Estimation of left ventricular diastolic pressures from precordial pulsed-Doppler analysis of pulmonary venous and mitral flow

Estimation of left ventricular diastolic pressures from precordial pulsed-Doppler analysis of pulmonary venous and mitral flow Because analysis of pulmonary venous flow (PVF) will be extensively used in comprehensive Doppler assessment of left ventricular diastolic function, this study was designed to (1) evaluate the feasibllity of PVF measurement in 116 consecutive pattents with various cardiac abnormalities by using precordial pulsed Doppler echocardfography; (2) Estimate mean pulmonary capillary pressure (MPCP) and left ventricular end-diastolic pressure (LVEDP) from Doppler variables of PVF and mitral inflow; and (3) evaluate the influence of clinical and hemodynemic varfables on PVF Doppler patterns. We adequately recorded anterograde PVF in 96 (82.7%) patients and retrograde PVF in 45 (38.7%) patients. The strongest correlation between MPCP and Doppler variables of PVF was found with systolic fraction (the systolic velocity tie integral expressed as a fraction of total anterograde PVF) (r = -0.88; p < 0.001). Age influenced this relation, with progressive increase of the systolic fraction in older patients. A good correlation (r = 0.72; p < 0.091) was found between LVEDP and the difference in duration of the reversal PVF and the mitral a wave. In conclusion, (1) PVF can be recorded adequately in most patients with pm~ordlal Doppler echocardiography; (2) left ventricular diastolii pressures can be estimated reftably by precordial Doppler echocardiography; and (3) the clinical meaning of Doppler-derived indexes of left ventricular diastolic performance is age-related. (AM HEART J 1994;128:293-300.)

Maria Cristiana Brunazzi, MD,8 Fabio Chirillo, MD,b Mario Pasqualini, MD, Marzio Gemelli, MD,a Enrico Franceschini-Grisolia, MD,b Carlo Longhini, MD, FACC,C Luigi Giommi, MD,b Franc0 Barbaresi, MD,” and Paolo Stritoni, MDb Legnago, Treviso, and Ferrara, Italy

The analysis of transmitral velocities by means of precordial pulsed wave Doppler echocardiography has been largely investigated and used as a noninvasive and easily obtainable method of evaluating the diastolic function of the left ventricle.le8 However, the dependence of mitral inflow patterns on multiple factors (such as left ventricular relaxation,g left ventricular chamber stiffness,‘O left atrial compliance,ll mitral regurgitation, l2 left ventricular loading condition,13 and pericardial restrainti4) has greatly limited the clinical value of this measurement. Recently, the analysis of pulmonary venous flow (PVF) by pulsed

From %he Department of Cardiology, Civic Hospital, Legnago; bthe Department of CardioIogy, Regional Hospital, Treviso; and Cthe Medical Clinics, University of Ferrara. Received for publication Aug. 11, 1993; accepted Dec. 10, 1993. Reprint requests: Maria Cristiana Brunazzi, MD, Department of Cardiology, Civic Hospital, Via Giannella 1, 37045 Legnago (VR), Italy. Copyright @ 1994 by Mosby-Year Book, Inc. oooz-8703/94/$3.00 + 0 4/l/56686

Doppler transesophageal echocardiography has provided an accurate estimation of mean pulmonary capillary pressure (MPCP)ls, I6 and left ventricular end-diastolic pressure (LVEDP).17 Transesophageal echocardiography cannot be used routinely, however, because it is semiinvasive, is costly, is not well tolerated by all patients, and is not easily repeatable. Because the analysis of PVF provides new and valuable findings and will be routinely used in comprehensive assessment of left ventricular diastoiic function,18-20 we undertook this study to (1) evaluate the feasibility of PVF measurement in an unselected population by using precordial pulsed wave Doppler echocardiography; (2) assess possible correlations between mitral inflow and PVF velocities and left ventricular diastolic pressures; and (3) evaluate the influence of certain clinical and hemodynamic variables on these relations (Fig. 1). METHODS Study population.

dial two-dimensional,

We prospectively performed precorM-mode, and pulsed Doppler echo293

294

Brunazzi et al.

