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Changes in transmitral and pulmonary venous flow velocity patterns after cardioversion of atrial fibrillation
Changes in transmitral and pulmonary venous flow velocity patterns after cardioversion of atrial fibrillation Arata Iuchi, MD, Takashi Old, MD, Nobuo Fukuda, MD, Tomotsugu Tabata, MD, Kazuyo Manabe, MD, Yoshimi Kageji, MD, Miwa Sasaki, MD, Minori Hama, MD, Hirotsugu Yamada, MD, and Susumu Ito, MD Tokushima, Japan To examine the recovery time of left atrial mechanical function after electrical cardioversion of atrial fibrillation, we recorded transmitral flow, pulmonary venous flow velocities, and interatrial septal motion during atrial systole within 24 hours (16 ± 5 hours) and 10 days after cardioversion in 25 patients with atrial fibrillation, including 6 patients with hypertension, 4 with ischemic heart disease, 2 with alcoholic heart disease, 5 with dilated cardiomyopathy, and 8 with no evidence of underlying heart disease. With the exception of the five patients with dilated cardiomyopathy, the peak atrial systolic transmitral and pulmonary venous flow velocities, peak first systolic velocity of pulmonary venous flow, duration of both atrial systolic waves, and amplitude of the interatrial septal motion during atrial systole decreased markedly within 24 hours after cardioversion and increased 10 days after cardioversion. These results suggest that active atrial systolic and relaxant variables obtained from transmitral and pulmonary venous flow velocities may reflect left atrial mechanical function after cardioversion of atrial fibrillation. (AM HEART J 1996;131:270-5.)
Assessment of left atrial systolic function immediately after cardioversion of atrial fibrillation (AF) has been performed by using transmitral flow velocity patterns with pulsed Doppler echocardiography and other modalities. 1-6 However, evaluation of left atrial mechanical function from this flow velocity only has been limited because blood in the left atrium is ejected into both the pulmonary veins and left ventricle through the mitral valve during atrial systole. The availability of transesophageal echocardiography in recent years has made it possible to obtain hemodynamic measurements between the left atrium and ventricle by examining the transmitral and pulmonary venous flow velocities; this From the Second Department of Internal Medicine, Tokushima University School of Medicine, Tokushima. Received for publication Jan. 23, 1995; accepted June 12, 1995. Reprint requests: Takashi Oki, MD, Second Department of Internal Medicine, Tokushima University School of Medicine, 2-50 Kuramoto-cho, Tokushima 770, Japan. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4/1167898
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approach has been d e m o n s t r a t e d to be more sensitive t h a n transthoracic echocardiography for evaluating the left atrial active systolic and diastolic function. 7-14 In this study, we recorded these flow velocity patterns by using transthoracic and transesophageal pulsed Doppler techniques and evaluated the relations of the different variables from these flow velocities and left atrial function after cardioversion of AF. METHODS Study population. Twenty-five patients (22 men and
3 women, mean age 55-+ 17 years) who successfully underwent electrical cardioversion of AF participated in this study. The patient population consisted of six patients with hypertension, four with ischemic heart disease, two with alcoholic heart disease, five with dilated cardiomyopathy, and eight with no underlying heart disease. The mean time interval from the onset of AF to successful cardioversion was 32 days (range 3 to 168 days). Disopyramide (300 mg/day) was administered to all patients beginning immediately after cardioversion and given until 10 days after the procedure. Of the six patients with dilated cardiomyopathy, one had recurrence of AF 7 days after cardioversion and was excluded from the study. Echocardiography. All patients underwent transthoracic and transesophageal pulsed Doppler echocardiography and M-mode echocardiography 24 hours before, 24 hours after (mean 16 ± 5 hours), and 10 days after cardioversion of AF. Cardioversion consisted of administering between 150 and 200 J of energy to each patient. Measurements of transmitral flow velocity and left atrial dimension at end systole were obtained by using the transthoracic approach. Pulmonary venous flow velocity and interatrial septal motion were assessed by transesophageal echocardiography by using a horizontal view that included both atria. Transmitral flow velocity was recorded after the sample volume was measured at the tip of mitral valve leaflets on long-axis view of the left ventricle, and a clear diastolic biphasic waveform was obtained. The peak atrial systolic (A), peak early diastolic (E) velocities, their ratio (A/E), and the duration of the atrial systolic wave (A-d) were measured from transmitral flow velocity (Fig. 1). Pulmonary
2
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Iuchi et al. 271
TMF
PVF
A-d
IAS
PVS2
,
LA
Pvs :, ~G
~
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PVA-d Fig. 1. Measurements of variables from transmitral and pulmonary venous flow velocities and interatrial
septal motion. TMF, Transmitral flow velocity pattern by transthoracic pulsed Doppler echocardiography; PVF, pulmonary venous flow velocity pattern by transesophageal pulsed Doppler echocardiography; IAS, interatrial septal motion obtained by transesophageal M-mode echocardiography; ECG, electrocardiogram;
PCG, phonocardiogram.
