment and evaluation of PDA flow velocity by the Doppler method. The accuracy with which Doppler velocity across the PDA predicted pulmonary arterial pressure and the influence of PDA size and shape on the Doppler velocity-pressure relationship were examined. Seventy percent had a cone-shaped PDA (narrowest at the pulmonary artery end), and the remainder were tubular. Narrowest PDA diameter ranged from 1.5 to 9 mm (mean 3.5 mm). Peak systolic and mean pulmonary arterial pressure ranged from 10 to 116 and 8 to 72 mm Hg, respectively. Twenty-one patients (group 1) had left-to-right shunting only. The following variables showed significant correlation in this group: peak instantaneous systolic aortic-to-main pulmonary arterial (MPA) pressure gradient and maximum Doppler velocity across the PDA (slope = 1.03, SEE = 13 mm Hg, r = .94, p less than .001), mean aortic-to-MPA pressure gradient and mean Doppler velocity (slope = 1.06, SEE = 10 mm Hg, r = .95, p less than .001), and end diastolic aortic-to-MPA pressure gradient and minimum Doppler velocity (slope = 1.12, SEE = 8 mm Hg, r = .96, p less than .001). Eight patients (group 2) had bidirectional shunting. In this group peak instantaneous aortic-to-MPA pressure gradient significantly correlated with maximum Doppler velocity measured from the left-to-right shunt (slope = .70, SEE = 2 mm Hg, r = .92, p less than .002) and mean pressure gradient correlated with mean Doppler velocity (slope = .83, SEE = 3 mm Hg, r = .78, p less than .003). Right-to-left Doppler velocities showed no correlation with pressures. In six patients with pulmonary hypertension Doppler velocity changes accurately predicted the effect of pulmonary vasodilation on pulmonary arterial pressure. Doppler velocity of PDA flow reliably predicts pulmonary arterial pressure over a wide range of pressures and PDA shapes and sizes.     

Evaluation of pulmonary artery pressure and resistance by pulsed Doppler echocardiography

Pulsed Doppler echocardiography was used to examine the relation between pulmonary valve motion and pulmonary artery (PA) flow velocity patterns in 39 adults. In 16 patients with normal PA pressure (mean pressure less than 20 mm Hg), PA flow velocity accelerated slowly to a peak flow velocity at midsystole (time to peak flow velocity, or acceleration time = 134 +/- 20 ms [mean +/- standard deviation]), followed by a slow deceleration to the end of ejection, producing a "dome-like" appearance. In contrast, in 23 patients with elevated PA pressure (mean pressure 20 mm Hg or more), flow velocity accelerated rapidly to a peak flow velocity in early systole (acceleration time = 88 +/- 25 ms, p less than 0.01), followed by rapid flow velocity deceleration to a nadir in midsystole. In 13 of these patients, a transient increase in flow velocity occurred in late systole, producing a "spike and dome" appearance. In patients with an acceleration time of 120 ms or less, there was a negative linear correlation with mean PA pressure, expressed by the equation: mean PA pressure = 90 - (0.62 X acceleration time). The standard error of the estimate was 8.3 mm Hg. A similar negative linear correlation was found between PA acceleration time and total pulmonary resistance. Using a PA acceleration time of 100 ms or less resulted in a 78% sensitivity and a 100% specificity for detection of elevated PA pressure. Although this Doppler method cannot precisely estimate PA pressure, it can be helpful in separating patients with normal pressure from those with elevated PA pressure.     