American

August 1994 Heart Journal

Fig. 1. Corresponding pulmonary capillary pressure (PCP) tracing and velocity-time profiles of pulmonary venous flow (PVF) and mitral inflow (MF) in normal heart. Velocity-time profile of PVF is triphasic, with systolic (s), diastolic fdj, and atria1 contraction fa) phases. It is related inversely to PCP waves, with peaks of anterograde flow corresponding to nadirs of x and y descents. Velocity-time profile of mitral flow is biphasic, with larger early (E) diastolic filling velocity and smaller atria1 (A) filling velocity.

cardiography in 116 consecutive patients undergoing elective cardiac catheterization for various cardiac abnormalities. No patient had evidence of congenital heart disease or atrioventricular conduction disturbances such as second- or third-degree atrioventricular block. All patients’ heartbeat demonstrated sinus rhythm, with a mean heart rate of 72 f 18 beatslmin. No patient required mechanical ventilation at the time of Doppler and catheter examination. Written informed consent was obtained from all patients. Cardiac catheterization. Left- and right-heart catheterization were performed through a femoral approach with fluid-filled catheters attached to manifold micromanometer transducers (P-50, Gould, Cleveland, Ohio). Pulmonary capillary wedge pressure readings were obtained with a balloon-tipped pulmonary artery catheter (SwanGanz, Baxter Healthcare, Irvine, Calif.). Pulmonary wedge position was verified by noting a 25 mm Hg decrease in pressure from mean pulmonary artery pressure and a change in the phasic waveform. Uncertain positions were verified by measuring oxygen saturation. Pulmonary wedge pressure data were obtained from both lungs and were recorded at end-tidal-volume apnea. Simultaneous recordings of pulmonary capillary wedge pressure and left ventricular pressure were obtained from all patients. All pressures were recorded on a strip chart at 100 mm/set. Left ventriculography was performed in the 30-degree right anterior oblique and 60-degree left oblique anterior projections. Left ventricular volumes and ejection fraction were

calculated by the method of Dodge et a1.21A standard examination of the coronary arteries followed. Echocardiography. Two-dimensional, M-mode, and Doppler echocardiograms were obtained with a HewlettPackard Sonos 1000 (Andover, Mass.) imaging system. The frequency of the transducer was 2.5 MHz. Flow velocity signals and the electrocardiogram were recorded on strip chart at 100 mm/set and recorded on videotape at an equivalent speed. Patients were examined in left lateral decubitus just before cardiac catheterization (mean interval between examinations 48 k 15 minutes, range 10 to 128 min). PVF velocities were recorded in the apical fourchamber view by positioning a 5 mm sample volume 1 to 2 cm proximal to the entrance of the right upper pulmonary vein into the left atrium. Color Doppler was used to identify the direction of the jet and to align the interrogating sample volume as parallel as possible to the flow. Angle correction was never used. Mitral inflow velocities were measured at the level of the leaflet tips in a standard four-chamber view. When atria1 contraction occurred before mitral deceleration slope had decreased to the zero baseline, the slope was linearly extrapolated to the baseline to obtain the deceleration time. All Doppler measurements were performed at endtidal-volume apnea, and five cardiac cycles were averaged. Mitral regurgitation was detected by color Doppler interrogation of the left atrium and graded according to standard criteria.22 Measurements and calculations. From Doppler trac-

Volume 128, Number 2 American Heart Journal

Brurzarzi

ct al.

295

SW-1 VTI SYSTOLIC FRACTION =s,,T, + d,,T,

aPV Fig. 2. Measurementsof pulmonary venous flow velocities. Systolic fraction of anterogradevelocity-time integrals (VTI) wascalculated asratio between systolic velocity-time integral (sVT1) and sumof sVTI and diastolic velocity-time integral (dVTZ). al+‘, Peak velocity of a wave; aVTI, velocity-time integral of a wave;DUR a, duration of a wave; DUR d, duration of diastolic wave; DUR s, duration of systolic wave; dPV, diastolic peak velocity; sPV, systolic peak velocity.

ings of mitral inflow, we measuredpeak early diastolic and peak late diastolic filling velocities, velocity-time integrals of early and late diastole, deceleration time, and duration of early and late diastolic mitral inflow. From the Doppler velocity profile of PVF, we measuredthe peak velocities of systolic, early-diastolic, and late-retrograde diastolic flows; the velocity-time integral; and the duration of the systolic and early- and late-diastolic flows (Fig. 2). When the systolic component was biphasic or triphasic, peak velocity wasconsideredthe greatest recorded value, and the velocity-time integral of the systolic wave wasobtained from the sum of all systolic components. The systolic peak velocity and the systolic velocity-time integral alsowere expressedas fractions of the sum of the systolic and early diastolic waves (systolic/systolic + anterogradediastolic = systolic fraction). According to the method introduced by Rossvoll and Hatle,23 the duration of the mitral a wave wascomparedwith the duration of the pulmonary venous wave at atria1 contraction to estimate LVEDP. Data analysis. To determine the relation of PVF variablesto MPCP and LVEDP, we correlated Doppler findings with left ventricular diastolic pressuresby meansof multiple stepwiseregressionanalysis.Age, sex, heart rate, left ventricular ejection fraction, and the presenceand severity of mitral regurgitation were included in the analysis to allow detection of the possibleeffects of these variables on the relation between Doppler and catheterization data. For purposesof analysis, patients were divided into two