venous flow velocity was recorded by measuring the sample volume within 1 to 2 cm of the junction of the pulmonary vein with the left atrium after sections of the left atrium, including the left superior pulmonary vein, were visualized and the pulmonary venous inflow to the left atrium was confirmed by color Doppler imaging. The peak first systolic (PVSz), peak second systolic (PVS2), peak early diastolic (PVD), peak atrial systolic (PVA), and duration of the atrial systolic wave (PVA-d) were measured from pulmonary venous flow velocity (Fig. 1). Furthermore, the amplitude of interatrial septal motion during atrial systole (IASA) was measured from an M-mode interatrial septal echogram (Fig. 1). The changes in A, PVA, and PVS1 after cardioversion were calculated as differences between values obtained 10 days after cardioversion and within 24 hours after cardioversion. The rate of change regarding each variable was obtained by dividing the calculated difference by the value of the corresponding variable obtained 10 days after cardioversion. M-mode and pulsed Doppler echocardiograms were recorded with a 5 MHz transesophageal transducer (Aloka SSD 870, Aloka CO. Ltd., Tokyo, Japan) and a 2.5 MHz transthoracic transducer (Toshiba SSH160A-HG, Toshiba Corp., Tokyo, Japan). The Doppler and M-mode echocardiograms were recorded on strip charts at a paper speed of 5 cm_/sec. Statistics. The mean of five consecutive heart beats was used for analysis. All data are expressed as mean _+ SD. The variables were compared before and after cardioversion by a paired t test. Ap value <0.05 was considered statistically significant. RESULTS Transmitral and pulmonary venous flow velocities before cardioversion. T h e atrial systolic wave of t h e
t r a n s m i t r a l flow velocity was a b s e n t in all patients. In addition, the negative PVA a n d PVS1 waves of the p u l m o n a r y venous flow velocity were also a b s e n t in all patients. However, the n e g a t i v e early systolic wave of the p u l m o n a r y venous flow velocity was clearly detected in almost all patients. Heart rate and M-mode variables after cardioversion.
T h e h e a r t r a t e d u r i n g AF (84 _+ 17 beats/min) was significantly h i g h e r t h a n t h a t w i t h i n 24 h o u r s (70 _+ 10 beats/min) (p < 0.01) and 10 days after cardioversion (69 _~ 14 beats/rain) (p < 0.01). However, t h e r e was no difference b e t w e e n the h e a r t r a t e w i t h i n 24 h o u r s and 10 days a f t e r cardioversion. T h e left atrial dimension 10 days a f t e r cardioversion (3.8 _+ 0.6 cm) was significantly smaller t h a n t h a t observed before cardioversion (4.0 _+ 0.7 cm) a n d w i t h i n 24 h o u r s (4.0 _+ 0.6 cm) after cardioversion (p < 0.05 for both). T h e IASA w i t h i n 24 h o u r s after cardioversion (2.6 _+0.7 mm) was significantly smaller t h a n t h a t observed 10 days after cardioversion (4.4 __ 1.0 ram) (p < 0.01) (Fig. 2). Transmitral flow velocity after cardioversion (Figs. 3
and 4). A and A-d w e r e significantly smaller w i t h i n 24 h o u r s after cardioversion (24 _+ 9 cm/sec and 100 _ 16 msec, respectively) relative to 10 days after (44 _+ 17 cm/sec and 134-+ 28 msec, respectively) cardioversion (p < 0.01 for both). In contrast, E was significantly g r e a t e r w i t h i n 24 h o u r s after cardioversion (64 _+ 16 cm/sec) t h a n 10 days (57 _+ 14 cm/ sec) after cardioversion (p < 0.05). T h e r e was no significant difference b e t w e e n E before cardioversion (68 _+ 13 cm/sec) and w i t h i n 24 h o u r s after cardioversion.