Spectrum of hemodynamic changes in cardiac tamponade

To investigate the pathophysiology of cardiac tamponade, the hemodynamics of 77 consecutive patients with greater than 150 ml of pericardial effusion were studied. Patients were classified into 3 groups based on the equilibration of intrapericardial with right atrial and pulmonary arterial wedge pressures (mm Hg): group I (n = 16), intrapericardial pressure was less than right atrial and pulmonary arterial wedge pressures; group II (n = 13), intrapericardial pressure was equilibrated with right atrial but not pulmonary arterial wedge pressures; group III (n = 48), intrapericardial pressure was equilibrated with right atrial and pulmonary arterial wedge pressures. Pericardiocentesis produced the following changes: group I--significant (p less than 0.03) decreases in intrapericardial pressure (7 +/- 2 mm Hg), right atrial pressure (3 +/- 2 mm Hg), pulmonary arterial wedge pressure (2 +/- 2 mm Hg), and the inspiratory decrease in arterial systolic pressure (3 +/- 4 mm Hg) but no significant change in cardiac output; group II--significant (p less than 0.02) decreases in intrapericardial pressure (11 +/- 5 mm Hg), right atrial pressure (6 +/- 4 mm Hg), pulmonary arterial wedge pressure (4 +/- 5 mm Hg), and inspiratory decrease in arterial systolic pressure (8 +/- 7 mm Hg), and increase in cardiac output (1.1 +/- 1.2 liters/min); group III--significant (p less than 0.001) decreases in intrapericardial pressure (16 +/- 7 mm Hg), right atrial pressure (9 +/- 4 mm Hg), pulmonary arterial wedge pressure (8 +/- 5 mm Hg), inspiratory decrease in arterial systolic pressure (17 +/- 11 mm Hg), and increase in cardiac output (2.8 +/- 1.5 liters/min). The changes after pericardiocentesis in all parameters were significantly (p less than 0.05) greater in group III than in groups I or II except for the change in right atrial pressure, which was not significantly different in groups II versus III. The changes after pericardiocentesis indicate pericardial effusion caused the greatest abnormalities in group III but also caused significant abnormalities of pressure and flow in group II and of pressure alone in group I.(ABSTRACT TRUNCATED AT 250 WORDS)     

"Overestimation" of catheter gradients by Doppler ultrasound in patients with aortic stenosis: a predictable manifestation of pressure recovery.

OBJECTIVES: This study sought to evaluate whether pressure recovery can cause significant differences between Doppler and catheter gradients in patients with aortic stenosis, and whether these differences can be predicted by Doppler echocardiography. BACKGROUND: Pressure recovery has been shown to be a source of discrepancy between Doppler and catheter gradients across aortic stenoses in vitro. However, the clinical relevance of this phenomenon for the Doppler assessment of aortic stenosis has not been evaluated in patients. METHODS: Twenty-three patients with various degrees of aortic stenosis were studied with Doppler echocardiography and catheter technique within 24 h. Using an equation previously validated in vitro, pressure recovery was estimated from peak transvalvular velocity, aortic valve area and cross-sectional area of the ascending aorta and compared with the observed differences between Doppler and catheter gradients. Doppler gradients were also corrected by subtracting the predicted pressure recovery and then were compared with the observed catheter gradients. RESULTS: Predicted differences between Doppler and catheter gradients due to pressure recovery ranged from 5 to 82 mm Hg (mean +/- SD, 19 +/- 16 mm Hg) and 3 to 54 mm Hg (12 +/- 11 mm Hg) for peak and mean gradients, respectively. They compared well with the observed Doppler-catheter gradient differences, ranging from -5 to 75 mm Hg (18 +/- 18 mm Hg) and -7 to 48 mm Hg (11 +/- 13 mm Hg). Good correlation between predicted pressure recovery and observed gradient differences was found (r = 0.90 and 0.85, respectively). Both the noncorrected and the corrected Doppler gradients correlated well with the catheter gradients (r = 0.93-0.97). However, noncorrected Doppler gradients significantly overestimated the catheter gradients (slopes, 1.36 and 1.25 for peak and mean gradients, respectively), while Doppler gradients corrected for pressure recovery showed good agreement with catheter gradients (slopes, 1.03 and 0.96; standard error of estimate [SEE] 8.1 and 6.9 mm Hg; mean difference +/- SD 0.4 +/- 8.0 mm Hg and 1.1 +/- 6.8 mm Hg for peak and mean gradients, respectively). CONCLUSIONS: Significant pressure recovery can occur in patients with aortic stenosis and can cause discrepancies between Doppler and catheter gradients. However, pressure recovery and the resulting differences between Doppler and catheter measurements may be predicted from Doppler velocity, aortic valve area and size of the ascending aorta.     

