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Anesth Analg 2001;93:14-19
© 2001 International Anesthesia Research Society


CARDIOVASCULAR ANESTHESIA

Atrial Fibrillation After Coronary Artery Bypass Graft Surgery Is Unrelated To Cardiac Abnormalities Detected By Transesophageal Echocardiography

Nikolaos J. Skubas, MD, Benico Barzilai, MD*, and Charles W. Hogue, Jr., MD

Division of Cardiothoracic Anesthesia, Department of Anesthesiology, and the *Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri

Address correspondence and reprint requests to Charles W. Hogue, Jr., MD, Department of Anesthesiology, Washington University School of Medicine, 660 South Euclid Ave, Box 8054, St. Louis, MO 63110. Address email to hoguec{at}notes.wustl.edu


    Abstract
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Atrial fibrillation is a common complication of coronary artery bypass graft (CABG) surgery that is associated with adverse patient outcomes. We evaluated whether preexisting abnormalities of cardiac structure or function detected with transesophageal echocardiography (TEE) are prevalent in patients later developing atrial fibrillation after CABG surgery. TEE imaging was performed after induction of general anesthesia, but before primary CABG surgery, in 62 consecutive patients without cardiac valvular disease or preexisting atrial fibrillation. Measurements included left atrial diameter, left ventricular wall thickness, left ventricular end-systolic and end-diastolic dimensions and fractional area change. Pulsed-wave Doppler measurements of pulmonary venous and trans-mitral blood flow velocity were obtained. Continuous monitoring with telemetry electrocardiography for the development of atrial fibrillation was performed. Eighteen patients (29%) developed postoperative atrial fibrillation. There were no significant differences in left atrial or left ventricular TEE variables or pulsed-wave Doppler pulmonary venous flow measurements between patients with and without postoperative atrial fibrillation. After adjusting for age and duration of aortic cross-clamping, there were no differences in the transmitral Doppler diastolic filling variables between these same groups. These data suggest that atrial fibrillation commonly occurs after CABG surgery in the absence of atrial enlargement or Doppler-derived cardiac functional abnormalities. The data imply that the use of TEE immediately before surgery would be an insensitive means for routine identification of patients susceptible to this arrhythmia.

Implications: Transesophageal echocardiography performed immediately before coronary arterybypass graft (CABG) surgery is not useful for prediction of susceptibility todevelop atrial fibrillation postoperatively. Postoperative atrial fibrillationcommonly occurs after CABG surgery in the absence of preoperative atrialenlargement or Doppler derived functional abnormalities.


    Introduction
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Postoperative atrial fibrillation is one of the most frequent complications of coronary artery bypass graft (CABG) surgery, occurring in as many as 27% to 40% of patients (16). The development of this arrhythmia may lead to hemodynamic deterioration in some patients but it is also associated with longer hospitalization, an increased risk of postoperative stroke, and increased hospital costs (13). Further, new onset atrial fibrillation has been identified as the single most common diagnosis leading to hospital readmission after early discharge after CABG surgery (6). Nonetheless, factors that predispose patients to postoperative atrial fibrillation are incompletely understood. Identifying variables that increase patient vulnerability to this complication could enhance insight into the pathophysiologic mechanisms of the arrhythmia and provide a means of risk-stratifying patients. The latter would be especially useful for appropriate targeting of pharmacologic prophylactic therapies to limit exposure to potential life-threatening complications of such drugs to those patients most likely to benefit from the treatment (4,5).

Several electrophysiologic-based measurements are associated with risk for postoperative atrial fibrillation, but routine use of these techniques have limitations, including the need for specialized equipment and the added time needed for testing (710). Echocardiography has been successfully used to identify cardiac abnormalities associated with susceptibility to atrial fibrillation in longitudinal studies of the general population and for patients with left ventricular dysfunction (11,12). Atrial dimensions and left ventricular mass, in particular, are related to risk for atrial fibrillation, whereas other data suggest that altered left ventricular diastolic filling dynamics measured with trans-mitral valve pulsed-wave Doppler echocardiography identify susceptibility for atrial fibrillation in some patients (11,12). There have been conflicting findings regarding whether risk for postoperative atrial fibrillation in CABG surgical patients is associated with preexisting cardiac structural abnormalities especially left atrial enlargement (2,13,14). Further, these data were obtained using transthoracic M-mode echocardiography and diastolic filling dynamics measured with Doppler echocardiography were not reported. Transesophageal echocardiography (TEE) is increasingly used during cardiac surgery, and this method might provide a practical means of routine screening for cardiac abnormalities that could be related to atrial fibrillation risk after surgery. The purpose of this study was to evaluate whether preexisting abnormalities of cardiac structure or function detected with TEE are prevalent in patients later developing atrial fibrillation after CABG surgery.