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10 hours after cardioversion
LA
10 days after cardioversion
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Fig. 2. Changes in interatrial septal motion after cardioversion in a patient with lone AF. Amplitude of interatrial septal motion during atrial systole (arrows) is minimal (1 ram) 10 hours after cardioversion but increases to 4 mm 10 days after cardioversion. LA, Left atrium; RA, right atrium. ECG, electrocardiogram; PCG, phonocardiogram. A
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Fig. 3. Comparisons of A of transmittal flow, PVA, and PVSl velocities of pulmonary venous flow within 24 hours and 10 days after cardioversion in patients with AF. DCM, Dilated cardiomyopathy.
Pulmonaryvenousflow velocityafter cardioversion (Figs. 3 and 5). PVA, PVA-d, PVS1, and PVS2 within 24 hours after cardioversion (PVA, 8.4 _+ 4.2 cm/sec; PVA-d, 77 _+ 32 msec; PVSl, 13 _+ 7 cm/sec; PVS2, 44 _+ 17 cm/sec)were significantly smaller compared with t h a t observed 10 days after cardioversion (PVA, 19.4 _+ 7.5 cm/sec; PVA-d, 117 +_ 40 msec; PVS1, 28 _+ 14 cm/sec; PVS2, 57 -+ 16 cm/sec) (p < 0.01 for each). There was a significant difference between the duration sum (d-sum, A-d + PVA-d) seen within 24 hours (170 _+ 39 msec) and 10 days (252 _+ 44 msec) after cardioversion (p < 0.01). There was no signifi-
cant difference between the PVS2 before (43 +_ 20 cm/sec) and within 24 hours after cardioversion. However, PVD was significantly greater within 24 hours after cardioversion (49 _+ 13 cm/sec) relative to 10 days after cardioversion ( 4 4 _+ 12 cm/sec) (p < 0.05). There was no significant difference between the PVD before (48 _+ 15 cm/sec) and within 24 hours after cardioversion.
Changesin variablesaftercardioversionin patients with dilatedcardiomyopathy(Fig. 3). H e r cazdioversion, the rat e of change in A of the t ransm i t r a l flow, PVA, and PVSl of the pulmonary venous flow were
Volume 131, Number 2 American Heart Journal
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Fig. 4. Changes' in transmitral flow velocity pattern after cardioversion in a patient with lone AF. A shows an amplitude of 38 cm/sec whereas E shows an amplitude of 75 cm/sec at 8 hours after cardioversion, or A/E < 1. Ten days after cardioversion, however, A increased to 52 cm/sec whereas E decreased to 50 cm/sec, or A/E > 1. ECG, Electrocardiogram; SV, sample volume; PCG, phonocardiogram.
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Fig. 5. Changes in pulmonary venous flow velocity pattern after cardioversion in same patient as Fig. 4. Eight hours after cardioversion, PVA and PVS1 velocities are minimal (7 cm/sec and 10 cm/sec, respectively). However, both PVA (22 cm/sec) and PVS1 (46 cm/sec) increased 10 days after cardioversion. PVD decreases (55 to 48 cm/sec) with time after cardioversion. ECG, Electrocardiogram; PCG, phonocardiogram.
