(Circulation. 1996;94:2138-2145.)
© 1996 American Heart Association, Inc.
Articles |
Assessment of Left Ventricular Filling Pressures by Doppler in the Presence of Atrial Fibrillation
the Department of Medicine, Section of Cardiology, Baylor College of Medicine, and The Methodist Hospital, Houston, Tex.
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Abstract |
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Background Although Doppler echocardiography can be used to estimate left ventricular filling pressures (LVFPs) in patients in sinus rhythm, its utility in atrial fibrillation is unknown.
Methods and Results An initial training population of 30 patients (17 men, 13 women; mean age, 69±9 years; range, 48 to 87 years) was studied. Measurements of LVFP were obtained simultaneously with pulsed Doppler recordings of mitral and pulmonary venous flow velocities and color M-mode recording of the flow propagation velocity of the mitral inflow. Measurements were averaged over 10 cardiac cycles. In addition, left atrial volume was derived from the apical four-chamber view. Significant relations were observed between LVFP and several parameters derived from the transmitral and pulmonary venous velocity and left atrial volume. The best relations were observed with the peak acceleration (PkAcc) of the mitral velocity (r=.84), isovolumic relaxation time (IVRT) (r=-.76), mean early (E) velocity (r=.6), and the ratio of peak E velocity to color M-mode flow propagation velocity (r=.65). The best model obtained by multilinear regression analysis (r=.88) included PkAcc and IVRT. The equation 
was tested in 30 additional patients (12 women and 18 men; mean age, 65±10.6 years; range, 43 to 87 years) with similar results (r=.87). When all 60 patients were combined, the mean±1SD difference between predicted and observed pressure was -0.88±3.6 mm Hg.
Conclusions LVFPs can be estimated with Doppler echocardiography in patients with atrial fibrillation.
Key Words: fibrillation • echocardiography • pressure • ventricles • diastole
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Introduction |
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In recent years, much has been learned about the relation of the transmitral and pulmonary vein velocities to left atrial and LV diastolic pressures.1 2 3 4 This knowledge has allowed the application of measurements derived from these velocities to the noninvasive estimation of LVFPs.5 6 7 8 These methods have been used exclusively in cardiac patients in sinus rhythm and have not been applied to atrial fibrillation for several reasons.
With atrial fibrillation, the A wave is absent from both mitral and pulmonary flow velocities, and therefore, one cannot apply the ratio of early filling to late filling velocity (E/A ratio), atrial filling fraction, or the pulmonary retrograde A velocity in the estimation of filling pressures. The systolic filling fraction in the pulmonary vein velocity is often reduced irrespective of the mean atrial pressure.9 In addition, patients with atrial fibrillation commonly have dilated atria, and hence the use of left atrial dimensions or volumes may not allow for good discrimination between elevated and normal pressures. Finally, the cycle variation in flow velocities, characteristic of atrial fibrillation, creates a real challenge in determining which cycles and how many of them should be measured. With the increasing age of our patient population, atrial fibrillation is nevertheless a common finding among patients referred to an echocardiography laboratory, and therefore, a Doppler method of estimating filling pressures in these patients will have important clinical utility.
The objective of this investigation, therefore, was to perform a detailed evaluation of the transmitral and pulmonary vein velocities, combined with measurements of left atrial volume in patients with atrial fibrillation, in an attempt to derive a noninvasive method of estimating filling pressures.
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Methods |
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The study was conducted at The Methodist Hospital, Houston, Tex, between January and June 1995. The protocol was approved by the Institutional Review Board of Baylor College of Medicine and The Methodist Hospital, and all patients gave informed consent. Patients with mitral stenosis, prosthetic mitral valves, and moderate or severe mitral regurgitation were excluded, as were those with cardiac tamponade and pericardial constriction. An initial training group of 30 consecutive patients (17 men and 13 women; mean age, 69±9 years; range, 48 to 87 years) provided the data needed for the development of the method. The group consisted of 22 patients in intensive care units, 3 patients in the cardiac catheterization laboratory, and 5 patients studied in the operating room before undergoing cardiovascular surgery. Twenty-two patients (73%) were on mechanical ventilation. The diagnoses of these patients are listed in Table 1
. LV ejection fraction for the group was determined echocardiographically10 and ranged from 20% to 75% (mean, 48±17%).
