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Assessment of left ventricular end-diastolic pressure by Doppler echocardiography: Contribution of duration of pulmonary venous versus mitral flow velocity curves at atrial contraction
Assessment of Left Ventricular End-Diastolic Pressure by Doppler Echocardiography: Contribution of Duration of Pulmonary Venous versus Mitral Flow Velocity Curves at Atrial Contraction Kazuhiro Yamamoto, MD, Rick A. Nishimura, MD, John C. Burnett, Jr., MD, and Margaret M. Redfield, MD, Rochester, Minnesota
The difference in the durations o f flow with atrial contraction (A duration) at the pulmonary veins and mitral valve has been reported to detect the presence o f elevated left ventricular end-diastolic pressure. It is postulated that with left ventricular filling during atrial contraction, reduced ventricular compliance results in the transmission o f increased pressure into the left atrium, resulting in prolongation o f the pulmonary venous flow with atrial contraction. However, the relationship between ventricular compliance during atrial contraction and the pulmonary venous and mitral A durations and their difference have not been carefully examined. We performed recordings o f left ventricular pressure and complete Doppler analysis o f pulmonary venous and transmitral flow in 87 patients" Operant ventricular compliance at atrial contraction was estimated by measuring the increase in ventricular pressure with atrial contraction (left ventricular a wave) and by using a compliance index, which incorporated an estimate o f flow into the ventricle with atrial contraction
from the Doppler transmitral a wave. The difference in pulmonary venous and mitral A durations correlated well with left ventricular end-diastolic pressure (r = 0.73, p < 0.01) and the pulmonary venous reversal duration exceeding the duration o f the mitral A velocity curve provided high sensitivity (82%) and specificity (92%) for the detection o f an end-diastolic pressure o f 20 m m H g or greater. The pulmonary venous A duration increased with a moderate decrease in ventricular compliance but was not increased further in patients with a severe decrease in compliance. In contrast, mitral A duration was not different in patients with moderate reduction in compliance, but was shorter in patients with severe decreases in ventricular compliance. Pulmonary venous and mitral A durations are related to ventricular compliance and they change in an opposite and progressive manner. Their difference is a sensitive method for the detection o f the elevated end-diastolic pressure associated with reduction in ventricular compliance. (J Am Soc Echocardiogr 1997;10:52-9.)
R e c e n t clinical studies ~,2 have shown that the relative difference in the durations o f flow with atrial contraction in the pulmonary veins (pulmonary venous A duration) and across the mitral valve (mitral A duration) as assessed by Doppler echocardiography correlates with left ventricular end-diastolic pressure. This concept was based on the demonstration that the left atrial pressure wave with atrial contraction
increased in magnitude and duration as left ventricular diastolic pressures increased? Investigators have concluded that the prolongation o f the left atrial pressure wave at atrial contraction may be caused by increased wave reflection from a n o n c o m p l i a n t left ventricle, causing prolongation o f p u l m o n a r y venous A d u r a t i o n ? As operant ventricular compliance becomes impaired, a rapid rate o f increase o f the ventricular pressure occurs during atrial contraction (left ventricular a wave) and the left ventricular pressure exceeds the left atrial pressure earlier than n o r m a l ? This may result in a rapid deceleration and abbreviation o f transmitral flow with atrial contraction. T h e relative changes between the p u l m o n a r y venous and mitral A durations with progressive abnormalities o f ventricular compliance have n o t been investigated. Therefore, complete D o p p l e r echocardiographic assessment and left ventricular pressure tracings were obtained in 87 patients with k n o w n or
From the Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic. Supported in part by grants from the Joseph P and Jeanne M Sullivan Foundation, Chicago, Illinois, and by the Mayo Foundation, Rochester, Minnesota. Dr. Yamamoto was supported by the Fellowship of the Uehara Memorial Foundation. Reprint requests: Margaret M. Redfield, MD, The Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First St., SW, Rochester, MN 55905. Copyright 9 1997 by the American Society of Echocardiography. 0894-7317/97 $5.00 + 0 27/1/74736 52
Journal of the AmericanSocietyof Echocardiography Volume 10 Number 1
suspected cardiac disease w h o were referred for cardiac catheterization. Pulmonary venous and mitral A durations and their differences were correlated with left ventricular diastolic pressures and estimates o f left ventricular compliance.
METHODS This p r o t o c o l was approved by the M a y o Clinic Institutional Review Board, and all patients provided written informed consent.
Study Population We studied 102 consecutive patients referred for cardiac catheterization (64 men and 38 women). The age of the patients ranged from 24 to 84 years (mean age 63 years). All patients had sinus rhythm without mitral stenosis or more than mild mitral regurgitation. Echocardiography Transthoracic echocardiographic examinations were conducted with the subjects in the left lateral position and during quiet respiration within 3 hours before the cardiac catheterization. All patients were in the fasting state, and medications were not withheld before the study. Blood pressure and heart rate were measured at the time of echocardiography. With the use of either a Hewlett-Packard (Andover, MA) or an Acuson (Mountain View, CA) echocardiographic instrument, pulsed wave Doppler transmitral flow velocity curves were recorded with the sample volume at the mitral tips. Pulmonary venous flow velocity curves were recorded with the sample volume 0 to 1 cm into the right superior pulmonary vein using the guidance of color flow Doppler imaging with the transducer placed at the cardiac apex. 1,4-6 During pulsed wave Doppler examination, the filter settings were minimized. Doppler velocity curves were recorded at a horizontal sweep speed of 100 mm/second. Cardiac Catheterization Through the femoral artery, a 7 F high-fidelity manometertipped catheter (Millar Instruments; Houston, TX) or a 6 F pigtail catheter connected with fluid-filled transducer was introduced across the aortic valve into the left ventricle just after access to the femoral artery was gained. The highfidelity left ventricular pressure was zeroed and calibrated to the fluid-filled left ventricular pressure measured by the fluid-filled lumen of the catheter before the recording. 4 Left ventricular pressure was digitized at high speed acquisition (5 ms intervals) onto an off-line computer.
Data Analysis Echocardiographic recordings were analyzed with the commercial analysis software supplied with the system. The transmitral flow velocity curve was analyzed for the mea-
Yamamoto et al.
53
surement of the mitral A duration, the time velocity integral and peak velocity of the mitral A velocity curve, and the peak velocity and the deceleration time of early transmitral filling (mitral E) velocity curve. 4 The pulmonary venous flow velocity curve was digitized for the measurement of the duration of the pulmonary venous A flow. 1,2 When the entire pulmonary A flow velocity curve was not recorded adequately, the pulmonary venous A duration was assessed with the time interval between the cessation of early diastolic flow and the start of forward systolic flow) From the left ventricular pressure tracing, we measured the left ventricular end-diastolic pressure, the increase in left ventricular pressure at atrial contraction (left ventricular a wave), and left ventricular pre-a wave pressure (left ventricular pressure before atrial contraction). To further assess operant left ventricular compliance at atrial contraction, a ratio of the time-velocity integral ofmitral A velocity curve to left ventricular a wave was calculated. 7 Averaged values of over 3 consecutive beats were used for statistical analysis. Statistical Analysis Values are expressed as mean -+ standard deviation (SD). The statistical significance of the difference among the data of groups was tested with an analysis of variance (ANOVA) and Scheffe's F test. Regression analysis was performed to compare two variables. Results were considered significant at a probability value of less than 0.05. All calculations were performed with the StatView II (Abacus Inc., Berkeley, CA) statistical program.