Noninvasive prediction of pulmonary hypertension in chronic obstructive pulmonary disease by Doppler echocardiography

Thirty-six patients with chronic obstructive pulmonary disease (COPD) were studied by pulsed Doppler echocardiography. In 32 of the 36 patients, adequate Doppler signals were obtained in the pulmonary arterial trunk and correlated with right cardiac hemodynamics. The studied group included 26 patients with mean pulmonary arterial pressure (MPAP) greater than 20 mm Hg at rest (group A, with pulmonary hypertension) and six patients with MPAP of 20 mm Hg or less (group B, without pulmonary hypertension). A control group (group C) consisted of 12 subjects with normal hemodynamic data and pulmonary function. Analysis of Doppler data included flow velocity curve pattern, presence of a negative presystolic velocity, right ventricular pre-ejection period (RVPEP) and ejection period (RVEP), time between onset and peak of pulmonary velocity (time to peak velocity, TPV) and derived ratios of TPV/RVPEP and TPV/RVEP. In patients with pulmonary hypertension, the Doppler flow velocity curve in the pulmonary trunk showed a rapid acceleration and an early deceleration. The mean value for TPV was 78 +/- 12 msec in group A, 115 +/- 11 msec in group B, and 127 +/- 10 msec in group C. In patients with COPD, significant correlations were observed between TPV and log10 MPAP (r = -0.77; SEE = 0.07) and between TPV and log10 total pulmonary resistances (r = -0.84; SEE = 0.05). Accordingly, pulsed Doppler echocardiography may be a useful tool to predict pulmonary hypertension due to chronic pulmonary disease.     

Effects of left ventricular preload and afterload on ascending aortic blood velocity and acceleration in coronary artery disease

Doppler measurements of the velocity and acceleration of ascending aortic blood flow have been used as indexes of left ventricular (LV) contractility. Conflicting data exist, however, on the influence of LV loading conditions on these measurements. Therefore, simultaneous LV micromanometer pressure measurements, 2-dimensional echocardiography and continuous-wave Doppler studies were performed before and after preload or afterload manipulation in 16 patients with coronary artery disease. Nitroprusside (n = 9) was administered in combination with saline to maintain preload and achieve a 10 to 20% reduction in mean aortic pressure. Saline (n = 7) was administered (850 +/- 240 ml) to increase LV end-diastolic pressure 25 to 50%. All measurements were obtained during atrial pacing at a heart rate 10 to 15 beats/min above resting sinus rate. The administration of nitroprusside plus saline decreased LV end-systolic wall stress (94 +/- 27 to 67 +/- 14 g/cm2 X 10(3), p = 0.011) without changing LV end-diastolic pressure and end-diastolic dimension. Peak velocity (0.8 +/- 0.2 to 0.9 +/- 0.3, p = 0.044), velocity time integral (11 +/- 4 to 13 +/- 5 cm, p = 0.049) and mean acceleration (12 +/- 4 to 17 +/- 7 m/s2, p = 0.0014) increased significantly. The administration of saline alone significantly increased LV end-diastolic pressure (10 +/- 4 to 22 +/- 4 mm Hg, p = 0.0006), LV end-diastolic dimension (4.8 +/- 0.5 to 5.1 +/- 0.5 cm, p = 0.0001), peak velocity (0.9 +/- 0.3 to 1.0 +/- 0.4 m/s, p = 0.008), velocity-time integral (14 +/- 5 to 18 +/- 7 cm, p = 0.005), and mean acceleration (14 +/- 6 to 17 +/- 7 m/s2, p = 0.041). Thus, even a modest change in either preload or afterload altered peak velocity, the velocity time integral and mean acceleration. These data have important clinical implications regarding the application of Doppler aortic flow indexes in the assessment of LV function.     