significantly smaller (p < 0.01,p < 0.01, a n d p < 0.05, respectively) in patients with dilated cardiomyopathy t h a n in patients with other cardiac disease. One patient with dilated cardiomyopathy had recurrent AF a week after cardioversion. DISCUSSION
Left atrial mechanical contractility is severely impaired immediately after electrical cardioversion of AF. This phenomenon has been referred to as the
"stunned left atrium. ''5, 6 Left atrial function has been assessed by evaluating the left atrial pressure curve during cardiac catheterization, 1 kinetocardiography, 2 transmitral flow velocity pattern by pulsed Doppler echocardiography,3, 4 and left atrial appendage blood flow pattern by transesophageal echocardiography.5, 6 Pulmonary venous flow velocity recordings obtained during transesophageal echocardiography consist of the following four-peaked waves: (1) PVA,
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which reflects active left atrial contraction; (2) PVS1, which is related to left atrial relaxation; (3) PVS2, which coincides with the reservoir function of the left atrium and left ventricular contractility; and (4) PVD, which is related to left ventricular diastolic function and reflects the conduit function of the left atrium. The purpose of this study was to evaluate changes in left atrial mechanical function after electrical cardioversion for treatment of AF with use of transmitral and pulmonary venous flow velocity patterns. Blood in the left atrium is ejected into both the pulmonary veins and left ventricle through the mitral valve during active atrial contraction. The majority of the left atrial blood is directed toward the left ventricle in healthy subjects. Under conditions of marked increase in left ventricular end-diastolic pressure, however, flow reversal of left atrial blood to the pulmonary veins is augmented because of left atrial afterload mismatch. 14 Thus many investigators have emphasized the importance of assessing atrial systolic waves by using both transmitral and pulmonary venous flow velocities when evaluating left atrial function in patients with cardiac disease.7, 10, 11, 15,16 It has been reported that A of the transmitral flow decreases immediately after electrical cardioversion o f AF. 3' 4 We have demonstrated that PVA of the pulmonary venous flow and I A S A also decrease significantly within 24 hours after cardioversion. Our results indicate that left atrial active systolic function is significantly impaired under this condition. It also has been reported that PVS1 of the pulmonary venous flow reflects left atrial relaxation from the absence of this wave in patients with AF. 14, 16 In this study, the PVS1 decreased within 24 hours after cardioversion but increased in peak velocity 10 days after cardioversion, as noted by atrial systolic waves of the transmitral and pulmonary venous flows. This finding suggests that active left atrial relaxation also i s impaired under this condition. Although a decrease and gradual recovery in the amplitude of PVS1, A, PVA, and IASA were noted in most patients, recovery of these variables was delayed significantly in patients with dilated cardiomyopathy. This finding m a y be explained by coexistent left atrial enlargement and atrial dysfunction, which occurred perhaps as a result of longstanding increases in atrial afterload from elevations in left ventricular end-diastolic pressures, myocardial failure, or both.14, 16 PVS2 of the pulmonary venous flow was significantly greater 10 days after cardioversion than during AF and 24 hours after cardioversion. These find-
ings suggest that in patients with AF, the left atrium before and within 24 hours after cardioversion is involved in active diastolic function and passive left atrial distensibility. E of the transmitral flow and PVD of the pulmonary venous flow decreased with time after cardioversion. In these patients, left ventricular inflow decreased during atrial systole within 24 hours after cardioversion. Therefore it is probable that left ventricular inflow during rapid filling was augmented to compensate for the decreased inflow during atrial systole under this condition. A close relation between the amplitude of the atrial systolic wave of the left ventricular pressure curve or the left ventricular end-diastolic pressure and the amplitude or duration of the atrial systolic wave of the pulmonary venous flow has been reported.10, 11, 14 These studies were performed under the assumption that the left atrial myocardium is not involved in these patients. Therefore when hemodynamic assessment between the left atrium and ventricle is performed by using atrial systolic waves of the transmitral and pulmonary venous flow velocity pattern, consideration should be given to abnormalities in left ventricular compliance and abnormalities in left atrial myocardial function, including the stunned left atrium that occurs after cardioversion of AF. Conclusions. Active left atrial contraction and relaxation are markedly impaired within 24 hours after electrical cardioversion of atrial fibrillation and subsequently improved 10 days after cardioversion. Our findings demonstrate that combined assessment of transmitral and pulmonary venous flow velocities are useful in evaluating the severity of left atrial dysfunction and obtaining serial measurements in patients undergoing electrical cardioversion of atrial fibrillation. REFERENCES
L Lawlands DJ, Logan WFWE, Howitt G. Atrial function after cardioversion. AM HEARTJ 1967;74:149-60. 2. Schweizer JMW, Burkart F. Atrial function after cardioversion for atrial fibrillation. Br Heart J 1973;35:24-7. 3. Manning WJ, Leeman DE, Gotch PJ, Come PC. Pulsed Doppler evaluation of atrial mechanical function after electrical cardioversion of atrial fibrillation. J Am Coll Cardiol 1989;13:617-23. 4. Miwa H, Arakawa M, Kagawa K, Noda T, Nishigaki K, Ito Y, Kawada T, Hirakawa S. Time-course of recovery of atrial contraction after cardioversion of chronic atrial fibrillation. Heart Vessels 1993;8:98-106. 5. Shapiro EP, Effron MB, Lima S, Ouyang P, Siu CO, Bush D. Transient atrial dysfunction after cardioversion of chronic atrial fibrillation to sinus rhythm. Am J Cardiol 1988;62:1202-7. 6. Fatkin D, Kuchar DL, Thorburn CW, Feneley MP. Transesophageal echocardiography before and during direct current cardioversion of atrial fibrillation: evidence for "atrial stunning" as a mechanism of thromboembolic complication. J Am Call Cardiol 1994;23:307-16. 7. Nishimura RA, Abel MD, Hatle LK, Tajik AJ. Relation of pulmonary
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8.