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Echocardiographic and Doppler Studies
Studies were performed with the patient in the supine position with the use of an HP-Sonos 1000 echocardiographic instrument (Hewlett Packard) equipped with 2.5- and 3.5-MHz transducers. Two-dimensional images were obtained in the standard parasternal and apical views. All Doppler and M-mode recordings were obtained at a sweep speed of 100 mm/s. A pulsed Doppler sample volume was placed at the tips of the mitral valve and the transmitral velocity recorded during 10 to 15 cardiac cycles. The Doppler cursor was then positioned between the mitral valve and the LV outflow, and a continuous wave Doppler recording was obtained to allow measurement of the IVRT.5 6 7 Flow within the right pulmonary vein was identified with the aid of color Doppler, and the sample volume was placed 1 cm into the vein to record the pulmonary venous velocity. Using color Doppler, we positioned the M-mode cursor within the mitral inflow stream, and an M-mode recording was obtained of the propagation of the early mitral inflow velocity into the left ventricle.11 Baseline shift was performed as needed to obtain a distinct color border of the propagation velocity that extended well into the distal third of the LV cavity (Fig 1).
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Echocardiographic Analysis
All measurements were made on an off-line analysis station (Digisonics EC 500) equipped with quantitative Doppler software. Ten cardiac cycles were selected for measurements, and the results were averaged. Selected cycles were not necessarily consecutive but were chosen on the basis of the quality of the Doppler recording, a cycle length equivalent to a heart rate ranging between 60 and 100 bpm, and an interval 
70 ms between the end of mitral flow and the onset of the QRS interval. The following parameters were derived from the transmitral velocity: peak early (E) velocity (cm/s), mean velocity (cm/s), time velocity integral (cm), PkAcc of the E velocity (cm/s2), ratio of acceleration time to diastolic filling period, mean acceleration derived as E velocity divided by acceleration time, and deceleration time (ms). PkAcc was derived by the computer after the transmitral velocity was traced. The computer algorithm used divided the time from the onset of mitral flow to peak velocity into 20 equal intervals, measured the change in velocity per unit of time in each interval, and reported the highest value as PkAcc. IVRT (ms) was measured from the end of the aortic flow to the onset of mitral inflow by use of continuous wave Doppler. The following variables were measured from the pulmonary venous flow velocity: peak systolic velocity and its velocity time integral, peak diastolic velocity and its velocity time integral, and the ratios of peak systolic to peak diastolic velocity and of systolic to diastolic velocity time integral. The slope of a line tangential to the linear component of the color border produced by the early propagation of the transmitral velocity into the left ventricle, as recorded by color M-mode, was measured (in centimeters per second) and used as an index of flow propagation velocity (Fig 1
).11 A dimensionless ratio of E velocity by pulsed Doppler to propagation velocity by color M-mode was calculated.
Left atrial volumes were measured in the apical four-chamber view by use of the method of multiple discs.12 The maximal left atrial volume (mL) was obtained before mitral valve opening and the minimal volume before valve closure. Left atrial emptying fraction was derived as the difference between volumes divided by the maximal volume. Volume measurements were averaged over three to five cycles.
Pressure Measurements
Pressures and echocardiographic/Doppler recordings were made simultaneously. All pressures were measured with the use of fluid-filled catheters and Medex transducers. LVFP consisted of the mean pulmonary artery balloon-occlusion pressure measured with the use of Swan-Ganz catheters in 27 patients and LV end-diastolic pressure measured in the catheterization laboratory in 3 patients. We verified occlusive pressure by comparing the pressure tracing waveforms to the waveforms observed in the pulmonary artery position and by looking for the expected rise in oxygen saturation. The pressures reported represented an average of 10 cardiac cycles. In the patients on mechanical ventilation, cycles were selected at end expiration.