groups according to levels of MPCP and LVEDP (normal 512 mm Hg and elevated >12 mm Hg). The clinical and hemodynamic characteristics of the two groups were compared by using Student’s unpaired t test. To identify determinants of systolic patterns (monophasic vs biphasic or triphasic flow) of the PVF, PQ interval, heart rate, MPCP, precontraction left ventricular pressure, the presenceof a C wave on the pulmonary wedgepressure tracing, and the morphologic appearance of the mitral leaflets (redundant vs normal) were compared between patients who presented one or more systolic peaks. To evaluate interobserver and intraobserver variabilities of Doppler and hemodynamic measurements,Doppler variables, MPCP, and LVEDP in 25 randomly selected patients were analyzed by two independent observersand by oneobserveron two different occasions.For determination of interobserver and intraobserver variabilities, the mean of the percentage differences between the two observers and that of the percentagedifferencesbetween the two occasions were calculated. All continuous values were expressedas mean +- SD. A p value
296

Brunazzi et al.

American

Table I. Characteristics dial Doppler recording flow

of patients with adequate of auterograde pulmonary

No. of patients Men/Women Age (yd

96

70126 58.4 f 18.1 (range 35-78) 76 + 21 49 21 28 12 0.27 + 0.09 11 10 6 8

Heart rate (beats/min) Coronary artery disease Single-vessel Multivessel Dilated cardiomyopathy Left ventricular ejection fraction Aortic stenosis (AVA < 0.8 cm2) Severe aortic regurgitation Mitral stenosis (MVA < 1 cm2) Severe mitral regurgitation AVA, Aortic

valve

precorvenous

area; MVA,

mitral valve area.

Table II. Clinical and hemodynamic with normal and elevated mean pressure

variables in patients pulmonary capillary

MPCP (mm Hg)

No. of patients Men/Women Age (~4 Heart rate (beats/min) MPCP (mm Hg) Left ventricular ejection fraction Mitral regurgitation 1+ 2+ 3+

112

>12

45 33112 56.8 + 14 64 + 19 7.8 + 3.6 0.71 f 0.18

37114 57.9 + 13 81 + 18 23.2 + 9 0.51 f 0.16

p Value

51

NS <0.05
38 5 3

36 6 5

Table Ill. Clinical and hemodyuamic variables in patients with normal and elevated left ventricular end-diastolic pressure LVEDP 512

LVEDP,

Left

ventricular

racic deformity (1). In six patients, because the left atrium was extremely large, it was impossible to sample the pulmonary veins because they were at the far field of the two-dimensional sector. In four patients with severe mitral regurgitation, the regurgitant jet entered the right upper pulmonary vein and masked the systolic component of the flow. Adequate recording of anterograde PVF was obtained in 96 (82.7 % ) patients. In 15 patients with an enlarged left atrium, pulsed-wave depth limitations of the ultrasound machine required modified precordial positions (off-axis views) to obtain an adequate sample volume location. Reverse flow at atria1 contraction was noted in all patients but was suitable for analysis in only 45 (38.7 % ). In 12 patients the atria1 reversal flow velocities were detected at a sample volume position different from that used to obtain the maximal anterograde velocities. Study group characteristics. The clinical and hemodynamic characteristics of the 96 patients in whom anterograde PVF was available for analysis are reported in Table I. There were no significant differences between patients with normal and elevated MPCP (Table II) and normal and elevated LVEDP (Table III) with regard to age, sex, or presence or grade of mitral regurgitation. Heart rate was greater in patients with elevated MPCP; left ventricular ejection fraction was lower in patients with elevated MPCP and LVEDP. Correlations of pulmonary venous flow variables with mean pulmonary capillary pressure. The strongest cor-

MPCP, Mean pulmonary capillary pressure; NS, not significant.

No. patients Men/women Age (yr) Heart rate (beats/min) LVEDP (mm Hg) Left ventricular ejection fraction Mitral regurgitation 1+ 2+ 3+

August 1994 Heart Journal

>12

15 1015 64 f 13 65 + 18 9 + 2.8 0.72 + 0.18

end-diastolic

(mm Hg)

8 2 2 pressure.