~S~TS
Patient Characteristics In 14 o f the 102 patients (14%), adequate Doppler recordings were n o t obtained, and in 1 patient, the systolic blood pressure had changed significantly (by m o r e than 50 m m H g ) at cardiac catheterization c o m p a r e d with the echocardiographic recording. T h u s the other 87 patients were included in this study (55 m e n and 32 w o m e n , m e a n age was 63 years). High-fidelity left ventricular pressure was recorded in 9 60 patients, and the fluid-filled left ventricular pressure was recorded in the other 27 patients. I n the 87 patients, the mean differences between systolic arterial pressures, diastolic arterial pressures, or heart rates at echocardiography and at catheterization were 4 + 20 m m H g , - 3 + 9 m m H g , and 1 ___ 6 beats per minute, respectively. O f the 87 patients, 55 patients had coronary artery disease (mean n u m b e r o f vessels with m o r e than 70% stenosis = 1.9), 2 had aortic stenosis, 5 had hypertrophic cardiomyopathy, 9 had dilated cardiomyopathy, and 16 had a chest pain syndrome with angiographically normal epicardial c o r o n a r y arteries.
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r = 0.73 p<0.01
100-
I
r = - 0 . 3 2 , p < 0.01, respectively) but the correlation was n o t as strong.
9
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Effects o f O p e r a n t V e n t r i c u l a r C o m p l i a n c e at Atrial C o n t r a c t i o n o n P t d m o n a r y V e n o u s a n d Mitral A D u r a t i o n s
50A
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~0
9
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EDP (mmHg) Figure 1 Correlation between the difference in pulmonary venous and mitral A durations (Ad)and left ventricular end-diastolic pressure (EDP)in all the subjects. The horizontal dotted line indicates that the difference in pulmonary venous and mitral A durations is equal to 0 ms, the vertical dotted line indicates that left ventricular end-diastolic pressure is equal to 20 mm Hg, and the solid line is a regression line. Relation of Pulmonary Venous and Mitral A D u r a t i o n s t o Left V e n t r i c u l a r Diastolic Pressures T h e difference in p u l m o n a r y venous and mitral A durations (pulmonary venous A duration minus mitral A duration) correlated with left ventricular end-diastolic pressure ( r = 0.73, p < 0.01, Figure l X). The difference in the durations o f 0 ms or greater predicted a left ventricular end-diastolic pressure o f 20 m m H g or greater with a sensitivity o f 82%, a specificity o f 92%, a positive predictive value o f 82%, and a negative predictive value o f 92%. T h e sensitivity o f this index for predicting a left ventricular end-diastolic pressure o f 20 m m H g or greater exceeded that o f traditional transmitral D o p p l e r parameters such as a shortened deceleration time o f the mitral E velocity curve (sensitivity o f deceleration time 150 ms or less for detecting left ventricular end-diastolic pressure 20 m m H g or greater = 33%) and an increased ratio o f peak mitral E velocity to peak mitral A velocity ( E / A ) (sensitivity o f an E / A ratio 2.0 or greater for detecting left ventricular end-diastolic pressure 20 m m H g or greater = 39%). P u l m o n a r y venous A duration and mitral A duration also correlated with left ventricular end-diastolic pressure (r = 0.58,
P u l m o n a r y venous and mitral A durations and their difference were c o m p a r e d with the magnitude o f the left ventricular a wave (Figure 2). The patients were assigned to three groups by the m a g n i t u d e o f the left ventricular a wave (group I = patients with a left ventricular a wave less than 5 m m H g ; g r o u p II = patients with a left ventricular a wave o f 5 m m H g or greater and 10 m m H g or lower; g r o u p III = patients with a left ventricular a wave o f m o r e than 10 m m H g ) . T h e p u l m o n a r y venous A duration was longer in groups I I and I I I than in g r o u p I, but there was no significant difference between groups I I and III, which indicated that the p u l m o nary venous A duration was p r o l o n g e d with a m o d erate increase in the left ventricular a wave but remaincd stable as the left ventricular a wave increased further. In contrast, mitral A duration was not different between groups I and II. H o w e v e r , the mitral A duration was shorter in g r o u p III, which indicated that mitral A duration was unchanged with a m o d e r a t e increase in the left ventricular a wave b u t was shortened with marked increases in the left ventricular a wave. As a result, the difference in the durations was the largest in group I I I and the smallest in g r o u p I. Examples o f representative patients in each o f the three groups are p r o v i d e d in Figures 3 A to C. T o further assess the effects o f operant left ventricular compliance at atrial contraction, the relationships between pulmonary venous A duration, mitral A duration, or the difference in the durations and a ratio o f the time-velocity integral o f mitral A velocity curve to left ventricular a wave were examined at three different levels o f compliance assessed in this manner (Figure 4). The group o f patients with moderate decreases in compliance (with a ratio o f greater than or equal to 1 but less than 2.6) had prolongation o f the pulmonary venous A duration but no change in mitral A duration when compared with the group with the highest ventricular compliance (the ratio more than 2.5). Compared with the group with moderate decreases in ventricular compliance, pulmonary venous A duration was not increased further but mitral A duration was decreased in the group with severe reductions in ventricular compliance (the ratio less than 1.0). The difference in pulmonary venous and mitral A durations increased progressively, with
Journal of the American Society of Echocardiography Volume 10 Number 1
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decreasing compliance being significantly greater in each group. Effects o f P r e l o a d f o r Atrial C o n t r a c t i o n o n P u l m o n a r y V e n o u s a n d Mitral A D u r a t i o n s
55
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Pulmonary venous and mitral A durations and their difference were compared with left ventricular pre-a wave pressure (Figure 5). These three indices were not significantly different between the patients with left ventricular pre-a wave pressure o f less than 10 m m H g and from 10 to 15 m m H g . Only in patients with markedly elevated pre-a wave pressure (pre-a wave pressure greater than 15 m m H g ) , was the difference in the durations prolonged, with prolongation o f pulmonary venous A duration and shortening of mitral A duration. The left ventricular a wave was significantly increased only in the patients with markedly elevated pre-a wave pressure as compared with the other patient groups.