Pulmonic valve insufficiency: a common cause of transient diastolic murmurs in renal failure

To study the transient diastolic murmur associated with renal failure, we used Doppler echocardiography to characterize flow across the semilunar valves in 10 patients on chronic hemodialysis with a diastolic murmur (group A), 26 patients on chronic hemodialysis without murmurs (group B), and 15 healthy persons (group C). Nine patients in group A had pulmonic valve insufficiency that encompassed 77 +/- 21% (SD) of diastole with peak regurgitant flow velocities of 1.7 +/- 0.3 m/s. Doppler-calculated mean pulmonary artery pressure in 8 of them was 43 +/- 7 mm Hg before dialysis and 20 +/- 12 mm Hg afterward (p less than 0.001). Dialysis reduced the duration of pulmonic insufficiency to 10 +/- 16% of diastole and lowered peak regurgitant flow velocities to 0.2 +/- 0.2 m/s (p less than 0.001 for each). Three patients in group B had aortic valve insufficiency and 3 had pulmonic valve insufficiency like that in group A. Three persons in group C had mild pulmonic valve insufficiency. Thus, transient diastolic murmurs associated with pulmonic valve insufficiency are not uncommon in patients with renal failure; they are related to fluid overload, are diminished by extracellular fluid removal, and reflect correctable pulmonary hypertension.     

Ultrasonic assessment of the St. Jude prosthetic valve: M mode, two-dimensional, and Doppler echocardiography

To determine whether the flow characteristics of aortic and mitral St. Jude Medical valves could be defined noninvasively, we analyzed Doppler transprosthetic flow velocity spectra in 23 relatively asymptomatic patients. Results were interpreted in the framework of M mode and two-dimensional echocardiographic data and were compared with Doppler transvalvular flow velocity spectra from native valves of healthy subjects. Although the morphologic characteristics of Doppler spectra were similar, peak and mean transprosthetic mitral flow velocities were higher than values obtained across native valves (1.38 +/- 0.3 m/sec and 0.73 +/- 0.1 m/sec vs 0.78 +/- 0.1 m/sec and 0.35 +/- 0.06 m/sec, respectively; p less than .001). However, calculated pressure half-times were not different (61.2 +/- 16.9 msec vs 57.2 +/- 13.2 msec; p greater than .05) and calculated transprosthetic mitral gradients were small (2.3 +/- 0.9 mm Hg). Similarly, the morphologic characteristics of aortic Doppler flow spectra in St. Jude and native valves were analogous. However, prosthetic valves exhibited higher peak and mean velocities (p less than .01) and slightly prolonged time-to-peak flow (p = .02). M mode and two-dimensional studies did not show useful quantitative measures of prosthetic function and did not demonstrate evidence of paravalvular leaks, which were detected in four cases by Doppler techniques. Thus Doppler echocardiography provides quantitative information about transprosthetic flow characteristics in patients with implanted St. Jude valves and is useful in identifying patients with prosthetic dysfunction.     

Clinical application of transpulmonary contrast-enhanced Doppler technique in the assessment of severity of aortic stenosis.

OBJECTIVE. The aim of this study was to demonstrate the clinical usefulness of the transpulmonary contrast-enhanced Doppler technique by using it to assess the severity of aortic stenosis. BACKGROUND. Sonicated albumin microbubbles can pass through the pulmonary circulation after peripheral venous injection and have been reported to enhance Doppler signals from the left side of the heart. Therefore, their use to determine aortic flow velocity would facilitate the assessment of the severity of aortic stenosis. METHODS. Twenty-two patients with aortic stenosis and seven normal volunteers were examined. Aortic flow velocity was recorded with continuous wave Doppler technique from an apical window before and after injection of 2 ml of sonicated albumin. RESULTS. In 10 patients with aortic stenosis, the aortic velocity envelope was too indistinct to determine the peak velocity before sonicated albumin was injected. After injection, the aortic flow Doppler signal was enhanced in 9 of the 10 patients and the velocity envelope became clear enough to measure the peak velocity, enabling calculation of the transaortic pressure gradient. In the remaining 12 patients with aortic stenosis and in all 7 normal volunteers, the velocity envelope was clear before injection and became much clearer after injection. The calculated transaortic pressure gradient showed a good agreement with catheterization measurements (y = 1.1x-6.5, r = 0.88, p less than 0.001, SEE = 16 mm Hg, n = 13). Duration of Doppler signal enhancement was measured as the time during which the envelope was clearer than before injection throughout the ejection period. The duration was significantly shorter in patients with aortic stenosis than in normal volunteers (16 +/- 5 vs. 52 +/- 32 s, p less than 0.01). There was a significant correlation between left ventricular systolic pressure measured by catheterization and the duration of signal enhancement (r = -0.69), suggesting that albumin microbubbles were fragile at high pressure. CONCLUSIONS. The transpulmonary contrast-enhanced Doppler technique using sonicated albumin is useful for assessing the severity of aortic stenosis even in patients with poor Doppler recordings, although the duration of signal enhancement might be affected by left ventricular systolic pressure.     