30 2119 62 + 8 73 + 22 17 * 5.3 0.60 + 0.22 14 4 1

p

Value

NS NS
relation between MPCP and the Doppler variables of the PVF was found with the systolic fraction of the velocity-time integrals (r = -0.88; standard error of the estimate [SEE] 3.1 mm Hg; Fig. 3). A systolic fraction <0.36 predicted MPCP ~18 mm Hg with a sensitivity of 0.90 and a specificity of 0.85. There was close agreement between the means of measured and predicted values and their differences (mean difference 0.51 mm Hg). However, the 95 % confidence intervals for upper (5.0 to 8.1 mm Hg) and lower (-7.5 to -4.9 mm Hg) limits were not small enough to provide a reliable estimation of normal borderline MPCP. Peak systolic velocity (r = 0.45; SEE 7.0 mm Hg), peak diastolic velocity (r = -0.38; SEE 7.5 mm Hg), and the systolic fraction of peak anterograde velocities (r = -0.56; SEE 4.8 mm Hg) correlated less well with MPCP. Influence of clinical and hemodynamic variables on the systolic pulmonary venous flow pattern. Systolic

PVF was monophasic in 65 (67.7 % ) patients, biphasic in 29 (30.2%; 18 with normal MPCP and 11 with elevated MPCP) patients, and triphasic in 2 patients (both with normal MPCP). No significant difference

Volume 128, Number 2 American Heart Journal

Brunazzi

et al.

297

CATHETERIZATION(MPCP) 50) mmHg

0

10

20 DOPPLER

30

40

(PVF SYSTOLIC

50

60

70 %

FRACTION)

Fig. 3. Systolic fraction of pulmonary venous flow IPVF) velocity-time

integrals versus mean pulmonary

capillary pressure (MPCP) .with regard to heart rate, PQ interval, MPCP, precontraction left ventricular pressure, presence of a C wave on the capillary wedge pressure tracing, or presence of redundant mitral leaflets was found between patients with one or more systolic waves on the PVF tracing. Pulmonary venous flow and mitral flow patterns in patients with elevated left ventricular end-diastolic pressure. The difference in duration between the PVF

reversal at atria1 contraction and the mitral a wave was calculated in 45 patients. A strong correlation (r = -0.72; p < 0.001) was found between the Doppler index and LVEDP. When LVEDP rises above normal, the mitral a wave shortens and the reversal flow into the pulmonary veins becomes longer. A longer pulmonary venous A wave than mitral A wave predicted LVEDP >16 mm Hg with a specificity of 0.82 and a sensitivity of 0.77. However, the agreement was poor (with a mean difference of 3.3 mm Hg) in the comparison of the means of measured and predicted values with their differences. Influence of clinical and hemodynamic variables. Sex,

heart rate, left ventricular ejection fraction, and mitral regurgitation did not affect the correlation between MPCP and the systolic fraction of the PVF. Only age influenced the relation. With age (Table IV), systolic peak velocity increased and diastolic peak velocity decreased; the same was found for the systolic and diastolic velocity-time integrals, with a consequent progressive increase of the systolic fraction. lntraobserver and interobserver variabilities of Doppler flow and catheterization measurements. For MPCP

and LVEDP,

interobserver

variability

was 3.2% it_

Table IV. Influence of age on pulmonary venous flow peak

systolic and diastolic velocities, systolic and diastolic velocity time-integrals, and systolic fraction of velocitytime integrals in patients with normal mean pulmonary capillary pressure Age (yr) Systolic peak velocity (cm/set) Diastolic peak velocity (cmhec) Systolic velocity timeintegral Diastolic velocity-time integral Systolic fraction of velocity-time integrals ( C6 )

540 48 It 13

41-50 50 r 11

51-60 55 It 12

261 60 i- 10

57 f 10

46 t 11

40 i 9

36 ? 14

11.7 t 4.1

12.5 i- 4.2

1X1

t- 3.3

15.1 + 4.2

12.7 t 2.5

11.4 I- 2.2

10.5 “- 4.3

9.7 + 4.4

47 J- 15

54 + 13

56 r 14

61 + 16

Values are mean t SD.

4.2 % and 3.0 % + 3.2 % , and intraobserver variability 0.7% + 4.0% and 0.6% 2 3.3%) respectively. For PVF, interobserver variability was 1.6 % + 3.8 % for peak velocities and 2.0 % rt 4.1% for the systolic fraction. The corresponding values for intraobserver variability were 0.8% +- 4.8% and 0.5% r 2.9%) respectively. For the duration of the mitral a wave and pulmonary reversal flow, interobserver variability was 2.2% +- 3.1% and 4.2% -+ 6.8% and intraobserver variability 1.2% f 2.1% and 2.5%, -t 3.4%, respectively.

298

Brunazzi et al.