Assessment of Beat-to-Beat Variability
The hypothesis was raised that in atrial fibrillation, the beat-to-beat variability in transmitral velocity is greater when the mean left atrial pressure is normal and less when the pressure is elevated. To test this hypothesis, the coefficient of variation, ie, the ratio of SD to mean, was calculated for each of the parameters derived from the transmitral velocity and compared between patients with LVFP below and above 15 mm Hg.
Test Population
The equation derived to estimate filling pressures was tested prospectively in 30 consecutive patients (12 women and 18 men; mean age, 65±10.6 years; range, 43 to 87 years). As in the training group, Doppler and pressure data were obtained simultaneously. The test population included 17 patients in intensive care units, 7 in the cardiac catheterization laboratory, and 6 studied before cardiovascular surgery; 19 patients (63%) were on mechanical ventilation. Criteria for exclusion were the same as in the training group. The diagnoses of the patients are listed in Table 1. The LV ejection fraction for the group averaged 45±15.5% (range, 20% to 75%). Mean pulmonary artery balloon-occlusion pressures were used in the 30 patients as a measurement of LVFP. All of the Doppler measurements and calculations were made without knowledge of the hemodynamic data.
Statistical Analysis
Comparison of data between the two groups divided according to the LVFP was performed by use of a two-tailed, unpaired Student's t test. Linear regression analysis was used to compare Doppler variables to LVFP. Stepwise multilinear regression analysis was used to develop an equation for the estimation of LVFP. Significance was established at P<.05.
Reproducibility
Seven studies were chosen at random for analysis of mitral inflow profile and derivation of LVFP. The studies were analyzed by a second observer and by the first observer at a later date. Reproducibility was assessed as the mean±1SD difference between the two sets of observations. In addition, mean percent error was calculated as the absolute difference divided by the average of the two observations.
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Results |
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Relation of Variables to LVFP
The hemodynamic data for the training and test population are listed in Table 2
. Although the mean heart rates listed for the two populations are near 100 bpm, the cycles chosen for Doppler measurements in all patients corresponded to a heart rate of 86±14 bpm. Several echocardiographic Doppler parameters were significantly related to LVFP in the training population (Table 3). Of all the mitral inflow variables, the best correlation with LVFP was observed with PkAcc (r=.84) (Fig 2A), followed by the IVRT (r=-.76) (Fig 2B) and mean velocity (r=.6). Weaker relations were observed with deceleration time (r=-.42); E velocity, alone (r=.42) or corrected for the velocity time integral (r=.45); and mean acceleration rate (r=.5). Interestingly, the relation between deceleration time and LVFP depended on the level of systolic performance. In patients with depressed ejection fractions (<45%), a good relation was observed between deceleration time and LVFP (r=-.78; P<.0001), whereas in the subgroup with preserved systolic function, no relation was found (Fig 3). This analysis was performed with data from the two patient populations (n=60) to increase the sample size.
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, patients with ejection fractions (EF) <45%; 
, patients with ejection fractions Four patients did not have adequate pulmonary venous recordings for analysis. In the remaining 26 patients, peak diastolic velocity and the ratio of peak systolic velocity to peak diastolic velocity had the best correlation with LVFP (r=.50 for both). Weaker relations were observed when the velocity time integrals were used. Systolic velocity and its time integral did not relate at all to LVFP.
Five patients did not have adequate color M-mode recordings for analysis. No significant relation was found between the flow propagation velocity and LVFP in the remaining 25 patients. However, the ratio of E velocity to flow propagation velocity was significantly related to LVFP (r=.65).
Of the measurements of atrial volumes, only the minimal atrial volume correlated significantly with LVFP (r=.55). Correction for body surface area did not improve any of the correlations.
Variability of Mitral Inflow Variables With Cycle Length
The coefficient of variation was higher for several mitral inflow parameters in patients with lower LVFPs (
15 mm Hg) than in those with higher pressures (Table 4). Variability in cycle length was similar in the two groups. To optimize sample size, this analysis was performed with data from the two populations of patients (n=60). These findings confirmed the hypothesis that variations in transmitral velocity with cycle length changes are less in the presence of higher filling pressures.