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DISCUSSION In the current study, the difference in pulmonary venous and mitral A durations correlated with left ventricular end-diastolic pressure and the increase in left ventricular pressure at atrial contraction (left ventricular a wave). This index was sensitive and specific for the detection o f elevated left ventricular enddiastolic pressure in patients in w h o m a transthoracic approach (84%) was possible. The pulmonary venous A duration was prolonged, with moderate decreases in compliance, but did not increase further in the presence o f severe decreases in ventricular compliance as estimated by pressure and combined pressure and flow measurements. In contrast, the mitral A duration was unchanged in the presence o f moderate decreases in ventricular compliance but decreased in the presence o f severely reduced compliance. The findings o f the current study confirm previous studies that examined the accuracy and feasibility o f transthoracic evaluation o f the transmitral and pulmonary venous flow velocity curves to assess ventricular diastolic pressures. These data extend the previous findings by offering insight into the mechanisms whereby the degree o f difference in pulmonary venous and mitral A durations corresponds with increasing left ventricular end-diastolic pressure. Rossvoll and Hatle 1 showed that the mitral A duration was decreased in patients with the highest left ventricular pre-a wave pressure, but did not show progressive increases in the pulmonary venous A duration with increasing pre-a wave pressure. When analyzed according to different levels o f compliance as estimated
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Figure 2 Bar charts show the mean (+ SD) of pulmonary venous A duration, mitral A duration, or the difference in the durations (Ad) in patients with an increase in left ventricular pressure at atrial contraction (left ventricular a wave, LVa) o f < 5 mm Hg (group I), from 5 to 10 mm Hg (group II) and >10 mm Hg (group III). * * p < 0 . 0 1 versus Lva <5 mm Hg; t p < 0 . 0 5 ; tl'P < 0.01 versus LVa from 5 to 10 mm Hg.
56
Journal of the American Society of Echocardiography January-February 1997
Yamamoto et al.
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0 Recordings of left ventricular pressure (left), pulmonary venous flow velocity curve (right upper) and transmitral flow velocity curve (rightlower) in three patients (panel A = group I, panel B = group II, panel C = group III). In A, left ventricular end-diastolic pressure (EDP) is not elevated with left ventricular a wave (LVa) o f < 5 mm Hg. In this case, pulmonary venous Figure 3
A duration was shorter than mitral A duration. In B, left ventricular end diastolic pressure is elevated with the prolongation of pulmonary venous A duration. In C, left ventricular enddiastolic pressure is more elevated; however, pulmonary venous A duration is not longer and mitral A duration is shorter than in B. The left ventricular a wave was 6 mm Hg in B and 15 mm Hg in C. The left ventricular pressure recording of panel C shows a simultaneous recording of high-fidelity and fluid-filled left ventricular pressure tracings and demonstrates that there is no significant difference in determining left ventricular diastolic pressures between these recordings. (A, mitral A velocity curve; D, diastolic pulmonary venous velocity curve; E, mitral E velocity curve; ECG, electrocardiogram; Pre-a, left ventricular pre-a wave pressure; pulmonary venousA, pulmonary venous A velocity curve; S, systolic pulmonary venous velocity curve.) by the left ventricular a wave, the previous study demonstrated that the p u l m o n a r y venous A duration increased progressively with an increasing left ventricular a wave but did n o t observe a significant decrease in the mitral A duration in such patients. In the current study with a larger n u m b e r o f patients and more varied cardiac diseases, changes in determinants o f the difference in p u l m o n a r y venous and mitral A durations were examined and insight was gained into the mechanism whereby this index provides a better correlation with left ventricular end-
diastolic pressure. As both c o m p o n e n t s that determine the difference in the durations change in an opposite and progressive but nonsimultaneous manner, the magnitude o f difference is linearly accentuated as ventricular compliance decreases and ventricular end-diastolic pressure increases. The nonlinear correlation o f pulmonary venous and mitral A durations to indices o f ventricular compliance and their weaker correlation with left ventricular end-diastolic pressure demonstrate that either index alone is a p o o r substitute for their difference and that both should be
Journal o f the American Society o f Echocardiography Volume 10 N u m b e r 1
measured when attempting to assess left ventricular end-diastolic pressure. The current findings are consistent with hemodynamic measurements demonstrating prolongation o f the left atrial a wave as the ventricular compliance decreases and ventricular diastolic pressures increase. 3 Although the previous study did not measure the period in which the left atrial pressure exceeded the left ventricular pressure, it appeared that this period, the determinant ofmitral A duration, was decreased in the presence o f marked increases in left ventricular pressure with atrial contraction. Left ventricular pre-a wave pressure can be used to estimate the preload for left atrial contraction, much as the mean left atrial and pulmonary capillary wedge pressures are used. 8,9 In the current study, a mild or moderate elevation o f the left ventricular pre-a wave pressure was not associated with prolongation o f the difference in pulmonary venous and mitral A durations and the difference in the durations was prolonged only in patients with markedly increased pre-a wave pressure. These results are compatible with the previously obtained results) The current study further extends these findings by demonstrating that only the patient group with markedly increased left ventricular pre-a wave pressure and the prolonged difference in the durations had a large left ventricular a wave. The left ventricular a wave was not increased in the other patient groups, even with moderate elevation o f the pre-a wave pressure (Figure 5). These findings suggest that left ventricular compliance or left ventricular late diastolic pressure plays an important role in determining the difference in the durations rather than exclusively the level o f preload for atrial contraction or mean left atrial pressure. Whereas ventricular compliance affects the left atrial pressure wave form at atrial contraction, atrial compliance and atrial systolic function also affect the atrial pressure wave form and the duration o f transmitral and pulmonary venous flow with atrial contraction. Changes in these factors may contribute to the pattern o f changes seen with the largest decreases in ventricular compliance where pulmonary venous A duration does not increase further despite decreases in ventricular compliance.
Study Limitations In this study, the left vemadcular volume was not measured, and thus left ventricular compliance could not bc calculated dirccfly. As described abovc, left ventricular a wave is affected by both lcft ventricular compliance and left ventricular filling volume at atrial contraction. Thcrcfore, we calculated a ratio of the time-velocity
Y a m a m o t o et al.
57
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Figure 4 Bar charts show that mean (+SD) of pulmonary venous A duration, mitral A duration, or the difference in the durations (Ad) in patients with the ratio of the time-velocity integral of mitral A velocity curve to left ventricular a wave (TVI-A/LVa) of>2.5 (with the highest left ventricular compliance), from 1 to 2.5 (with moderately decreased left ventricular compliance) and <1.0 c m / m m Hg (with severely decreased left ventricular compliance). *p < 0.05 and **p < 0.01 versus TVI-A/LVa >2.5 c m / m m Hg; t t P < 0.01 versus TVI-A/LVa of 1-2.5 c m / m m Hg.
58
Journal of the American Society of Echocardiography January February 1997
Y a m a m o t o e t al.