DISCUSSION

In the 1970s Rajagopalan et a1.24-26demonstrated the phasic nature of the extraparenchymal PVF and its dependence on left atria1 pressure; in the 1980s Keren et a1.27v28 studied PVF velocity patterns with precordial pulsed-Doppler echocardiography. Since then the analysis of PVF has rarely drawn the attention of investigators, perhaps because of technical difficulties in sampling the pulmonary veins from the precordial approach and the apparent lack of clinical utility. The introduction of transesophageal echocardiography has made the analysis of the PVF feasible and accurate in almost all patients. Many studies have demonstrated the utility of PVF analysis for evaluating the diastolic properties of the left ventricle,20 the severity of mitral stenosis2g>30 and regurgitation31$ 32 and the presence of pericardial constriction. However, most of these studies were performed with transesophageal echocardiography, a technique not easily applicable to routine or follow-up examinations. With transesophageal echocardiography PVF measurement can be accomplished in most patients (4.9% failure rate reported by Bartzokis et a1.34). In subjects without cardiac disease, precordial echocardiography has failed to yield adequate PVF tracings in 18% of cases,35 and the feasibility of PVF measurement from the precordial approach has been assessed only in restricted groups of patients with heart disease. In the present study, adequate recording of forward PVF was obtained in most patients from the apical approach, and its feasibility was independent of the underlying cardiac abnormality and level of MPCP. Reverse flow at atria1 contraction has been reported in as many as 100% of subjects in sinus rhythm in transesophageal echocardiographic studies36; extremely variable detection rates have been reported for precordial echocardiography. 18136 In our study acquisition of adequate reverse PVF (a low-velocity signal) was highly dependent on gain and filter settings and was often disturbed by wall motion artifacts from prominent atria1 contraction. Biphasic systolic forward flow has been detected in heart disease 73% to 100% of subjects without studied with transesophageal echocardiography, whereas this pattern was encountered less frequently (0% to 37% )36 in studies with precordial echo.18p I9236 Such different rates of adequately recorded PVF and such marked variations of its systolic pattern may be related to technological improvements in echo Doppler instrumentation, the greater ease and accuracy of transesophageal measurements,36 the influence of postural changes,37 to the location of the sample volume, and the pulmonary vein being interrogated.i2, 36

American

August 1994 Heart Journal

In agreement with the transesophageal echocardiographic study by Kuecherer et a1.,15we found that the systolic fraction of the PVF velocity-time integrals had the best correlation with MPCP. Unlike other investigatorsi lg we found no significant correlation between MPCP and peak systolic velocity or systolic fraction of peak anterograde velocities: in many patients with normal MPCP diastolic peak velocity was greater than systolic peak velocity, but velocity-time integrals were almost equal. The statistical values of our study are similar to those found by Kuecherer et a1.,i5 but there are some important differences. All patients evaluated by Kuecherer et al. were mechanically ventilated; the influence of mechanical ventilation on PVF pattern is controversial.38, 3g We calculated left ventricular ejection fraction by contrast ventriculography, whereas left ventricular systolic shortening fraction calculated by M-mode echocardiography, as in the Kuecherer et al. study, may not reflect the overall left ventricular systolic performance in patients with segmental wall motion abnormalities. Most patients in the group studied by Kuecherer et al. had coronary artery disease, whereas our population had a variety of cardiac disorders. Variations of PVF patterns with age in our study population are in accordance with those reported by Klein and Tajik, I9 Masuyama et a1.,35 and Arakawa et a1.40 and may be related to prolonged left ventricular relaxation with aging.41r 42 The age distribution of the population studied by Kuecherer et a1.15 was rather homogeneous, with 85 % of patients >60 years old, whereas age distribution was markedly greater in our population. The different age distribution can explain our smaller cutoff value of PVF systolic fraction (0.36 vs 0.55) for identifying patients with elevated MPCP. Adopting such a small cutoff value, we limited falsepositive findings especially in younger patients, whereas the identification of older patients with borderline MPCP was more problematic. Further investigation in younger patients with heart disease is warranted to establish ranges of PVF variables in the presence of normal or elevated MPCP. It has been hypothesized that in the presence of increased MPCP caused by pathologic conditions producing an increase in a wave pressure, forward PVF might appear, not predominant, but normal during early diastole. 43 As a consequence the correlation between MPCP and the systolic fraction of PVF velocity-time integrals would be not valid in the presence of pathologic conditions such as left ventricular hypertrophy and myocardial ischemia leading to impaired relaxation.