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Multiple Linear Regression Analysis
All of the parameters that were significantly related to LVFP in the training population were included in a stepwise multiple linear regression analysis. The best model obtained for the estimation of LVFP included PkAcc and IVRT. The inclusion of other variables did not improve the estimation of LVFP. The derived equation correlated with measured LVFP with a value of r=.88 (r2=.77) and an SEE of 3.6 mm Hg (Fig 4A).
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Test Population
The equation derived from multiple linear regression analysis in the initial group was tested in the test population. The Doppler analysis was performed without knowledge of the filling pressures. Estimation of LVFP was possible with a value of r=.87 (r2=.757) and an SEE of 4 mm Hg (Fig 4B). When all 60 patients were combined, the equation predicted LVFP with a value of r=.88 (Fig 5A). The mean difference between predicted and measured pressures was -0.88 mm Hg, and the 95% confidence limits (2 SD) were ±7 mm Hg (Fig 5B). The sensitivity and specificity for LVFP >15 mm Hg were 98% and 82%, respectively; accuracy was 93%.
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No differences were observed in the accuracy of estimating LVFP between patients with mechanical ventilators (r=.86; n=41) and those without (r=.91; n=19).
Simplification of Method for Clinical Use
The results shown above were obtained by use of the average of 10 heartbeats. In an attempt to reduce measurement and analysis time, two simpler versions of the method were tested in the 60 patients. One version consisted of averaging 3 nonconsecutive beats with cycle lengths representing a heart rate within 10% to 20% of the average heart rate. In the second version, one cardiac cycle with an RR interval equivalent to a heart rate of 70 to 80 bpm was used. When the average of three cardiac cycles was used, the correlation coefficient between Doppler and catheter LVFP dropped modestly to .82 and the 95% confidence limits increased to ±9 mm Hg, with a mean difference between predicted and measured pressure of 1.9 mm Hg. The correlation coefficient dropped further when only one cardiac cycle was used (r=.74), and the 95% confidence limits increased to ±11 mm Hg, with a mean difference between predicted and measured pressures of 0.2 mm Hg.
Accurate recognition of high filling pressures can be very useful in everyday clinical practice. Accordingly, the sensitivity of several Doppler parameters for detecting an increased LVFP >15 mm Hg was determined in all 60 patients. These consisted of PkAcc, IVRT, deceleration time, and the ratio of E velocity to propagation velocity. Using receiver operating characteristic curves, we selected cutoff values for each parameter to keep specificity at 88%. Table 5 lists the sensitivity and specificity of these parameters with the average of 3 cardiac cycles and 1 representative cycle as described above (averaging 10 cycles gave similar results). For all patients combined, PkAcc, IVRT, and the ratio of E velocity to propagation velocity had comparable sensitivities that were higher than deceleration time. However, in the subgroup of 20 patients with depressed ejection fraction (<45%), deceleration time had comparable sensitivity to the other parameters (76% for 3 cycles; 71% for 1 cycle), with a specificity of 100%. Detecting one or more abnormal values in any given patient improved the sensitivity of the method to 91% and 95% with 3 cycles and 1 cycle, respectively; specificity fell to 71% and 65%, respectively. Many commercially available systems are currently not programmed to measure PkAcc. Combining the other parameters without PkAcc resulted in a slight reduction in sensitivity to 88%, with a specificity of 76%, regardless of the number of cycles used.
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Reproducibility
The interobserver and intraobserver reproducibilities for the parameters listed in Table 5 are reported in Table 6. Considerable variability was observed for individual measurements, with a mean percent error ranging from 6% to 24% between observers and 5% to 22% for the same observer. The parameters with greater variability were PkAcc, flow propagation velocity, and consequently, the ratio of E velocity to propagation velocity. Although in terms of percent error, the variability of estimated LVFP was similar to that of the individual measurements, in terms of absolute values, the variability ranged from 0 to 6 mm Hg between observers and from 0 to 4 mm Hg for the same observer.