Accuracy and pitfalls of Doppler evaluation of the pressure gradient in aortic coarctation

Although the pressure gradient in aortic coarctation can usually be obtained by comparison of upper and lower limb blood pressures measured by sphygmomanometry, some patients may have upper or lower limb arterial compromise as a result of prior procedures or anomalous origin of the subclavian arteries, either of which may preclude accurate gradient measurement. To determine whether Doppler echocardiography could predict the pressure gradient, the Doppler method was used to predict transcoarctation gradients in 35 studies and the data were compared with the gradients measured at catheterization. Jet velocities were not adequately obtained by Doppler recording in three neonates with coarctation and patent ductus arteriosus, leaving 32 studies for analysis. The mean age of the study patients was 6 +/- 5.8 years. The mean Doppler-estimated gradient, calculated using only jet velocities distal to the obstruction (V2) in the modified Bernoulli equation, was 44 +/- 17 mm Hg, and the mean catheterization gradient was 36 +/- 21 mm Hg (p = NS; r = 0.91, SEE = 7.0 mm Hg; slope = 0.75, y = 17.3 mm Hg). The mean Doppler-estimated gradient using both the pre- and postcoarctation velocities (V1 and V2) in the modified Bernoulli equation (n = 26) was 36 +/- 20 mm Hg, and the mean catheterization gradient was 36 +/- 21 mm Hg (p = NS; r = 0.98, SEE = 4.2 mm Hg; slope = 0.91, y = 2.8 mm Hg). Doppler echocardiography closely estimated the pressure gradient in aortic coarctation, and estimation of the gradient improved when the velocities proximal as well as distal to the obstruction were included in the modified Bernoulli equation.     

Noninvasive prediction of transvalvular pressure gradient in patients with pulmonary stenosis by quantitative two-dimensional echocardiographic Doppler studies

Recent studies suggest that maximal Doppler velocities measured within the jets that form downstream from stenotic valves can be used to predict aortic valve gradients. To test whether the Doppler method would be useful for evaluation and management of pediatric patients with right ventricular outflow obstruction, we evaluated pulmonary artery flow before catheterization in 16 children with pulmonary valve stenosis. We used a 3.5-MHz, quantitative, range-gated, two-dimensional, pulsed, echocardiographic Doppler scanner with fast Fourier transform spectral output and a 2.5-MHz phased array with pulsed or continuous-mode Doppler. Peak systolic pulmonary artery flow velocities in the jet were recorded distal to the domed pulmonary valve leaflets in short-axis parasternal echocardiographic views. The pulsed Doppler scanner, because of its limitations for resolving high velocities, could quantify only the mildest stenoses; but, especially with the continuous Doppler technique, a close correlation was found between maximal velocity recorded in the jet and transpulmonary gradients between 11 and 180 mm Hg. A simplified Bernoulli equation (transvalvular gradient = 4 x [maximal velocity]2) proposed by Hatle and Angelsen could be used to predict the gradients found at catheterization with a high degree of accuracy (r = 0.98, SEE = +/- 7 mm Hg). Our study shows that recording of maximal Doppler jet velocities appears to provide a reliable measure of the severity of valvular pulmonic stenosis.     