    Methods
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
All procedures used in this study were approved by the Washington University School of Medicine Human Studies Committee. Sixty-two consecutive patients undergoing elective, primary CABG surgery at Barnes-Jewish Hospital, St. Louis, Missouri anesthetized by the same physician (CWH) were included in the study. Exclusion criteria for the study included a history of atrial fibrillation before surgery, the presence of a cardiac pacemaker, a history of sinus node dysfunction, or cardiac valvular disease. Patients received thiopental 2–4 mg and fentanyl 10–15 µg/kg with pancuronium given for muscle relaxation and isoflurane for anesthesia maintenance. Standard patient monitoring was used, including a pulmonary artery catheter and direct radial artery blood pressure monitoring.

After tracheal intubation a multiplane TEE probe (Hewlett Packard, Andover, MA) was inserted and connected to an intraoperative echocardiography system. Echocardiographic examination was systematically performed before incision. Color and pulsed-wave Doppler echocardiography evaluations of the cardiac valves were performed to exclude valvular regurgitation or stenosis. Pulsed-wave Doppler echocardiographic measurements of trans-mitral valve blood flow velocity were performed by sampling at the tips of the mitral valve leaflets from the four-chamber view. Pulsed-wave Doppler examinations of pulmonary blood flow were performed after the left superior vein was identified with color flow Doppler and two-dimensional TEE imaging and Doppler data were acquired 1 cm proximal to the confluence of left superior pulmonary vein with the left atrium. All TEE images were recorded on videotape for later analysis. Cardiopulmonary bypass was conducted with nonocclusive roller pumps using a membrane oxygenator (Cobe, Denver, CO) and a single two-stage cannula inserted directly into the atrium. Catheters for venting the left ventricle were inserted via the right superior pulmonary vein. High potassium, cold (3°C–5°C) blood cardioplegia was administered after aortic cross-clamping under mild systemic hypothermia (venous temperature >32°C). Patients received standard institutional care postoperatively, including the resumption of ß-adrenergic receptor blocking drugs for patients receiving this therapy before surgery, but there were no other drugs given for arrhythmia prophylaxis. Potassium and magnesium were administered postoperatively to keep serum concentrations within the normal range. After surgery, the patients were continuously monitored until the time of hospital discharge for arrhythmias with telemetry electrocardiography. The definition of atrial fibrillation was irregular heart rhythm with a fluctuating baseline without well-defined P wave. The diagnosis was made by attending medical staff based on telemetry findings confirmed with 12-lead electrocardiograms. Only sustained arrhythmia episodes were considered.

Off-line analysis of the recorded echocardiographic images and pulsed-wave Doppler results were performed by an investigator blinded to the patient outcomes. Measurements were performed using the calculation software package of the echocardiography machine (Hewlett Packard, Andover, MA). Left atrial dimensions were measured from the four-chamber view immediately before diastolic valve opening. The horizontal diameter of the atrium was defined as the maximal distance from the inner portion of the mid-septum to the inner portion of the midlateral atrial wall. Left ventricular wall thickness was measured from the posterior ventricular wall using images from the midpapillary short axis view at end-diastole. Left ventricular area was measured from this same view at end-systole and end-diastole. Transmitral valve blood flow velocity curves were analyzed for the following variables: early filling (E) wave (the highest initial velocity in early diastole) and late filling (A) wave caused by atrial contraction. The peak E and A velocities, E/A velocities ratio, and the E and A velocity-time integrals were calculated. The deceleration time of the E-wave was the time from the peak E-wave until the velocity crossed zero. This was extrapolated when the A-wave velocity was superimposed on the E-wave. Pulmonary venous blood flow velocity curves were analyzed for the following variables: peak reverse velocity at atrial contraction (PV-A wave), highest peak forward velocity during ventricular systole (PV-S wave), which was further defined as two distinct peaks, an early (SE) and a late (SL) one, and diastole (PV-D wave) (15). The systolic (including both SE and SL) and diastolic integrals were measured, and the S/D ratio was calculated using the S and D velocities. All TEE and Doppler echocardiography measurements were made from three consecutive cycles at end-exhalation during a period of relatively stable R-R intervals corresponding to the baseline heart rate.