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Discussion |
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This investigation has demonstrated that despite the absence of atrial contraction and the increased variability of measurements, the interactions of the transmitral velocity with left atrial pressure in atrial fibrillation are analogous to those observed in sinus rhythm. Consequently, one can combine measurements derived from the transmitral velocity to estimate LVFPs in patients with a variety of cardiovascular disorders and a wide range of ejection fractions even when such patients are ventilated mechanically.
Relation of Transmitral Flow and IVRT to Filling Pressures
The relations observed in this study between parameters derived from the transmitral velocity and LVFP are similar to previous studies in animals4 13 and in patients in sinus rhythm.14 The multifactorial influence of LV relaxation, filling pressures, and net atrioventricular compliance on transmitral flow probably accounts for the weak relations observed with many of the parameters tested. On the other hand, PkAcc rate related very well with LVFP. This finding was not surprising given the direct relationship between acceleration and pressure predicted by Newton's second law. Thomas and Weyman15 demonstrated in a mathematical model of LV filling that PkAcc is greatly affected by changes in left atrial pressure compared with peak velocity, peak deceleration, and the total integral of the inflow velocity. Interestingly, the value for PkAcc predicted by the computer model at a left atrial pressure of 20 mm Hg (2400 cm/s2) was nearly identical to the value that related to a filling pressure of 20 mm Hg in the training population (2333 cm/s2; Fig 2A).
Despite the theoretical observations by Thomas and Weyman,15 PkAcc has not been used clinically before the present investigation. There are two possible reasons for this: one is that most of the commercially available on-line and off-line quantitation systems do not include a program for PkAcc, and the other relates to the concern that this index may be less reproducible than other Doppler parameters of diastolic function. However, when put to the test, we found that PkAcc was only slightly less reproducible than the other parameters measured. The impact of this variability in the estimation of LVFP in absolute values was minimal, with a range of 0 to 6 mm Hg. Although clinical studies are lacking, it is likely that PkAcc will also relate well to LVFP in cardiac patients in the presence of sinus rhythm.
Compared with PkAcc, mean acceleration did not relate as well to LVFP. One possible explanation is that PkAcc occurs at a certain moment in time that relates directly to the transmitral pressure gradient and left atrial pressure. On the other hand, mean acceleration incorporates all of the acceleration throughout the rise in velocity, including lower values that occur during the later phase when the transmitral pressure gradient is lower.
IVRT has become an important noninvasive index of diastolic function that can be measured in the majority of patients with the aid of continuous wave Doppler. IVRT has been shown to relate directly to the time constant of relaxation and end-systolic pressure and inversely to left atrial pressure.16 The strong relation between IVRT and LVFP observed in the present study is similar to earlier findings from our laboratory and others in patients in sinus rhythm.1 5 6 7 Importantly, multilinear regression analysis included IVRT in the model for prediction of LVFP, which was similar to our previous observations in sinus rhythm.
Several investigations4 13 17 demonstrated the dependence of the E velocity on LV relaxation and left atrial pressure in both the experimental animal and the clinical setting. Consequently, a high E velocity can be a reflection of normal relaxation with low filling pressures or a manifestation of elevated left atrial pressure in patients with impaired relaxation (the so-called pseudo-normal pattern). The velocity of propagation of the early mitral inflow from LV base to apex, determined with the use of color M-mode, has been demonstrated to be a noninvasive index of LV relaxation.11 18 Very recent observations from our laboratory and also by Ares et al19 and by Takatsuji and associates18 have shown that in sinus rhythm, the flow propagation velocity remains abnormally depressed in patients with impaired relaxation and a pseudo-normal mitral velocity pattern due to high filling pressures.18 19 20 Both Ares et al19 and our group demonstrated in addition that the ratio of E velocity to flow propagation velocity (or its reciprocal) related significantly to LVFP.19 20 Our observations in patients in atrial fibrillation are similar and suggest that the flow propagation velocity may be used to correct for the influence of relaxation on the E velocity regardless of the presence or absence of atrial contraction.