Volume 126, Number 2 American Heart Journal

In patients with prominent left ventricular a wave and normal MPCP we found a systolic predominance in PVF velocity-time integrals, whereas diastolic predominance was noted only in the presence of elevated MPCP. We conclude that the inverse relation between the systolic fraction of PVF and the level of MPCP was good in a vast spectrum of cardiac diseases. This finding validates in a broader clinical setting the correlation found by Kuecherer et a1.15in the operating theater, and extends its clinical value. In agreement with Rossvoll and Hatle,23 we found that a prolonged PVF reversal and a shortened mitral A wave identified patients with elevated LVEDP. In both studies, however, the number of patients was limited; measurements of the two waves were not simultaneous; and the influence of some technical, clinical, and hemodynamic variables on this relation was not assessed. Further investigations are needed to standardize and validate this method on larger clinical scale. Several limitations of the study must be considered. The Doppler and the catheterization measurements were not simultaneous. Although the condition of all patients was hemodynamically stable and medications were not changed between the two studies, the possibility of variations in the hemodynamic status cannot be excluded. The position of the tip of the balloon-tipped pulmonary artery catheter was not standardized; the measured MPCP may differ by 1 to 3 mm Hg if the catheter is placed in one anterior or posterior pulmonary segmental branch with the patient supine. 44Pulmonary capillary wedge pressure measured with fluid-filled catheters was assumed to be equal to left atria1 pressure.45j 46 Direct measurement of left atria1 pressure with Millar micromanometers would have been more precise. However, our purpose was to compare an invasive, indirect, and largely used measure of left atria1 pressure with Doppler-derived indices. We did not evaluate the influence of left atria1 size and function or the descent of the base of the heart on PVF patterns. The importance of these variables on PVF is controversial.47-4g Moreover, the echocardiographic methods used to measure left atria1 volumes were based on geometric assumptions50 that are not applicable to enlarged and deformed left atria such as those found in chronic mitral valve diseases (as in our study population). Despite these limitations, this study provides evidence that over a wide range of MPCP and in patients with various cardiac abnormalities, MPCP can be estimated accurately by precordial pulsed Doppler analysis of PVF. The combination of PVF and mitral velocity can supplement mitral flow studies in de-

Rrunnzzi

et al.

299

tecting elevated LVEDP in patients with pseudonormalization of mitral flow velocity pattern due to elevated MPCP. With application of these Dopplerderived indexes, precordial echocardiography may provide accurate assessment and follow-up of different cardiac abnormalities in which progressive left. ventricular diastolic dysfunction occurs with or in the absence of systolic impairment. We thank Giorgio Rossello for his skilled technical assistance.

REFERENCES

. Rokey R, Kuo LC, Zoghbi WA, Limacher MC, Quinones MA. Determination of narameters of diastolic fillina with nulsed Doppler echocardibgraphy. Circulation 1985;717543-50: 2. Friedman BJ, Drincovic N, Miles H, Shih WJ, Mazzoleni A, De Maria AN. Assessment of left ventricular diastolic function: comparison of Doppler and gated blood pool scintigraphy. J Am Co11 Cardioi 1986;8:1348-54. 3. Channer S, Wilde P, Culling W, Jones JV. Estimation of left ventricular end-diastolic pressure by pulsed Doppler ultrasound. Lancet 1986;3:1005-7. 4. Aronoff RD, Zoghbi WA, Rokey R, Bolli R, Quinones MA. Assessment of diastolic pressure-volume relation in the intact left ventricle by pulsed-Doppler echocardiography [Abstract]. J Am Co11 Cardiol 1986,73224A. 5. Labovitz AJ, Pearson AC. Evaluation of left ventricular diastolic function: clinical relevance and recent Doppler echocardiographic insights. AM HEART J 1987;114:836-51. 6. Kuecherer H, Ruffmann K, Kuebler W. Determination of left ventricular filling parameters by pulsed Doppler echocardiography: a noninvasive method to predict high filling pressures in patients with coronary artery disease. AM HEAR’I‘ J 1988: 116:1017-21. 7.

8.

9.

10.

11.

12.

Hanrath P, Mathey DG, Siegert R, Bleifeld W. Left ventricular relaxation and filling patterns in different forms of left ventricular hypertrophy: an echocardiographic study. Am J Cardiol 1980;45:15-23. De Maria AN, Wisenbaugh T. Identification and treatment of diastolic dysfunction: role of transmitral Doppler recordings. J Am Co11 CardioI 1987;9:1106-7. Appleton CP, Hatle LK, Popp RL. Relations of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Co11 Cardiol 1988;12:426-40. Lin SL, Tak T, Kawanishi DT, McKay CR, Rahimtoola SH, Chandraratna AN. Comparison of Doppler echocardiographic and hemodynamic indexes of left ventricular diastolic properties in coronary artery disease. Am d Cardiol 1988;62:882-6. Ishida Y, Meisner JS, Tsujioka K, Gallo JI, Yoran C, Frater RW, Yellin EL. Left ventricular filling dynamics: influence of left ventricular relaxation and left atria1 pressure. Circulation 1986;74:18’7-96. Grodecki PV, Klein AL. Pitfalls in the echo-Doppler assessment of diastolic dysfunction. Echocardiography 1993;10:21334.