9.
10.
11.
vein to mitral flow velocities by transesophageal Doppler echocardiography: effect of different loading conditions. Circulation 1990;81:148897. Kuecherer HF, Muhiudeen IA, Kusumoto FM, Lee E, Moulinier LE, Caharan MK, Shiller NB. Estimation of mean left atrial pressure from transesophageal pulsed Doppler echocardiography of pulmonary venous flow. Circulation 1990;82:1127-39. Kuccherer ttF, Kusumoto F, Muhiudeen IA, Cahalan MK, Shiller NB. Pulmonary venous flow patterns by transesophageal pulsed Doppler echocardiography: relation to parameters of left ventricular systolic and diastolic function. AM HEARTJ 1991;122:1683-93. Rossvoll O, Hatle LK. Pulmonary venous flow velocities recorded by transthoracic Doppler ultrasound: relation to left ventricular diastolic pressure. J Am Coll Cardiol 1993;21:1687-96. Appleton CP, Galloway JM, Gonzales MS, Gaballa M, Basnight MA. Estimation of left ventricular filling pressure using two-dimensional and Doppler echocardio~aphy in adult patients with cardiac disease: additional value of analyzing left atrial size, left atrial ejection function and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction. J Am Coll Cardiol 1993;22:1972-82.
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12. Hoit BD, Shao Y, Gabel M, Walsh RA. Influence of loading conditions and contractile state on pulmonary venous flow: validation of Doppler velocimetry. Circulation 1992;86:651-9. 13. KagejiY, Oki T, Iuchi A, Tabata T, Fukuda N. Noninvasive assessment of left atrial and ventricular relationship during atrial contraction from transesophageal pulsed Doppler echocardiography of pulmonary venous flow and left ventricular inflow. Jpn J Med Ultrasonics 1994; 21:443-50. 14. Oki T, Fukuda N, Ara N, Iuchi A, Tabata T, Tanimoto M, Manabe K, Kageji Y, Sasaki M, Ito S. Evaluation of left atrial active contraction and relaxation in various myocardial diseases by transesophageal pulsed Doppler echocardiography of left ventricular inflow and pulmonary venous flow. Am J Noninvas Cardiol 1994;8:140-5. 15. Yamag~chi M, Arakawa M, Tanaka T, Takaya T, Nagano T. Study on left atrial contractile performance: participation of Frank-Starling mechanism. Jpn Circ J 1987;51:1001-9. 16. Naito M, Dreifus LS, David D, Michelson EL, Mardelli TJ, Kmetzo JJ. Reevaluation of atrial systole to cardiac hemodynamics: evidence for pulmonary venous regurgitation during abnormal atrioventricular sequencing. AM HEARTJ 1983;105:295-302.
Assessment of left atrial systolic function immediately after cardioversion of atrial fibrillation (AF) has been performed by using transmitral flow velocity patterns with pulsed Doppler echocardiography and other modalities. 1-6 However, evaluation of left atrial mechanical function from this flow velocity only has been limited because blood in the left atrium is ejected into both the pulmonary veins and left ventricle through the mitral valve during atrial systole. The availability of transesophageal echocardiography in recent years has made it possible to obtain hemodynamic measurements between the left atrium and ventricle by examining the transmitral and pulmonary venous flow velocities; this From the Second Department of Internal Medicine, Tokushima University School of Medicine, Tokushima. Received for publication Jan. 23, 1995; accepted June 12, 1995. Reprint requests: Takashi Oki, MD, Second Department of Internal Medicine, Tokushima University School of Medicine, 2-50 Kuramoto-cho, Tokushima 770, Japan. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4/1167898
270
approach has been d e m o n s t r a t e d to be more sensitive t h a n transthoracic echocardiography for evaluating the left atrial active systolic and diastolic function. 7-14 In this study, we recorded these flow velocity patterns by using transthoracic and transesophageal pulsed Doppler techniques and evaluated the relations of the different variables from these flow velocities and left atrial function after cardioversion of AF. METHODS Study population. Twenty-five patients (22 men and