Statistical Analysis
Continuous data were analyzed with analysis of variance using Bonferroni post hoc test when appropriate and with Wilcoxon’s rank sum test when the data were nonparametrically distributed. Categorical data were analyzed with Fisher’s exact test. The relationship between left atrial size and risk for postoperative atrial fibrillation was evaluated both as a continuous variable and as a dichotomous variable. For the latter, patients were categorized based on atrial size in 0.1-cm increments. Stepwise logistic regression analysis was used to assess for the potential of any echocardiographic variable to be of value in predicting postoperative atrial fibrillation. In this analysis, age and duration of aortic cross-clamping were included because of the strength of these variables to identify risk for this arrhythmia in other series. All values are expressed as mean ± SD. A significant difference was considered to exist for P <= 0.05.


    Results
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Atrial fibrillation developed in 18 of the 62 (29%) patients after surgery, occurring between postoperative days 1 through 5. Characteristics and perioperative data for patients developing atrial fibrillation and for those remaining in sinus rhythm are listed in Table 1. Patients with atrial fibrillation tended to be older and were more likely to have noninsulin dependent diabetes mellitus compared with patients without atrial arrhythmias. There were no other differences in the listed variables between the patients with and without postoperative atrial fibrillation.


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Table 1. Patient Demographic and Operative Data
 
TEE-derived cardiac structural and systolic functional measurements are listed in Table 2. The mean left atrial diameter for patients developing postoperative atrial fibrillation was no different compared with the patients remaining in sinus rhythm after surgery. Further, there was no significant relationship between left atrial dimensions between these same groups when left atrial diameter was dichotomized in 0.1-cm increments. There were no differences in left ventricular thickness or in the frequency of left ventricular hypertrophy (LV thickness >1.3 cm) between patients with and without postoperative atrial fibrillation. End-systolic and end-diastolic areas were not significantly different between the patients with and without postoperative arrhythmias. Further, left ventricular systolic function assessed as fractional area change was not different between the Atrial Fibrillation and the Sinus Rhythm groups. The number of patients with a left ventricular fractional area change <35% was not significantly different between the patients with postoperative atrial fibrillation compared with those patients remaining in sinus rhythm. To further describe atrial size between the patients, left atrial width was categorized based on increments of 0.5 cm between 4 and 6 cm (Table 3). There were no differences between the number of patients in each category for patients with and without atrial fibrillation.


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Table 2. Transesophageal Echocardiographic Derived Cardiac Dimensions and Indices of Systolic Function
 

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Table 3. Number of Patients (%) Versus Left Atrial Width for Patients with and without Postoperative Atrial Fibrillation
 
TEE pulmonary venous and transmitral Doppler measurement results are listed in Tables 4 and 5, respectively. There were no differences between the Postoperative Atrial Fibrillation and the Sinus Rhythm groups in any of the pulmonary venous Doppler measurements. Eight of the 44 (17%) patients remaining in sinus rhythm after surgery had a systolic/diastolic ratio <1, whereas 3 of 18 (18%) patients developing atrial fibrillation had this finding. For the most part, transmitral diastolic Doppler measurements were not different between the patients with and without postoperative atrial fibrillation. Three (17%) patients developing atrial fibrillation and 7 (16%) patients without this arrhythmia had a peak early to peak atrial transmitral flow (E/A ratio) >1.5. The deceleration time of the early transmitral diastolic wave was significantly longer in the patients remaining in sinus rhythm postoperatively compared with the patients developing atrial fibrillation after surgery. To evaluate whether this finding would have predictive value in identifying risk for postoperative atrial fibrillation, regression analysis was used to adjust for other factors associated with risk for the arrhythmia. When adjusting for age, and the duration of aortic cross-clamping, there was no significant relationship between any of the echocardiographic variables and risk for atrial fibrillation.