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Figure 5 Bar charts show that mean (_+SD) of pulmonary venous A duration, mitral A duration, the difference in the durations (Ad), or left ventricular a wave (LVa) in patients with left ventricular (LV) pre-a wave pressure of <10, from 10 to 15, and >15 mm Hg. **p < 0.01 versus LV pre-a wave pressure < 1 0 mm Hg; t~fp < 0.01 versus LV pre-a wave pressure of 10~15 mm Hg. integral o f mitral A vclocity curve to left ventricular a wave to minimize the effects o f various filling volumes a m o n g patients. Because this ratio is n o t equal to left ventricular compliance, we assessed the relation between D o p p l e r indices and left ventricular compliance qualitatively. In addition, the results were similar even if either left ventricular a wave or this ratio was used as an index o f operant compliance. Thus although the direct determination ofventricular volumes to determine operant compliance w o u l d m o r e firmly establish o u r con-
clusions, the use o f the left ventricular a wave and this ratio provides a reasonable estimate o f operant compliance. Left ventricular pressure was r e c o r d e d with either high-fidelity m a n o m e t e r - t i p p e d catheters o r fluidfilled catheters. W e c o n f i r m e d , however, that such a m e t h o d o l o g i c difference p r o d u c e d o n l y small differences in m e a s u r e d left ventricular diastolic pressure w h e n the left ventricular pressure was m e a s u r e d by a high-fidelity m a n o m e t e r - t i p p e d c a t h e t e r as c o m -
Journal of the AmericanSocietyof Echocardiography Volume 10 Number 1
p a r e d w i t h fluid-filled left ventricular pressure tracings (Figure 3C). D o p p l e r e c h o c a r d i o g r a p h y was n o t r e c o r d e d sim u l t a n e o u s l y w i t h left ventricular pressure. H o w ever, we c o n f i r m e d t h a t systolic a n d diastolic arterial pressures a n d the h e a r t rate d i d n o t significantly c h a n g e at c a t h e t e r i z a t i o n c o m p a r e d w i t h e c h o c a r d i o graphic r e c o r d i n g in t h e 87 patients w h o s e d a t a w e r e used for analysis. T h e s e patients were u n d e r g o i n g elective o u t p a t i e n t a n g i o g r a p h y a n d n o n e h a d unstable o r rest angina o r e x p e r i e n c e d a n g i n a attack b e f o r e o r d u r i n g t h e p r o c e d u r e o n the e x a m i n a t i o n day. W e c o n f i r m e d t h a t n o n e h a d clinically significant arrhythmias, such as f r e q u e n t atrial o r ventricular p r e m a t u r e c o n t r a c t i o n s , at e c h o c a r d i o g r a p h i c r e c o r d i n g a n d catheterization. F u r t h e r m o r e , t h e left ventricular pressure was r e c o r d e d as the first p r o c e d u r e before c o r o n a r y a n g i o g r a p h y a n d left v e n t r i c u l o g r a p h y . I n a d d i t i o n , w e r e c o r d e d p u l s e d wave D o p p l e r transmitral flow velocity curves at c a t h e t e r i z a t i o n in 20 patients. T h e absolute value o f the difference in p e a k mitral A velocity was 5.7 c m / s (SD = 5.2 c m / s ) , a n d the a b s o l u t e value o f t h e difference in mitral A d u r a t i o n was 6.3 ms ( S D = 4.2 ms). T h u s , n o n s i m u l t a n e o u s m e a s u r e m e n t s h o u l d n o t significantly affect o u r conclusions.
Conclusions T h e difference in p u l m o n a r y v e n o u s a n d mitral A d u r a t i o n s as assessed b y transthoracic p u l s e d wave D o p p l e r e c h o c a r d i o g r a p h y correlates w i t h left ventricular e n d - d i a s t o l i c pressure. T h e d e t e r m i n a n t s o f this n e w i n d e x are closely related t o the o p e r a n t left ventricular c o m p l i a n c e at atrial c o n t r a c t i o n . A p r o l o n g a t i o n o f the difference in the d u r a t i o n s w i t h an increase in left ventricular end-diastolic pressure is caused by a p r o l o n g a t i o n o f p u l m o n a r y v e n o u s A d u r a t i o n w i t h m o d e r a t e decreases in o p e r a n t left ventricular c o m p l i a n c e a n d by a s h o r t e n i n g o f mitral
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A d u r a t i o n w i t h severe decreases in o p e r a n t compliance. These indices change in an o p p o s i t e a n d p r o gressive b u t n o n s i m u l t a n e o u s m a n n e r as ventricular c o m p l i a n c e decreases, a n d their difference correlates closely with increases in left ventricular end-diastolic pressure.
REFERENCES 1. Rossvoll O, Hatle LK. Pulmonary venous flow velocities recorded by transthoracic Doppler ultrasound: relation to left vcntricular diastolic pressures. J Am Coil Cardiol 1993;21: 1687-96. 2. Appleton CP, Galloway JM, Gonzalez MS, Gaballa M, Basnight MA. Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease. Additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction. J Am Coil Cardiol 1993;22:1972-82. 3. Matsuda Y, Toma Y, Matsuzaki M, et al. Change of left atrial systolic pressure waveform in relation to left ventricular enddiastolic pressure. Circulation 1990;82:1659-67. 4. Nishimura RA, Schwartz RS, Holmes DR, Jr, Tajik A]. Failure of calcium channel blockers to improve ventricular relaxation in humans. J Am Coil Cardiol 1993;21:182-8. 5. Masuyama T, Lee JM, Nagano R, et al. Doppler echocardiographic pulmonary venous flow-velocity pattern for assessment of the hemodynamic profile in acute congestive heart failure. Am Heart J 1995;129:107-13. 6. Yamamoto K, Masuyama T, Tanouchi J, et al. Intraventricular dispersion of early diastolic filling: a new marker of left ventricular diastolic dysfunction. Am Heart J 1995;129:291-9. 7. Bristow JD, Van Zee BE, Judkins MP. Systolic and diastolic abnormalities of the left ventricle in coronary artery disease: studies in patients with little or no enlargement ofventricular volume. Circulation 1970;42:219-28. 8. Braunwald E, Brockenbrough EC, Frahm CJ, Ross J. Left atrial and left ventricular pressures in subjects without cardiovascular disease. Circulation 1961;24:267-9. 9. Rahimtoola SH, Ehsani A, Sinno MZ, Loeb HS, Rosen KM, Gunnar RM. Left atrial transport function in myocardial infarction: importance of its booster pump function. Am J Med 1975;59:686-94.