3 women, mean age 55-+ 17 years) who successfully underwent electrical cardioversion of AF participated in this study. The patient population consisted of six patients with hypertension, four with ischemic heart disease, two with alcoholic heart disease, five with dilated cardiomyopathy, and eight with no underlying heart disease. The mean time interval from the onset of AF to successful cardioversion was 32 days (range 3 to 168 days). Disopyramide (300 mg/day) was administered to all patients beginning immediately after cardioversion and given until 10 days after the procedure. Of the six patients with dilated cardiomyopathy, one had recurrence of AF 7 days after cardioversion and was excluded from the study. Echocardiography. All patients underwent transthoracic and transesophageal pulsed Doppler echocardiography and M-mode echocardiography 24 hours before, 24 hours after (mean 16 ± 5 hours), and 10 days after cardioversion of AF. Cardioversion consisted of administering between 150 and 200 J of energy to each patient. Measurements of transmitral flow velocity and left atrial dimension at end systole were obtained by using the transthoracic approach. Pulmonary venous flow velocity and interatrial septal motion were assessed by transesophageal echocardiography by using a horizontal view that included both atria. Transmitral flow velocity was recorded after the sample volume was measured at the tip of mitral valve leaflets on long-axis view of the left ventricle, and a clear diastolic biphasic waveform was obtained. The peak atrial systolic (A), peak early diastolic (E) velocities, their ratio (A/E), and the duration of the atrial systolic wave (A-d) were measured from transmitral flow velocity (Fig. 1). Pulmonary
2
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Iuchi et al. 271
TMF
PVF
A-d
IAS
PVS2
,
LA
Pvs :, ~G
~
PCG
~k[ ECGI I PVA .. _: ~1 ~ -~ F
_
,,
- -
2'~ ECG
PCG
PVA-d Fig. 1. Measurements of variables from transmitral and pulmonary venous flow velocities and interatrial
septal motion. TMF, Transmitral flow velocity pattern by transthoracic pulsed Doppler echocardiography; PVF, pulmonary venous flow velocity pattern by transesophageal pulsed Doppler echocardiography; IAS, interatrial septal motion obtained by transesophageal M-mode echocardiography; ECG, electrocardiogram;
PCG, phonocardiogram.
venous flow velocity was recorded by measuring the sample volume within 1 to 2 cm of the junction of the pulmonary vein with the left atrium after sections of the left atrium, including the left superior pulmonary vein, were visualized and the pulmonary venous inflow to the left atrium was confirmed by color Doppler imaging. The peak first systolic (PVSz), peak second systolic (PVS2), peak early diastolic (PVD), peak atrial systolic (PVA), and duration of the atrial systolic wave (PVA-d) were measured from pulmonary venous flow velocity (Fig. 1). Furthermore, the amplitude of interatrial septal motion during atrial systole (IASA) was measured from an M-mode interatrial septal echogram (Fig. 1). The changes in A, PVA, and PVS1 after cardioversion were calculated as differences between values obtained 10 days after cardioversion and within 24 hours after cardioversion. The rate of change regarding each variable was obtained by dividing the calculated difference by the value of the corresponding variable obtained 10 days after cardioversion. M-mode and pulsed Doppler echocardiograms were recorded with a 5 MHz transesophageal transducer (Aloka SSD 870, Aloka CO. Ltd., Tokyo, Japan) and a 2.5 MHz transthoracic transducer (Toshiba SSH160A-HG, Toshiba Corp., Tokyo, Japan). The Doppler and M-mode echocardiograms were recorded on strip charts at a paper speed of 5 cm_/sec. Statistics. The mean of five consecutive heart beats was used for analysis. All data are expressed as mean _+ SD. The variables were compared before and after cardioversion by a paired t test. Ap value <0.05 was considered statistically significant. RESULTS Transmitral and pulmonary venous flow velocities before cardioversion. T h e atrial systolic wave of t h e
t r a n s m i t r a l flow velocity was a b s e n t in all patients. In addition, the negative PVA a n d PVS1 waves of the p u l m o n a r y venous flow velocity were also a b s e n t in all patients. However, the n e g a t i v e early systolic wave of the p u l m o n a r y venous flow velocity was clearly detected in almost all patients. Heart rate and M-mode variables after cardioversion.