Noninvasive estimation of the left ventricular pressure waveform throughout ejection in young patients with aortic stenosis

Validation of a totally noninvasive method for estimating instantaneous left ventricular pressure and constructing a pressure waveform throughout ejection in patients with aortic stenosis is reported. In 20 patients (aged 8.75 +/- 10 years) with congenital aortic stenosis (measured peak left ventricular pressure 120 to 260 mm Hg; transvalvular gradient 18 to 165 mm Hg), transaortic valve continuous wave Doppler ultrasound, indirect carotid pulse tracing, peripheral blood pressure and measured left ventricular pressure were recorded simultaneously at cardiac catheterization. Data were entered into a microcomputer using a digitizing tablet and the instantaneous Doppler gradient was calculated and added to instantaneous aortic pressure, derived from the time-corrected and calibrated carotid pulse tracing, to estimate instantaneous left ventricular pressure. Estimated left ventricular pressure waveforms reproduced measured left ventricular pressure closely. The mean error at peak left ventricular pressure was 0.2 +/- 4.8 mm Hg (r = 0.98, p = 0.001). The average error throughout ejection was 0.9 +/- 5.1 mm Hg. The error of estimated pressure was not related to age or the severity of aortic stenosis. The Doppler peak instantaneous gradient was observed to correlate closely (r = 0.97, p = 0.001) with peak to peak gradient. With this technique, the left ventricular pressure waveform throughout ejection can be accurately estimated noninvasively in patients with aortic stenosis. This methodology enables determination of mean, total and instantaneous systolic left ventricular pressure.     

Determination of the stenotic aortic valve area in adults using Doppler echocardiography

The severity of aortic stenosis was evaluated by Doppler echocardiography in 48 adults (mean age 67 years) undergoing cardiac catheterization. Maximal Doppler systolic gradient correlated with peak to peak pressure gradient (r = 0.79, y = 0.63x + 25.2 mm Hg) and mean Doppler gradient correlated with mean pressure gradient (r = 0.77, y = 0.59x + 10.0 mm Hg) by manometry. The transvalvular pressure gradient is flow dependent, however, and associated left ventricular dysfunction was common in our patients (33%). Thus, of the 32 patients with an aortic valve area less than or equal to 1.0 cm2 at catheterization, 6 (19%) had a peak Doppler gradient less than 50 mm Hg. To take into account the influence of volume flow, aortic valve area was calculated as stroke volume, measured simultaneously by thermodilution, divided by the Doppler systolic velocity integral in the aortic jet. Aortic valve areas calculated by this method were compared with results at catheterization in the total group (r = 0.71). Significant aortic insufficiency was present in 71% of the population. In the subgroup without significant coexisting aortic insufficiency, closer agreement of valve area with catheterization was noted (n = 14, r = 0.91, y = 0.83x + 0.24 cm2). Transaortic stroke volume can be determined noninvasively by Doppler echocardiographic measures in the left ventricular outflow tract, just proximal to the stenotic valve. Aortic valve area can then be calculated as left ventricular outflow tract cross-sectional area times the systolic velocity integral of outflow tract flow, divided by the systolic velocity integral in the aortic jet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Doppler evaluation of left ventricular diastolic filling in children with systemic hypertension

To assess left ventricular (LV) diastolic function in children with systemic hypertension, 11 patients with hypertension (mean blood pressure 99 mm Hg) and 7 normal patients (mean blood pressure 78 mm Hg) underwent M-mode echocardiography and pulsed Doppler examination of the LV inflow. From a digitized trace of the LV endocardium and a simultaneous phonocardiogram, echocardiographic diastolic time intervals, peak rate of increase in LV dimension (dD/dt), and dD/dt normalized for LV end-diastolic dimension (dD/dt/D) were measured. Doppler diastolic time intervals, peak velocities at rapid filling (E velocity) and atrial contraction (A velocity), and the ratio of E and A velocities were measured. The following areas under the Doppler curve and their percent of the total area were determined: first 33% of diastole (0.33 area), first 50% of diastole, triangle under the A velocity (A area), and the triangle under the E velocity (E area). The A velocity (patients with hypertension = 0.68 +/- 0.11 m/s, normal subjects = 0.49 +/- 0.08 m/s), the 0.33 area/total area (patients with hypertension = 0.49 +/- 0.09, normal subjects = 0.58 +/- 0.08), the A area (patients with hypertension = 0.17 +/- 0.05, normal subjects = 0.12 +/- 0.03), and the A area/total area (patients with hypertension = 0.30 +/- 0.11, normal subjects = 0.20 +/- 0.07) were significantly different between groups (p less than 0.05). M-mode and Doppler time intervals, (dD/dt)/D, E velocity, and the remaining Doppler areas were not significantly different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)