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Table 4. Transesophageal Echocardiographically Measured Pulmonary Venous Doppler Results
 

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Table 5. Transesophageal Echocardiographically Measured Transmitral Doppler Results
 

    Discussion
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
These results show that there were no baseline differences in left atrial width, left ventricular end-systolic and end-diastolic areas or fractional area change between patients who developed atrial fibrillation after CABG surgery compared with those remaining in sinus rhythm. Further, the number of patients with left ventricular hypertrophy or dysfunction was no different between these groups. Assessment of atrial and ventricular filling dynamics with TEE Doppler measurement of pulmonary venous and transmitral blood flow velocity did not reveal differences between patients with and without atrial fibrillation, with the exception of early transmitral deceleration. When statistically adjusting for patient demographic variables, the latter finding was not a significant predictor of risk for postoperative atrial fibrillation.

Identifying patients predisposed to atrial fibrillation after CABG surgery would allow for more appropriate targeting of patient electrocardiogram monitoring and preventative drug therapy. It is hypothesized that patients susceptible to postoperative atrial arrhythmias have a preexisting electrophysiologic substrate that becomes vulnerable as a result of surgical perturbations (16). Experimentally, atrial distention promotes the electrophysiologic conditions for atrial fibrillation by reducing action potential duration, decreasing the effective refractory period and shortening the wavelength of depolarization (1719). Further, myocardial stretching can induce ectopic beats and after-depolarizations that may promote the initiation of arrhythmias (20,21). The mechanisms for these processes, termed mechanoelectrical feedback, appears to be activation of selective and nonselective sarcolemmal ion channels as a result of myocardial stretch (stretch-activated ion channels) as well as volume-sensitive ion channels (2225).

Experimentally, thus, there is an electrophysiologic association between increased atrial dimensions and the electrophysiologic conditions conducive to the development and maintenance of atrial fibrillation. Further, in the general population, there is a well appreciated relationship between atrial enlargement and atrial fibrillation, although a causal role of atrial size in arrhythmogenesis (as opposed to secondary enlargement from the arrhythmia) has not always been clear (2628). Other prospective longitudinal studies of elderly, nonsurgical patients initially in sinus rhythm, have shown that left atrial enlargement, left ventricular wall thickness and left ventricular fractional shortening are predictive of the development of atrial fibrillation after a mean follow-up of 7.2 years (11).

Although there appears to be a plausible basis to suspect that patients prone to develop atrial fibrillation after CABG surgery might have preexisting cardiac structural or functional abnormalities, our results suggest that such cardiac abnormalities are uncommon for many patients developing this arrhythmia. These findings are similar to those previously reported where transthoracic M-mode echocardiography was used to measure left atrial size (2,14). Others, however, have reported that left atrial size detected before surgery with two-dimensional transthoracic echocardiography was associated with postoperative atrial fibrillation (13). In that report, patients with a history of atrial fibrillation were included in the analysis. Atrial fibrillation induces cardiac structural changes including hypocontractility or atrial "stunning" that could confound the results (2931). Our study included only patients without valvular heart disease and excluded those with a history of atrial fibrillation.

Doppler echocardiography allows for the assessment of the dynamics of cardiac blood flow that provide insight into atrial and ventricular diastolic function and compliance (32). There are few data, however, on whether Doppler echocardiography derived assessments are related to susceptibility for postoperative atrial fibrillation. In nonsurgical populations such abnormalities have been reported (12). Further, in a study of patients undergoing pulmonary resection, transvalvular Doppler echocardiography indices after surgery were independently associated with risk for postoperative supraventricular arrhythmias (33). Our results showed that although some patients may have had diastolic dysfunction as indicated by the ratio of systolic-to-diastolic pulmonary venous wave ratio >1.0 and transmitral early wave-to-atrial wave ratio <1.0 (Tables 4 and 5), there were no differences in the frequency of such abnormalities or in the mean blood flow velocity patterns between patients with and without postoperative arrhythmias. We did find that, compared with patients developing atrial fibrillation, the patients remaining in sinus rhythm had significantly longer transmitral deceleration time of the early diastolic wave. These findings would be compatible with abnormalities in diastolic relaxation of the left ventricle. Nonetheless, when adjusting for patient age and duration of aortic cross-clamping, there were no differences in any other Doppler derived indices suggesting that abnormal left atrial and ventricular filling dynamics are not prevalent in patients susceptible to postoperative atrial fibrillation.