T h e h e a r t r a t e d u r i n g AF (84 _+ 17 beats/min) was significantly h i g h e r t h a n t h a t w i t h i n 24 h o u r s (70 _+ 10 beats/min) (p < 0.01) and 10 days after cardioversion (69 _~ 14 beats/rain) (p < 0.01). However, t h e r e was no difference b e t w e e n the h e a r t r a t e w i t h i n 24 h o u r s and 10 days a f t e r cardioversion. T h e left atrial dimension 10 days a f t e r cardioversion (3.8 _+ 0.6 cm) was significantly smaller t h a n t h a t observed before cardioversion (4.0 _+ 0.7 cm) a n d w i t h i n 24 h o u r s (4.0 _+ 0.6 cm) after cardioversion (p < 0.05 for both). T h e IASA w i t h i n 24 h o u r s after cardioversion (2.6 _+0.7 mm) was significantly smaller t h a n t h a t observed 10 days after cardioversion (4.4 __ 1.0 ram) (p < 0.01) (Fig. 2). Transmitral flow velocity after cardioversion (Figs. 3
and 4). A and A-d w e r e significantly smaller w i t h i n 24 h o u r s after cardioversion (24 _+ 9 cm/sec and 100 _ 16 msec, respectively) relative to 10 days after (44 _+ 17 cm/sec and 134-+ 28 msec, respectively) cardioversion (p < 0.01 for both). In contrast, E was significantly g r e a t e r w i t h i n 24 h o u r s after cardioversion (64 _+ 16 cm/sec) t h a n 10 days (57 _+ 14 cm/ sec) after cardioversion (p < 0.05). T h e r e was no significant difference b e t w e e n E before cardioversion (68 _+ 13 cm/sec) and w i t h i n 24 h o u r s after cardioversion.
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10 hours after cardioversion
LA
10 days after cardioversion
LA
RA
l~cm
RA
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Fig. 2. Changes in interatrial septal motion after cardioversion in a patient with lone AF. Amplitude of interatrial septal motion during atrial systole (arrows) is minimal (1 ram) 10 hours after cardioversion but increases to 4 mm 10 days after cardioversion. LA, Left atrium; RA, right atrium. ECG, electrocardiogram; PCG, phonocardiogram. A
(cm/sec)
(cm/sec)
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40
20 23.5
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Fig. 3. Comparisons of A of transmittal flow, PVA, and PVSl velocities of pulmonary venous flow within 24 hours and 10 days after cardioversion in patients with AF. DCM, Dilated cardiomyopathy.
Pulmonaryvenousflow velocityafter cardioversion (Figs. 3 and 5). PVA, PVA-d, PVS1, and PVS2 within 24 hours after cardioversion (PVA, 8.4 _+ 4.2 cm/sec; PVA-d, 77 _+ 32 msec; PVSl, 13 _+ 7 cm/sec; PVS2, 44 _+ 17 cm/sec)were significantly smaller compared with t h a t observed 10 days after cardioversion (PVA, 19.4 _+ 7.5 cm/sec; PVA-d, 117 +_ 40 msec; PVS1, 28 _+ 14 cm/sec; PVS2, 57 -+ 16 cm/sec) (p < 0.01 for each). There was a significant difference between the duration sum (d-sum, A-d + PVA-d) seen within 24 hours (170 _+ 39 msec) and 10 days (252 _+ 44 msec) after cardioversion (p < 0.01). There was no signifi-
cant difference between the PVS2 before (43 +_ 20 cm/sec) and within 24 hours after cardioversion. However, PVD was significantly greater within 24 hours after cardioversion (49 _+ 13 cm/sec) relative to 10 days after cardioversion ( 4 4 _+ 12 cm/sec) (p < 0.05). There was no significant difference between the PVD before (48 _+ 15 cm/sec) and within 24 hours after cardioversion.
Changesin variablesaftercardioversionin patients with dilatedcardiomyopathy(Fig. 3). H e r cazdioversion, the rat e of change in A of the t ransm i t r a l flow, PVA, and PVSl of the pulmonary venous flow were
Volume 131, Number 2 American Heart Journal
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Fig. 5. Changes in pulmonary venous flow velocity pattern after cardioversion in same patient as Fig. 4. Eight hours after cardioversion, PVA and PVS1 velocities are minimal (7 cm/sec and 10 cm/sec, respectively). However, both PVA (22 cm/sec) and PVS1 (46 cm/sec) increased 10 days after cardioversion. PVD decreases (55 to 48 cm/sec) with time after cardioversion. ECG, Electrocardiogram; PCG, phonocardiogram.