The difference in the durations o f flow with atrial contraction (A duration) at the pulmonary veins and mitral valve has been reported to detect the presence o f elevated left ventricular end-diastolic pressure. It is postulated that with left ventricular filling during atrial contraction, reduced ventricular compliance results in the transmission o f increased pressure into the left atrium, resulting in prolongation o f the pulmonary venous flow with atrial contraction. However, the relationship between ventricular compliance during atrial contraction and the pulmonary venous and mitral A durations and their difference have not been carefully examined. We performed recordings o f left ventricular pressure and complete Doppler analysis o f pulmonary venous and transmitral flow in 87 patients" Operant ventricular compliance at atrial contraction was estimated by measuring the increase in ventricular pressure with atrial contraction (left ventricular a wave) and by using a compliance index, which incorporated an estimate o f flow into the ventricle with atrial contraction
from the Doppler transmitral a wave. The difference in pulmonary venous and mitral A durations correlated well with left ventricular end-diastolic pressure (r = 0.73, p < 0.01) and the pulmonary venous reversal duration exceeding the duration o f the mitral A velocity curve provided high sensitivity (82%) and specificity (92%) for the detection o f an end-diastolic pressure o f 20 m m H g or greater. The pulmonary venous A duration increased with a moderate decrease in ventricular compliance but was not increased further in patients with a severe decrease in compliance. In contrast, mitral A duration was not different in patients with moderate reduction in compliance, but was shorter in patients with severe decreases in ventricular compliance. Pulmonary venous and mitral A durations are related to ventricular compliance and they change in an opposite and progressive manner. Their difference is a sensitive method for the detection o f the elevated end-diastolic pressure associated with reduction in ventricular compliance. (J Am Soc Echocardiogr 1997;10:52-9.)
R e c e n t clinical studies ~,2 have shown that the relative difference in the durations o f flow with atrial contraction in the pulmonary veins (pulmonary venous A duration) and across the mitral valve (mitral A duration) as assessed by Doppler echocardiography correlates with left ventricular end-diastolic pressure. This concept was based on the demonstration that the left atrial pressure wave with atrial contraction
increased in magnitude and duration as left ventricular diastolic pressures increased? Investigators have concluded that the prolongation o f the left atrial pressure wave at atrial contraction may be caused by increased wave reflection from a n o n c o m p l i a n t left ventricle, causing prolongation o f p u l m o n a r y venous A d u r a t i o n ? As operant ventricular compliance becomes impaired, a rapid rate o f increase o f the ventricular pressure occurs during atrial contraction (left ventricular a wave) and the left ventricular pressure exceeds the left atrial pressure earlier than n o r m a l ? This may result in a rapid deceleration and abbreviation o f transmitral flow with atrial contraction. T h e relative changes between the p u l m o n a r y venous and mitral A durations with progressive abnormalities o f ventricular compliance have n o t been investigated. Therefore, complete D o p p l e r echocardiographic assessment and left ventricular pressure tracings were obtained in 87 patients with k n o w n or
From the Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic. Supported in part by grants from the Joseph P and Jeanne M Sullivan Foundation, Chicago, Illinois, and by the Mayo Foundation, Rochester, Minnesota. Dr. Yamamoto was supported by the Fellowship of the Uehara Memorial Foundation. Reprint requests: Margaret M. Redfield, MD, The Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First St., SW, Rochester, MN 55905. Copyright 9 1997 by the American Society of Echocardiography. 0894-7317/97 $5.00 + 0 27/1/74736 52
Journal of the AmericanSocietyof Echocardiography Volume 10 Number 1
suspected cardiac disease w h o were referred for cardiac catheterization. Pulmonary venous and mitral A durations and their differences were correlated with left ventricular diastolic pressures and estimates o f left ventricular compliance.
METHODS This p r o t o c o l was approved by the M a y o Clinic Institutional Review Board, and all patients provided written informed consent.
Study Population We studied 102 consecutive patients referred for cardiac catheterization (64 men and 38 women). The age of the patients ranged from 24 to 84 years (mean age 63 years). All patients had sinus rhythm without mitral stenosis or more than mild mitral regurgitation. Echocardiography Transthoracic echocardiographic examinations were conducted with the subjects in the left lateral position and during quiet respiration within 3 hours before the cardiac catheterization. All patients were in the fasting state, and medications were not withheld before the study. Blood pressure and heart rate were measured at the time of echocardiography. With the use of either a Hewlett-Packard (Andover, MA) or an Acuson (Mountain View, CA) echocardiographic instrument, pulsed wave Doppler transmitral flow velocity curves were recorded with the sample volume at the mitral tips. Pulmonary venous flow velocity curves were recorded with the sample volume 0 to 1 cm into the right superior pulmonary vein using the guidance of color flow Doppler imaging with the transducer placed at the cardiac apex. 1,4-6 During pulsed wave Doppler examination, the filter settings were minimized. Doppler velocity curves were recorded at a horizontal sweep speed of 100 mm/second. Cardiac Catheterization Through the femoral artery, a 7 F high-fidelity manometertipped catheter (Millar Instruments; Houston, TX) or a 6 F pigtail catheter connected with fluid-filled transducer was introduced across the aortic valve into the left ventricle just after access to the femoral artery was gained. The highfidelity left ventricular pressure was zeroed and calibrated to the fluid-filled left ventricular pressure measured by the fluid-filled lumen of the catheter before the recording. 4 Left ventricular pressure was digitized at high speed acquisition (5 ms intervals) onto an off-line computer.
Data Analysis Echocardiographic recordings were analyzed with the commercial analysis software supplied with the system. The transmitral flow velocity curve was analyzed for the mea-
Yamamoto et al.
53
surement of the mitral A duration, the time velocity integral and peak velocity of the mitral A velocity curve, and the peak velocity and the deceleration time of early transmitral filling (mitral E) velocity curve. 4 The pulmonary venous flow velocity curve was digitized for the measurement of the duration of the pulmonary venous A flow. 1,2 When the entire pulmonary A flow velocity curve was not recorded adequately, the pulmonary venous A duration was assessed with the time interval between the cessation of early diastolic flow and the start of forward systolic flow) From the left ventricular pressure tracing, we measured the left ventricular end-diastolic pressure, the increase in left ventricular pressure at atrial contraction (left ventricular a wave), and left ventricular pre-a wave pressure (left ventricular pressure before atrial contraction). To further assess operant left ventricular compliance at atrial contraction, a ratio of the time-velocity integral ofmitral A velocity curve to left ventricular a wave was calculated. 7 Averaged values of over 3 consecutive beats were used for statistical analysis. Statistical Analysis Values are expressed as mean -+ standard deviation (SD). The statistical significance of the difference among the data of groups was tested with an analysis of variance (ANOVA) and Scheffe's F test. Regression analysis was performed to compare two variables. Results were considered significant at a probability value of less than 0.05. All calculations were performed with the StatView II (Abacus Inc., Berkeley, CA) statistical program.
~S~TS
Patient Characteristics In 14 o f the 102 patients (14%), adequate Doppler recordings were n o t obtained, and in 1 patient, the systolic blood pressure had changed significantly (by m o r e than 50 m m H g ) at cardiac catheterization c o m p a r e d with the echocardiographic recording. T h u s the other 87 patients were included in this study (55 m e n and 32 w o m e n , m e a n age was 63 years). High-fidelity left ventricular pressure was recorded in 9 60 patients, and the fluid-filled left ventricular pressure was recorded in the other 27 patients. I n the 87 patients, the mean differences between systolic arterial pressures, diastolic arterial pressures, or heart rates at echocardiography and at catheterization were 4 + 20 m m H g , - 3 + 9 m m H g , and 1 ___ 6 beats per minute, respectively. O f the 87 patients, 55 patients had coronary artery disease (mean n u m b e r o f vessels with m o r e than 70% stenosis = 1.9), 2 had aortic stenosis, 5 had hypertrophic cardiomyopathy, 9 had dilated cardiomyopathy, and 16 had a chest pain syndrome with angiographically normal epicardial c o r o n a r y arteries.