Our TEE measurements were obtained after induction of anesthesia and institution of positive pressure ventilation, both of which could alter cardiac preload and, thus, the TEE cardiac structural and functional measurements. Although these results might not necessarily be readily extrapolated to the awake state, the conditions of this study are similar to the usual clinical conditions where TEE might potentially be implemented for detecting any abnormalities associated with postoperative atrial fibrillation. Further, in this study we did not report right atrial size or hepatic venous and tricuspid valve Doppler measurements. The latter are difficult to consistently obtain in patients with TEE because of the position of these structures in relation to the posterior and rotated position of the TEE probe. Despite the increased prevalence of postoperative atrial fibrillation in this series, the sample size of this study is a limitation in light of the small differences for many of our TEE findings between patients with and without atrial fibrillation. Consequently, we cannot exclude a Type II error for failing to distinguish these two groups with our TEE assessments. Based on our results, a study of nearly 3500 patients would be required to exclude the latter with confidence. Thus, our results do not eliminate that patients with preexisting left atrial enlargement or other cardiac abnormalities may be prone to postoperative atrial fibrillation. Our findings do suggest, though, that atrial fibrillation commonly occurs in the absence of atrial enlargement or Doppler derived cardiac functional abnormalities. The data imply that the use of TEE immediately before surgery would be an insensitive means for routinely identifying many patients susceptible to this arrhythmia.