significantly smaller (p < 0.01,p < 0.01, a n d p < 0.05, respectively) in patients with dilated cardiomyopathy t h a n in patients with other cardiac disease. One patient with dilated cardiomyopathy had recurrent AF a week after cardioversion. DISCUSSION
Left atrial mechanical contractility is severely impaired immediately after electrical cardioversion of AF. This phenomenon has been referred to as the
"stunned left atrium. ''5, 6 Left atrial function has been assessed by evaluating the left atrial pressure curve during cardiac catheterization, 1 kinetocardiography, 2 transmitral flow velocity pattern by pulsed Doppler echocardiography,3, 4 and left atrial appendage blood flow pattern by transesophageal echocardiography.5, 6 Pulmonary venous flow velocity recordings obtained during transesophageal echocardiography consist of the following four-peaked waves: (1) PVA,
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which reflects active left atrial contraction; (2) PVS1, which is related to left atrial relaxation; (3) PVS2, which coincides with the reservoir function of the left atrium and left ventricular contractility; and (4) PVD, which is related to left ventricular diastolic function and reflects the conduit function of the left atrium. The purpose of this study was to evaluate changes in left atrial mechanical function after electrical cardioversion for treatment of AF with use of transmitral and pulmonary venous flow velocity patterns. Blood in the left atrium is ejected into both the pulmonary veins and left ventricle through the mitral valve during active atrial contraction. The majority of the left atrial blood is directed toward the left ventricle in healthy subjects. Under conditions of marked increase in left ventricular end-diastolic pressure, however, flow reversal of left atrial blood to the pulmonary veins is augmented because of left atrial afterload mismatch. 14 Thus many investigators have emphasized the importance of assessing atrial systolic waves by using both transmitral and pulmonary venous flow velocities when evaluating left atrial function in patients with cardiac disease.7, 10, 11, 15,16 It has been reported that A of the transmitral flow decreases immediately after electrical cardioversion o f AF. 3' 4 We have demonstrated that PVA of the pulmonary venous flow and I A S A also decrease significantly within 24 hours after cardioversion. Our results indicate that left atrial active systolic function is significantly impaired under this condition. It also has been reported that PVS1 of the pulmonary venous flow reflects left atrial relaxation from the absence of this wave in patients with AF. 14, 16 In this study, the PVS1 decreased within 24 hours after cardioversion but increased in peak velocity 10 days after cardioversion, as noted by atrial systolic waves of the transmitral and pulmonary venous flows. This finding suggests that active left atrial relaxation also i s impaired under this condition. Although a decrease and gradual recovery in the amplitude of PVS1, A, PVA, and IASA were noted in most patients, recovery of these variables was delayed significantly in patients with dilated cardiomyopathy. This finding m a y be explained by coexistent left atrial enlargement and atrial dysfunction, which occurred perhaps as a result of longstanding increases in atrial afterload from elevations in left ventricular end-diastolic pressures, myocardial failure, or both.14, 16 PVS2 of the pulmonary venous flow was significantly greater 10 days after cardioversion than during AF and 24 hours after cardioversion. These find-
ings suggest that in patients with AF, the left atrium before and within 24 hours after cardioversion is involved in active diastolic function and passive left atrial distensibility. E of the transmitral flow and PVD of the pulmonary venous flow decreased with time after cardioversion. In these patients, left ventricular inflow decreased during atrial systole within 24 hours after cardioversion. Therefore it is probable that left ventricular inflow during rapid filling was augmented to compensate for the decreased inflow during atrial systole under this condition. A close relation between the amplitude of the atrial systolic wave of the left ventricular pressure curve or the left ventricular end-diastolic pressure and the amplitude or duration of the atrial systolic wave of the pulmonary venous flow has been reported.10, 11, 14 These studies were performed under the assumption that the left atrial myocardium is not involved in these patients. Therefore when hemodynamic assessment between the left atrium and ventricle is performed by using atrial systolic waves of the transmitral and pulmonary venous flow velocity pattern, consideration should be given to abnormalities in left ventricular compliance and abnormalities in left atrial myocardial function, including the stunned left atrium that occurs after cardioversion of AF. Conclusions. Active left atrial contraction and relaxation are markedly impaired within 24 hours after electrical cardioversion of atrial fibrillation and subsequently improved 10 days after cardioversion. Our findings demonstrate that combined assessment of transmitral and pulmonary venous flow velocities are useful in evaluating the severity of left atrial dysfunction and obtaining serial measurements in patients undergoing electrical cardioversion of atrial fibrillation. REFERENCES
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