54
Journal of the American Society of Echocardiography January-February 1997
Y a m a m o t o et al.
r = 0.73 p<0.01
100-
I
r = - 0 . 3 2 , p < 0.01, respectively) but the correlation was n o t as strong.
9
I
Effects o f O p e r a n t V e n t r i c u l a r C o m p l i a n c e at Atrial C o n t r a c t i o n o n P t d m o n a r y V e n o u s a n d Mitral A D u r a t i o n s
50A
E
~0
9
-50-
-100
9
ab
I
2b
3b
EDP (mmHg) Figure 1 Correlation between the difference in pulmonary venous and mitral A durations (Ad)and left ventricular end-diastolic pressure (EDP)in all the subjects. The horizontal dotted line indicates that the difference in pulmonary venous and mitral A durations is equal to 0 ms, the vertical dotted line indicates that left ventricular end-diastolic pressure is equal to 20 mm Hg, and the solid line is a regression line. Relation of Pulmonary Venous and Mitral A D u r a t i o n s t o Left V e n t r i c u l a r Diastolic Pressures T h e difference in p u l m o n a r y venous and mitral A durations (pulmonary venous A duration minus mitral A duration) correlated with left ventricular end-diastolic pressure ( r = 0.73, p < 0.01, Figure l X). The difference in the durations o f 0 ms or greater predicted a left ventricular end-diastolic pressure o f 20 m m H g or greater with a sensitivity o f 82%, a specificity o f 92%, a positive predictive value o f 82%, and a negative predictive value o f 92%. T h e sensitivity o f this index for predicting a left ventricular end-diastolic pressure o f 20 m m H g or greater exceeded that o f traditional transmitral D o p p l e r parameters such as a shortened deceleration time o f the mitral E velocity curve (sensitivity o f deceleration time 150 ms or less for detecting left ventricular end-diastolic pressure 20 m m H g or greater = 33%) and an increased ratio o f peak mitral E velocity to peak mitral A velocity ( E / A ) (sensitivity o f an E / A ratio 2.0 or greater for detecting left ventricular end-diastolic pressure 20 m m H g or greater = 39%). P u l m o n a r y venous A duration and mitral A duration also correlated with left ventricular end-diastolic pressure (r = 0.58,
P u l m o n a r y venous and mitral A durations and their difference were c o m p a r e d with the magnitude o f the left ventricular a wave (Figure 2). The patients were assigned to three groups by the m a g n i t u d e o f the left ventricular a wave (group I = patients with a left ventricular a wave less than 5 m m H g ; g r o u p II = patients with a left ventricular a wave o f 5 m m H g or greater and 10 m m H g or lower; g r o u p III = patients with a left ventricular a wave o f m o r e than 10 m m H g ) . T h e p u l m o n a r y venous A duration was longer in groups I I and I I I than in g r o u p I, but there was no significant difference between groups I I and III, which indicated that the p u l m o nary venous A duration was p r o l o n g e d with a m o d erate increase in the left ventricular a wave but remaincd stable as the left ventricular a wave increased further. In contrast, mitral A duration was not different between groups I and II. H o w e v e r , the mitral A duration was shorter in g r o u p III, which indicated that mitral A duration was unchanged with a m o d e r a t e increase in the left ventricular a wave b u t was shortened with marked increases in the left ventricular a wave. As a result, the difference in the durations was the largest in group I I I and the smallest in g r o u p I. Examples o f representative patients in each o f the three groups are p r o v i d e d in Figures 3 A to C. T o further assess the effects o f operant left ventricular compliance at atrial contraction, the relationships between pulmonary venous A duration, mitral A duration, or the difference in the durations and a ratio o f the time-velocity integral o f mitral A velocity curve to left ventricular a wave were examined at three different levels o f compliance assessed in this manner (Figure 4). The group o f patients with moderate decreases in compliance (with a ratio o f greater than or equal to 1 but less than 2.6) had prolongation o f the pulmonary venous A duration but no change in mitral A duration when compared with the group with the highest ventricular compliance (the ratio more than 2.5). Compared with the group with moderate decreases in ventricular compliance, pulmonary venous A duration was not increased further but mitral A duration was decreased in the group with severe reductions in ventricular compliance (the ratio less than 1.0). The difference in pulmonary venous and mitral A durations increased progressively, with
Journal of the American Society of Echocardiography Volume 10 Number 1
Y a m a m o t o et al.
decreasing compliance being significantly greater in each group. Effects o f P r e l o a d f o r Atrial C o n t r a c t i o n o n P u l m o n a r y V e n o u s a n d Mitral A D u r a t i o n s
55
E
v
.o "ID
Pulmonary venous and mitral A durations and their difference were compared with left ventricular pre-a wave pressure (Figure 5). These three indices were not significantly different between the patients with left ventricular pre-a wave pressure o f less than 10 m m H g and from 10 to 15 m m H g . Only in patients with markedly elevated pre-a wave pressure (pre-a wave pressure greater than 15 m m H g ) , was the difference in the durations prolonged, with prolongation o f pulmonary venous A duration and shortening of mitral A duration. The left ventricular a wave was significantly increased only in the patients with markedly elevated pre-a wave pressure as compared with the other patient groups.
W
0 e-
C O 1
E
D.
<5 5-10 >10 (group I) (group II) (group III) LVa (mmHg)
E e-
DISCUSSION In the current study, the difference in pulmonary venous and mitral A durations correlated with left ventricular end-diastolic pressure and the increase in left ventricular pressure at atrial contraction (left ventricular a wave). This index was sensitive and specific for the detection o f elevated left ventricular enddiastolic pressure in patients in w h o m a transthoracic approach (84%) was possible. The pulmonary venous A duration was prolonged, with moderate decreases in compliance, but did not increase further in the presence o f severe decreases in ventricular compliance as estimated by pressure and combined pressure and flow measurements. In contrast, the mitral A duration was unchanged in the presence o f moderate decreases in ventricular compliance but decreased in the presence o f severely reduced compliance. The findings o f the current study confirm previous studies that examined the accuracy and feasibility o f transthoracic evaluation o f the transmitral and pulmonary venous flow velocity curves to assess ventricular diastolic pressures. These data extend the previous findings by offering insight into the mechanisms whereby the degree o f difference in pulmonary venous and mitral A durations corresponds with increasing left ventricular end-diastolic pressure. Rossvoll and Hatle 1 showed that the mitral A duration was decreased in patients with the highest left ventricular pre-a wave pressure, but did not show progressive increases in the pulmonary venous A duration with increasing pre-a wave pressure. When analyzed according to different levels o f compliance as estimated
.o "ID m
m
<5 5-10 >10 (group I) (group II) (group III) l.Va (mmHg)
E
01
I,~f
fY'l
i <5 (groupl)
5-10 >10 (groupll) (group III) LVa (mmHg)
Figure 2 Bar charts show the mean (+ SD) of pulmonary venous A duration, mitral A duration, or the difference in the durations (Ad) in patients with an increase in left ventricular pressure at atrial contraction (left ventricular a wave, LVa) o f < 5 mm Hg (group I), from 5 to 10 mm Hg (group II) and >10 mm Hg (group III). * * p < 0 . 0 1 versus Lva <5 mm Hg; t p < 0 . 0 5 ; tl'P < 0.01 versus LVa from 5 to 10 mm Hg.