Deceleration time is affected primarily by the net atrioventricular compliance and mitral valve area.21 Therefore, it is not surprising to see a weaker relation between this parameter and LVFP, a finding that we previously observed in patients with sinus rhythm.5 Furthermore, deceleration time seems to also be influenced by systolic performance, as was observed in the present investigation. Deceleration time related well to filling pressures in patients with depressed systolic performance and did not relate at all in the group with normal function. Giannuzzi and associates22 found a good correlation between deceleration time and LVFP in patients with myocardial infarction, sinus rhythm, and poor ventricular function, whereas Symanski et al23 observed a poor relation between this parameter and LVFP in patients with hypertrophic cardiomyopathy and normal systolic function. Furthermore, Himura and associates24 evaluated the relation between deceleration time and measurements of LV stiffness in patients with different degrees of LV dysfunction. In the group with dilated cardiomyopathy, deceleration time related well to stiffness parameters. In contrast, no relation was observed in patients with diastolic dysfunction secondary to hypertrophy or ischemic heart disease and with preserved systolic function. Also of interest is the observation that in patients with dilated or infiltrative cardiomyopathy, short deceleration times have been associated with worse clinical outcomes.25 26 It is fair, therefore, to conclude that in ventricles with depressed function, a short deceleration time is an index of restrictive filling that is almost always associated with high filling pressures. The weak relation between deceleration time and LVFP found in this and previous studies results from the inclusion of patients with normal and depressed ejection fractions.
Pulmonary Venous Flow Velocity and Left Atrial Volumes
Forward systolic flow in the pulmonary veins is dependent in part on atrial relaxation. Consequently, forward systolic venous flow is reduced in atrial fibrillation regardless of the atrial pressure. This is true for both the left and right atria9 27 and explains the lack of correlation between peak systolic velocity and mean LVFP observed in the present study. A better relation was observed between peak diastolic velocity and LVFP, with a correlation coefficient in the same range as that observed with the E velocity. This finding is not surprising, because previous studies have shown a good relation between these two Doppler parameters.3 The frequent occurrence of left atrial enlargement in atrial fibrillation probably explains the weak relations found in the present study between left atrial volumes and LVFP. The best correlation observed was with minimal left atrial volume, a finding previously noted by Appleton et al6 in the presence of sinus rhythm. None of the relations observed between pulmonary vein velocities or left atrial size were of sufficient magnitude to be of clinical use in estimating filling pressures.
Cycle-to-Cycle Variation in Transmitral Velocity
LV filling dynamics are dependent on the length of diastole, particularly when relaxation is impaired. Accordingly, with a shorter cycle length, ventricular filling depends more on a higher driving pressure that increases the transmitral velocity. The opposite occurs with a longer cycle length. However, if left atrial pressure is constantly elevated, the transmitral velocity will tend to be high throughout the variations in cycle length. This hypothesis was explored with the use of the coefficient of variation of parameters derived from the transmitral velocity. Patients with higher LVFP (>15 mm Hg) demonstrated less variability in acceleration, velocity, and deceleration time than those with lower pressures. One is unlikely to measure the coefficient of variation of Doppler parameters in clinical practice. However, this concept may have clinical application as a qualitative observation. For instance, the absence of a noticeable variation in E velocity in a patient with atrial fibrillation can raise the suspicion of an increased LVFP and make one look more closely for other more sensitive and specific findings such as increased PkAcc or shortened IVRT.