Choong CY, Herrmann HC, Weyman AE, Fifer MA. Preload dependence of Doppler-derived indexes of left ventricular diastolic function in humans. J Am Co11 Cardiol 1987;10800-8. 14 Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomvopathv bv DODpler echocardiography. Circulation 1989;79:357-70.’ ” 1 15. Kuecherer HF. Muhiudeen IA. Kusumoto FM. Lee E. Moulinier LE, Cahalan MK, Schiller NB. Estimation of mean left atria1 pressure from transesophageal pulsed Doppler echocardiographyofpulmonaryvenousflo~.Circ~~lation1990;82:112739. 13.

300

Brunmzi et al.

16. Habu H, Sasaki T, Naito T, Hirano Y, Ikawa H, Katori R. What is the most appropriate variable for estimation of mean pulmonary capillary wedge pressure by transesophageal pulsed Doppler echocardiography? [Abstract]. J Am Co11 Cardiol 1992;19:236A. 17. Nishimura RA, Abel MD, Hatle LK, Tajik AJ. Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocardiography: effect of different loading conditions. Circulation 1990;81:1488-97. 18. Basnight MA, Gonzalez MS, Kershenovich SC, Appleton CP. Pulmonary venous flow velocity: relation to hemodynamics, mitral flow velocity and left atrial volume, and ejection fraction. J Am Sot Echocardiogr 1991;4:457-58. 19. Klein AL, Tajik AJ. Doppler assessment of pulmonary venous flow in healthy subjects and in patients with heart disease. J Am Sot Echocardiogr 1991;4:379-92. 20. Appleton CP, Hatle LK. The natural history of left ventricular filling abnormalities: assessment by two-dimensional and Doppler echocardiography. Echocardiography 1992;9:437-57. 21. Dodge HT, Sandler H, Ballew DW, Lord JD Jr. The use of biplane angiocardiography for the measurement of left ventricular volume in man. AM HEARTJ 1960;60:762-8. 22. Mohr-Kahaly S, Erbel R, Zenker G, Drexler M, Wittlich N, Schaudig M, Bohlander M, Esser M, Meyer J. Semiquantitative grading of mitral regurgitation by color-coded Doppler echocardiogranhv. Int J Cardiol 1989;23:223-30. 23. Rossvoll 0, Hail, LK. Pulmonary venous flow velocities recorded by transthoracic Doppler ultrasound: relation to left ventricular diastolic pressures. J Am CollCardiol1993;21:168796. 24. Rajagopalan B, Friend JA, Stallard T, Lee GJ. Blood flow in pulmonary veins: I. Studies in dog and man. Cardiovasc Res 1979;13:667-76. 25. Rajagopalan B, Friend JA, Stallard T, Lee GJ. Blood flow in pulmonary veins: II. The influence of events transmitted from the right and left sides of the heart. Cardiovasc Res 1979;13:67783. 26.

27.

28.

29.

30.

31.

32.

33.

Rajagopalan B, Bertram CD, Stallard T, Lee GJ. Blood flow in pulmonary veins: III. Simultaneous measurements of their dimensions, intravascular pressure and flow. Cardiovasc Res 1979;13:684-92. Keren G, Sherez J, Megidish R, Levitt B, Laniado S. Pulmonary venous flow pattern-its relationship to cardiac dynamics: a pulsed Donnler echocardiographic - _ study. Circulation 1985;71:1105-12. - Keren G, Bier A, Sherez J, Miura D, Keefe D, LeJemtel T. Atrial contraction is an important determinant of pulmonary venous flow. J Am Co11 Cardiol 1986;7:693-5. Klein AL, Bailey AS, Cohen GI, Stewart WJ, Husbands K, Pearce GL, Salcedo EE. Effects of mitral stenosis on pulmonary venous flow as measured by Doppler transesophageal echocardiography. Am J Cardiol 1993;72:66-72. Jolly N, Arora R, Mohan J, Khalilullah M. Pulmonary venous flow dynamics before and after balloon mitral valvuloplasty as determined by transesophageal Doppler echocardiography. Am J Cardiol 1992;70:780-4. Klein AL, Stewart WJ, Bartlett J, Cohen GI, Kahan F, Pearce G, Husbands K, Bailey AS, Salcedo EE, Cosgrove DM. Effects of mitral regurgitation on pulmonary venous flow and left atria1 pressure: an intraoperative transesophageal echocardiographic study. J Am Co11 Cardiol 1992;20:1345-52. Jain S, Moos S, Awad M, Far PH, Helmcke F. Assessment of mitral regurgitation severity using pulmonary venous flow by transesophageal echocardiography [Abstract]. Circulation 1989;8O(suppl II):II-571. Schiavone WA, Calaliore PA, Currie PJ, Lytle BW. Doppler

American

34.