56
Journal of the American Society of Echocardiography January-February 1997
Yamamoto et al.
.
~
.
.
,
,
+
.
.
.
.
.
.
.
.
.
+
.
.
.
.
,
.
.
.
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oL B
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0 Recordings of left ventricular pressure (left), pulmonary venous flow velocity curve (right upper) and transmitral flow velocity curve (rightlower) in three patients (panel A = group I, panel B = group II, panel C = group III). In A, left ventricular end-diastolic pressure (EDP) is not elevated with left ventricular a wave (LVa) o f < 5 mm Hg. In this case, pulmonary venous Figure 3
A duration was shorter than mitral A duration. In B, left ventricular end diastolic pressure is elevated with the prolongation of pulmonary venous A duration. In C, left ventricular enddiastolic pressure is more elevated; however, pulmonary venous A duration is not longer and mitral A duration is shorter than in B. The left ventricular a wave was 6 mm Hg in B and 15 mm Hg in C. The left ventricular pressure recording of panel C shows a simultaneous recording of high-fidelity and fluid-filled left ventricular pressure tracings and demonstrates that there is no significant difference in determining left ventricular diastolic pressures between these recordings. (A, mitral A velocity curve; D, diastolic pulmonary venous velocity curve; E, mitral E velocity curve; ECG, electrocardiogram; Pre-a, left ventricular pre-a wave pressure; pulmonary venousA, pulmonary venous A velocity curve; S, systolic pulmonary venous velocity curve.) by the left ventricular a wave, the previous study demonstrated that the p u l m o n a r y venous A duration increased progressively with an increasing left ventricular a wave but did n o t observe a significant decrease in the mitral A duration in such patients. In the current study with a larger n u m b e r o f patients and more varied cardiac diseases, changes in determinants o f the difference in p u l m o n a r y venous and mitral A durations were examined and insight was gained into the mechanism whereby this index provides a better correlation with left ventricular end-
diastolic pressure. As both c o m p o n e n t s that determine the difference in the durations change in an opposite and progressive but nonsimultaneous manner, the magnitude o f difference is linearly accentuated as ventricular compliance decreases and ventricular end-diastolic pressure increases. The nonlinear correlation o f pulmonary venous and mitral A durations to indices o f ventricular compliance and their weaker correlation with left ventricular end-diastolic pressure demonstrate that either index alone is a p o o r substitute for their difference and that both should be
Journal o f the American Society o f Echocardiography Volume 10 N u m b e r 1
measured when attempting to assess left ventricular end-diastolic pressure. The current findings are consistent with hemodynamic measurements demonstrating prolongation o f the left atrial a wave as the ventricular compliance decreases and ventricular diastolic pressures increase. 3 Although the previous study did not measure the period in which the left atrial pressure exceeded the left ventricular pressure, it appeared that this period, the determinant ofmitral A duration, was decreased in the presence o f marked increases in left ventricular pressure with atrial contraction. Left ventricular pre-a wave pressure can be used to estimate the preload for left atrial contraction, much as the mean left atrial and pulmonary capillary wedge pressures are used. 8,9 In the current study, a mild or moderate elevation o f the left ventricular pre-a wave pressure was not associated with prolongation o f the difference in pulmonary venous and mitral A durations and the difference in the durations was prolonged only in patients with markedly increased pre-a wave pressure. These results are compatible with the previously obtained results) The current study further extends these findings by demonstrating that only the patient group with markedly increased left ventricular pre-a wave pressure and the prolonged difference in the durations had a large left ventricular a wave. The left ventricular a wave was not increased in the other patient groups, even with moderate elevation o f the pre-a wave pressure (Figure 5). These findings suggest that left ventricular compliance or left ventricular late diastolic pressure plays an important role in determining the difference in the durations rather than exclusively the level o f preload for atrial contraction or mean left atrial pressure. Whereas ventricular compliance affects the left atrial pressure wave form at atrial contraction, atrial compliance and atrial systolic function also affect the atrial pressure wave form and the duration o f transmitral and pulmonary venous flow with atrial contraction. Changes in these factors may contribute to the pattern o f changes seen with the largest decreases in ventricular compliance where pulmonary venous A duration does not increase further despite decreases in ventricular compliance.
Study Limitations In this study, the left vemadcular volume was not measured, and thus left ventricular compliance could not bc calculated dirccfly. As described abovc, left ventricular a wave is affected by both lcft ventricular compliance and left ventricular filling volume at atrial contraction. Thcrcfore, we calculated a ratio of the time-velocity
Y a m a m o t o et al.
57
~" 200
E
tO om
150-
T
qD
lOO0 e.-
Q,) >
E" 5oC 0
E " O,.
0
>2.5 -2.5 <1.0 TVI-A/LVa (cm/mmHg)
200
150.O m
100"ID
,< m
50-
>2.5 1-2.5 <1.0 "FVI-A/LVa (cm/mmHg)
5025E
0-
qD <1
-25 -50>2.5 1-2.5 <1.0 "FVI-A]LVa (cm/mmHg)
Figure 4 Bar charts show that mean (+SD) of pulmonary venous A duration, mitral A duration, or the difference in the durations (Ad) in patients with the ratio of the time-velocity integral of mitral A velocity curve to left ventricular a wave (TVI-A/LVa) of>2.5 (with the highest left ventricular compliance), from 1 to 2.5 (with moderately decreased left ventricular compliance) and <1.0 c m / m m Hg (with severely decreased left ventricular compliance). *p < 0.05 and **p < 0.01 versus TVI-A/LVa >2.5 c m / m m Hg; t t P < 0.01 versus TVI-A/LVa of 1-2.5 c m / m m Hg.
58
Journal of the American Society of Echocardiography January February 1997
Y a m a m o t o e t al.
""r 200 E
200
(-
A
o
,m 4-1
E 150
150-
L_
'ID < (n
o
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,
T I,.
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o to >
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100
'1o <
50
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I
m to
mE a.