    References
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Creswell LL, Schuessler RB, Rosenbloom M, Cox JL. Hazards of postoperative atrial arrhythmias. Ann Thorac Surg 1993; 56: 539–49.[Abstract]
  2. Mathew JP, Parks R, Savino JS, et al. Atrial fibrillation following coronary artery bypass graft surgery. JAMA 1996; 276: 300–6.[Abstract/Free Full Text]
  3. Aranki SF, Shaw DP, Adams DH, et al. Predictors of atrial fibrillation after coronary artery surgery: current trends and impact on hospital resources. Circulation 1996; 94: 390–7.[Abstract/Free Full Text]
  4. Hogue CW Jr, Hyder ML. Atrial fibrillation after cardiac operation: risks, mechanisms, and treatment. Ann Thorac Surg 2000; 69: 300–6.[Abstract/Free Full Text]
  5. Weber UK, Osswald S, Huber M, et al. Selective versus non-selective antiarrhythmic approach for prevention of atrial fibrillation after coronary surgery: is there a need for pre-operative risk stratification? Eur Heart J 1998; 19: 794–800.[Abstract/Free Full Text]
  6. Lahey SJ, Campos CT, Jennings B, et al. Hospital readmission after cardiac surgery: does "fast track" cardiac surgery result in cost saving or cost shifting? Circulation 1998; 98 (Suppl II): II35–40.
  7. Steinberg JS, Zelenkofske S, Wong S-C, et al. Value of the P-wave signal-averaged ECG for predicting atrial fibrillation after cardiac surgery. Circulation 1993; 88: 2618–22.[Abstract/Free Full Text]
  8. Klein M, Evans SJL, Blumberg S, et al. Use of P-wave-triggered, P-wave signal-averaged electrocardiogram to predict atrial fibrillation after coronary artery bypass surgery. Am Heart J 1995; 129: 895–901.[Web of Science][Medline]
  9. Hogue CW Jr, Domitrovich PP, Stein PK, et al. RR interval dynamics before atrial fibrillation in patients after coronary artery bypass graft surgery. Circulation 1998; 98: 429–34.[Abstract/Free Full Text]
  10. Hogue CW Jr, Filos KS, Schuessler RB, Sundt TM. Sinus nodal function and risk for atrial fibrillation after coronary artery bypass graft surgery. Anesthesiology 2000; 92: 1286–92.[Web of Science][Medline]
  11. Vaziri SM, Larson MG, Benjamin EJ, Levy D. Echocardiographic predictors of nonrheumatic atrial fibrillation: the Framingham Heart Study. Circulation 1994; 89: 724–30.[Abstract/Free Full Text]
  12. Pozzoli M, Cioffi G, Traversi E, et al. Predictors of primary atrial fibrillation and concomitant clinical and hemodynamic changes in patients with chronic heart failure: a prospective study in 344 patients with baseline sinus rhythm. J Am Coll Cardiol 1998; 32: 197–204.[Abstract/Free Full Text]
  13. Ducceschi V, D’Andrea A, Liccardo B, et al. Perioperative clinical predictors of atrial fibrillation occurrence following coronary artery surgery. Eur J Cardiothorac Surg 1999; 16: 435–39.[Abstract/Free Full Text]
  14. Parikka H, Toivonen L, Pellinen T, et al. The influence of intravenous magnesium on the occurrence of atrial fibrillation after coronary artery by-pass operation. Eur Heart J 1993; 14: 251–8.[Abstract/Free Full Text]
  15. Bartzokis T, Lee R, Yeoh TK, et al. Transesophageal echo-Doppler echocardiographic assessment of pulmonary venous flow patterns. J Am Soc Echocardiogr 1991; 4: 457–64.[Medline]
  16. Cox JL. A perspective on postoperative atrial fibrillation in cardiac operations. Ann Thorac Surg 1993; 56: 405–9.[Web of Science][Medline]
  17. Smeets JL, Allessie MA, Lammers WJ, et al. The wave-length of the cardiac impulse and reentrant arrhythmias in isolated rabbit atrium: the role of heart rate, autonomic transmitters, temperature, and potassium. Circ Res 1986; 58: 96–108.[Abstract/Free Full Text]
  18. Solti F, Vecsey T, Kékesi V, Juhasz-Nagy A. The effect of atrial dilatation on the genesis of atrial arrhythmias. Cardiovasc Res 1989; 23: 882–6.[Web of Science][Medline]
  19. Ravelli F, Allessie M. Effects of atrial dilatation on refractory period and vulnerability to atrial fibrillation in the isolated Langendorff-perfused rabbit heart. Circulation 1997; 96: 1686–95.[Abstract/Free Full Text]
  20. Wijffels MC, Kirchhof CJ, Dorland R, et al. Electrical remodeling due to atrial fibrillation in chronically instrumented conscious goats: the role of neurohumoral changes, ischemia, atrial stretch, and high rates of electrical activation. Circulation 1997; 96: 3710–20.[Abstract/Free Full Text]
  21. Lab MJ. Transient depolarisation and action potential alterations following mechanical changes in isolated myocardium. Cardiovasc Res 1980; 14: 624–37.[Web of Science][Medline]
  22. Franz MR, Cima R, Wang D, et al. Electrophysiological effects of myocardial stretch and mechanical determinants of stretch-activated arrhythmias. Circulation 1992; 86: 968–78.[Abstract/Free Full Text]
  23. Craelius W, Chen V, El-Sherif N. Stretch activated ion channels in ventricular myocytes. Biosci Rep 1988; 8: 407–14.[Web of Science][Medline]
  24. Bustamante JO, Ruknudin A, Sachs F. Stretch-activated anion currents of rabbit cardiac myocytes. J Physiol 1992; 456: 285–302.[Abstract/Free Full Text]
  25. Sorota S. Swelling-induced chloride-sensitive current in canine atrial cells revealed by whole-cell patch-clamp method. Circ Res 1992; 70: 679–87.[Abstract/Free Full Text]
  26. Davies MJ, Pomerance A. Pathology of atrial fibrillation in man. Br Heart J 1972; 34: 520–5.[Free Full Text]
  27. Henry WL, Morganroth J, Pearlman AS, et al. Relation between echocardiographically determined left atrial size and atrial fibrillation. Circulation 1976; 53: 273–9.[Abstract/Free Full Text]
  28. Keren G, Etzion T, Sherez J, et al. Atrial fibrillation and atrial enlargement in patients with mitral stenosis. Am Heart J 1987; 114: 1146–55.[Web of Science][Medline]
  29. Shachnow N, Spellman S, Rubin I. Persistent supraventricular tachycardia: case report with review of literature. Circulation 1954; 10: 232–6.[Web of Science][Medline]
  30. Gillette PC, Smith RT, Garson A, et al. Chronic supraventricular tachycardia, a curable cause of congestive cardiomyopathy. JAMA 1985; 253: 391–2.[Abstract/Free Full Text]
  31. 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.[Abstract]
  32. Choong CY. Left ventricle V. Diastolic function—its principles and evaluation. In: Weyman AE, ed. Principles and practice of echocardiography. 2nd ed. Philadelphia: Lea & Febiger, 1994: 721–80.
  33. Amar D, Roistacher N, Burt M, et al. Clinical and echocardiographic correlates of symptomatic tachydysrhythmias after noncardiac thoracic surgery. Chest 1995; 108: 349–54.[Abstract/Free Full Text]
Accepted for publication March 28, 2001.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press