35.

36.

37.

38. 39.

40.

August 1994 Heart Journal

echocardiographic demonstration of pulmonary venous flow velocity in three patients with constrictive pericarditis before and after pericardiectomy. Am J Cardiol 1989;43:145-7. Bartzokis T, Lee R, Yeoh TK, Grogin H, Schnittger I. Transesophageal echo Doppler echocardiographic assessment of pulmonary venous flow patterns. J Am Sot Echocardiogr 1991;4:457-64. Masuyama T, Lee JM, Tamai M, Tanouchi J, Kitabatake A, Kamada T. Pulmonary venous flow pattern as assessed with transthoracic pulsed Doppler echocardiography in subjects without cardiac disease. Am J Cardiol 1991;67:1396-404. Caste110 R, Pearson AC, Lenzen P, Labovitz AJ. Evaluation of pulmonary venous flow by transesophageal echocardiography in subjects with a normal heart: comparison with transthoracic echocardiography. J Am Co11 Cardiol 1991;18:65-71. Tanabe K, Ooyake N, Ishibashi Y, Ohta T, Shimada T, Morioka S, Moriyama K. Influence of postural change on pulmonary venous flow pattern in heart failure [Abstract]. Circulation 1991;84(suppl II):II-164. Orihashi K, Goldiner PL, Oka Y. Intraoperative assessment of pulmonary vein flow. Echocardiography 1990;7:261-71. Akamatsu S, Terazawa E, Kagawa K, Takeda T, Arakawa M, Dohi S. Effect of PEEP on left atrial filling dynamics assessed by transesophageal pulsed Doppler echocardiography [Abstract]. Circulation 1990;82(suppl III):III-722. Arakawa M, Akamatsu S, Terazawa E, Dohi S, Miwa H, Kaeawa K. Nishieaki K. Ito Y. Hirakawa S. Ape-related increase m systolic fracvtion of pulmonary vein flow velocity-time integral from transesophageal echocardiography in subjects without cardiac disease. Am J Cardiol 1992;70:1190-4. Hausdorf G, Morf G, Berdjis, Lange PE. Age dependence of diastolic function [Abstract]. Circulation 1991;84(suppl II):III

I

7

41.

382.

Byrg RJ, Williams GA, Labovitz AJ. Effect of aging on left ventricular diastolic filline in normal subjects. Am J Cardiol 198;59:971-4. 43. Kuecherer HF, Kusumoto F, Muhiudeen IA, Cahalan MK, Schiller NB. Pulmonary venous flow patterns by transesophageal echocardiography: relation to parameters of left ventricularsvstolicanddiastolicfunction.A~H~~~~J1991: 122:168342.

93. 44.

45.

46.

47.

48.

49.

50

”

Rajacich N, Burchard KW, Hasan FM, Singh A. Central venous pressure and pulmonary capillary wedge pressure as estimates of left atria1 pressure: effects of positive end-expiratory pressure and catheter tip malposition. Crit Care Med 1989;17:7-11. Luchsinger PC, Seipp HW, Pate1 DJ. Relationship of pulmonary artery wedge pressure to left atria1 pressure in man. Circ Res 1962;11:315-8. Werko L, Varnauskas E, Eliasch H, Lagerlof H, Senning A, Thomasson B. Further evidence that the pulmonary capillary venous pressure pulse in man reflects cyclic pressure changes in the left atrium. Circ Res 1953:1:337-44. Keren G, Meisner JS, Sherez J, Yellin EL, Laniado S. Interrelationship of mid-diastolic mitral valve motion, pulmonary venous flow, and transmitral flow. Circulation 19867436-44. Hoit BD. Shao Y. Gabel M. Walsh RA. Influence of loading conditions and contractile state on pulmonary venous flow: validation of Doppler velocimetry. Circulation 1992;86:651-9. Jue J, Gin K, Pollick C. Pulmonary venous flow: relation to mitral annular motion [Abstract]. J Am Co11 Cardiol 1993; 21:41A. Pearlman JD, Triulzi MO, King ME, Abascal VM, Newell BA, Weyman AE. Left atria1 dimensions in growth and development: normal limits for two-dimensional echocardiography. J Am Co11 Cardiol 1990;16:1168-74.