0
0 <10 10-15 >15 LV pre-a wave pressure (mmHg)
<10 10-15 >15 LV pre-a wave pressure (mmHg)
lttt
tt A
o)
A
"I-
E --,0
E E "-'5
"o
-25
--I.
<10 10-15 >15 LV pre-a wave pressure (mmHg)
<10 10-15 >15 LV pre-a wave pressure (mmHg)
Figure 5 Bar charts show that mean (_+SD) of pulmonary venous A duration, mitral A duration, the difference in the durations (Ad), or left ventricular a wave (LVa) in patients with left ventricular (LV) pre-a wave pressure of <10, from 10 to 15, and >15 mm Hg. **p < 0.01 versus LV pre-a wave pressure < 1 0 mm Hg; t~fp < 0.01 versus LV pre-a wave pressure of 10~15 mm Hg. integral o f mitral A vclocity curve to left ventricular a wave to minimize the effects o f various filling volumes a m o n g patients. Because this ratio is n o t equal to left ventricular compliance, we assessed the relation between D o p p l e r indices and left ventricular compliance qualitatively. In addition, the results were similar even if either left ventricular a wave or this ratio was used as an index o f operant compliance. Thus although the direct determination ofventricular volumes to determine operant compliance w o u l d m o r e firmly establish o u r con-
clusions, the use o f the left ventricular a wave and this ratio provides a reasonable estimate o f operant compliance. Left ventricular pressure was r e c o r d e d with either high-fidelity m a n o m e t e r - t i p p e d catheters o r fluidfilled catheters. W e c o n f i r m e d , however, that such a m e t h o d o l o g i c difference p r o d u c e d o n l y small differences in m e a s u r e d left ventricular diastolic pressure w h e n the left ventricular pressure was m e a s u r e d by a high-fidelity m a n o m e t e r - t i p p e d c a t h e t e r as c o m -
Journal of the AmericanSocietyof Echocardiography Volume 10 Number 1
p a r e d w i t h fluid-filled left ventricular pressure tracings (Figure 3C). D o p p l e r e c h o c a r d i o g r a p h y was n o t r e c o r d e d sim u l t a n e o u s l y w i t h left ventricular pressure. H o w ever, we c o n f i r m e d t h a t systolic a n d diastolic arterial pressures a n d the h e a r t rate d i d n o t significantly c h a n g e at c a t h e t e r i z a t i o n c o m p a r e d w i t h e c h o c a r d i o graphic r e c o r d i n g in t h e 87 patients w h o s e d a t a w e r e used for analysis. T h e s e patients were u n d e r g o i n g elective o u t p a t i e n t a n g i o g r a p h y a n d n o n e h a d unstable o r rest angina o r e x p e r i e n c e d a n g i n a attack b e f o r e o r d u r i n g t h e p r o c e d u r e o n the e x a m i n a t i o n day. W e c o n f i r m e d t h a t n o n e h a d clinically significant arrhythmias, such as f r e q u e n t atrial o r ventricular p r e m a t u r e c o n t r a c t i o n s , at e c h o c a r d i o g r a p h i c r e c o r d i n g a n d catheterization. F u r t h e r m o r e , t h e left ventricular pressure was r e c o r d e d as the first p r o c e d u r e before c o r o n a r y a n g i o g r a p h y a n d left v e n t r i c u l o g r a p h y . I n a d d i t i o n , w e r e c o r d e d p u l s e d wave D o p p l e r transmitral flow velocity curves at c a t h e t e r i z a t i o n in 20 patients. T h e absolute value o f the difference in p e a k mitral A velocity was 5.7 c m / s (SD = 5.2 c m / s ) , a n d the a b s o l u t e value o f t h e difference in mitral A d u r a t i o n was 6.3 ms ( S D = 4.2 ms). T h u s , n o n s i m u l t a n e o u s m e a s u r e m e n t s h o u l d n o t significantly affect o u r conclusions.
Conclusions T h e difference in p u l m o n a r y v e n o u s a n d mitral A d u r a t i o n s as assessed b y transthoracic p u l s e d wave D o p p l e r e c h o c a r d i o g r a p h y correlates w i t h left ventricular e n d - d i a s t o l i c pressure. T h e d e t e r m i n a n t s o f this n e w i n d e x are closely related t o the o p e r a n t left ventricular c o m p l i a n c e at atrial c o n t r a c t i o n . A p r o l o n g a t i o n o f the difference in the d u r a t i o n s w i t h an increase in left ventricular end-diastolic pressure is caused by a p r o l o n g a t i o n o f p u l m o n a r y v e n o u s A d u r a t i o n w i t h m o d e r a t e decreases in o p e r a n t left ventricular c o m p l i a n c e a n d by a s h o r t e n i n g o f mitral
Yamamoto et al.
59
A d u r a t i o n w i t h severe decreases in o p e r a n t compliance. These indices change in an o p p o s i t e a n d p r o gressive b u t n o n s i m u l t a n e o u s m a n n e r as ventricular c o m p l i a n c e decreases, a n d their difference correlates closely with increases in left ventricular end-diastolic pressure.
REFERENCES 1. Rossvoll O, Hatle LK. Pulmonary venous flow velocities recorded by transthoracic Doppler ultrasound: relation to left vcntricular diastolic pressures. J Am Coil Cardiol 1993;21: 1687-96. 2. Appleton CP, Galloway JM, Gonzalez MS, Gaballa M, Basnight MA. Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease. Additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction. J Am Coil Cardiol 1993;22:1972-82. 3. Matsuda Y, Toma Y, Matsuzaki M, et al. Change of left atrial systolic pressure waveform in relation to left ventricular enddiastolic pressure. Circulation 1990;82:1659-67. 4. Nishimura RA, Schwartz RS, Holmes DR, Jr, Tajik A]. Failure of calcium channel blockers to improve ventricular relaxation in humans. J Am Coil Cardiol 1993;21:182-8. 5. Masuyama T, Lee JM, Nagano R, et al. Doppler echocardiographic pulmonary venous flow-velocity pattern for assessment of the hemodynamic profile in acute congestive heart failure. Am Heart J 1995;129:107-13. 6. Yamamoto K, Masuyama T, Tanouchi J, et al. Intraventricular dispersion of early diastolic filling: a new marker of left ventricular diastolic dysfunction. Am Heart J 1995;129:291-9. 7. Bristow JD, Van Zee BE, Judkins MP. Systolic and diastolic abnormalities of the left ventricle in coronary artery disease: studies in patients with little or no enlargement ofventricular volume. Circulation 1970;42:219-28. 8. Braunwald E, Brockenbrough EC, Frahm CJ, Ross J. Left atrial and left ventricular pressures in subjects without cardiovascular disease. Circulation 1961;24:267-9. 9. Rahimtoola SH, Ehsani A, Sinno MZ, Loeb HS, Rosen KM, Gunnar RM. Left atrial transport function in myocardial infarction: importance of its booster pump function. Am J Med 1975;59:686-94.