Study Limitations
Mean pulmonary occlusive pressure, rather than LV end-diastolic pressure, was measured in 57 of the 60 patients. Rahimtoola et al28 measured mean pulmonary wedge pressure with Swan-Ganz catheters using the balloon occlusion technique and compared them to LV diastolic pressures in 54 patients with acute myocardial infarction. All patients were in sinus rhythm. The authors noted the similarity between mean wedge pressure and LV diastolic pre–A-wave pressure with a correlation coefficient of .90 and a regression line along the identity line. On the other hand, LV end-diastolic pressure was consistently higher than mean wedge pressure. Identical findings were reported recently by Appleton et al.6 Therefore, in the absence of atrial contraction and/or severe mitral regurgitation, it is unlikely that significant differences will be observed between mean pulmonary occlusive pressure and LV end-diastolic pressure. Furthermore, mean pulmonary occlusive pressure is an index of mean left atrial pressure and is therefore clinically important as a determinant of pulmonary congestion.
The patient population was overall an elderly group, with the younger individuals having significant cardiac disease. Thus, our findings cannot be extrapolated to younger, healthy patients with lone atrial fibrillation. Fortunately, such patients are usually recognized by the absence of clinical signs of heart disease or hypertension and echocardiographic evidence of normal LV size and function.29 It is conceivable that the ratio of E velocity to propagation velocity could be useful in this unique subgroup because it may correct for the influence of relaxation on the transmitral velocity. This could be a subject of future investigations.
Two thirds of the patients were on mechanical ventilation, reflecting the severity of their illnesses and the clinical need for invasive monitoring. Although data are lacking in atrial fibrillation, studies of patients in sinus rhythm and on mechanical ventilation have demonstrated no significant changes in transmitral velocity even with the use of positive end-expiratory pressure up to 20 cm of H2O.30 Furthermore, measurement of pulmonary occlusive pressure in patients on mechanical ventilation has been shown to be accurate when taken at end expiration.31 Importantly, when data obtained from the 60 patients in the present study were combined, the accuracy of the estimation of LVFP was not altered by mechanical ventilation.
Although the estimation of LVFP correlated well with measured LVFP, the 95% limits of agreement (±7 mm Hg) were wider than those we observed previously with sinus rhythm (±5 mm Hg),7 reflecting the complexity of atrial fibrillation and the increased variability of the Doppler measurements. In addition, the 95% limits of agreement as well as specificity for detection of normal filling pressures could have been affected by the unequal distribution of patients with normal and high LVFPs (17 and 43 patients, respectively). However, these limits of agreement are still clinically useful, particularly at the higher ranges of LVFP. One must remember that there is also variability in catheter measurements of LVFP even in the presence of sinus rhythm. Reyes and associates32 evaluated the intraobserver variability in measurements of pulmonary capillary wedge pressures in patients with mitral stenosis; they found the 95% confidence limits to be between 2.4 and 4.8 mm Hg. One might expect these limits to increase in the presence of atrial fibrillation.
Clinical Implications
The inclusion in this study of patients with a wide range of cardiac conditions allows for the methodology to be used by physicians caring for these types of patients. For greater accuracy, measurements from 10 cardiac cycles should be averaged. However, one can use a single cycle with a longer RR interval simply to detect the presence of elevated filling pressures. Although measurement of PkAcc is not currently available in most echocardiography systems, inclusion of this parameter in future upgrades should not be a difficult task. In the absence of measurement of PkAcc, the combination of IVRT with deceleration time and the ratio of E velocity to propagation velocity can be used with minimal loss of sensitivity. Deceleration time by itself is quite useful in the subset of patients with depressed LV function.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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The excellent assistance of Almanubia Cespedes in the preparation of the manuscript is gratefully acknowledged.
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Footnotes |
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Reprint requests to Miguel A. Quinones, MD, Professor of Medicine, Director, Echocardiography Laboratory, Baylor College of Medicine, The Methodist Hospital, Section of Cardiology, 6550 Fannin, SM-677, Houston, TX 77030. E-mail guelq@bcm.tmc.edu.
Guest editor for this article was Dr Richard Popp, Stanford (Calif) University Medical Center.
Presented in part at the 68th Scientific Sessions of the American Heart Association, Anaheim, Calif, November 13-16, 1995, and published in abstract form (Circulation. 1995;92(suppl I):I-397).
Received February 1, 1996; revision received April 30, 1996; accepted May 10, 1996.
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References |
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