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J Thorac Cardiovasc Surg 1998;115:139-147
© 1998 Mosby, Inc.

SURGERY FOR CONGENITAL HEART DISEASE

Effect of the Cox maze procedure on the secretion of atrial natriuretic peptide

From the Department of Thoracic and Cardiovascular Surgery and InternalMedicine, Seoul National University College of Medicine,^a and Departmentof Clinical Pathology, Chung Ang University,^b Seoul, Korea. Supportedby grant No. 05-95-004 from the Seoul National University Hospital ResearchFund.

Read at the Seventy-seventh Annual Meeting of The American Associationfor Thoracic Surgery, Washington, D.C., May 4-7, 1997.

Received for publication May 7, 1997; revisions requested June 24,1997; revisions received July 24, 1997. Accepted for publication July 25, 1997. Reprints: Ki-Bong Kim, MD, Department of Thoracic and CardiovascularSurgery, Seoul National University Hospital, 28 Yeunkun-Dong, Chongro-Ku,Seoul 110-744, Korea.

	Abstract

Top Abstract Introduction Patients and methods Results Discussion Conclusions Discussion References

 
Objectives:TheCox maze procedure has been confirmed to be effective in curing atrial fibrillation.Some authors have reported severe fluid retention after the Cox maze procedureand have suggested decreased secretion of atrial natriuretic peptide as apossible mechanism. This study was designed (1) to examine the serial changesin atrial natriuretic peptide after the Cox maze procedure as compared withchanges occurring after coronary artery bypass grafting and (2) to elucidateany differences in atrial natriuretic peptide levels between patients withtransient recurrence of atrial fibrillation after the Cox maze procedure andthose without recurrence of atrial fibrillation.
Methods:Blood samples were drawn from theright and left atria in patients undergoing the Cox maze procedure (n = 19) and from the rightatrium in patients undergoing coronary artery bypass grafting (n = 6) before and 1, 2, and 3 daysafter the operation. In six patients undergoing the Cox maze procedure, sampleswere also drawn from the radial artery before and 1, 2, 3, 5, and 7 days afterthe operation. The plasma samples were prepared by refrigerated centrifugationand stored until radioimmunoassay. In the Cox maze procedure group, atrialnatriuretic peptide levels in the right atrium were 629 ± 366,154 ± 112, 162 ± 112, and 183 ± 97 pg/mland those in the left atrium were 276 ± 168, 152 ±91, 162 ± 111, and 145 ± 80 pg/ml before and 1, 2,and 3 days after the operation, respectively. A marked decrease in atrialnatriuretic peptide levels was evident after the Cox maze procedure (p < 0.001). There was nosignificant correlation between atrial natriuretic peptide levels and atrialpressures after the Cox maze procedure, which suggests that secretion of atrialnatriuretic peptide by the atria was impaired. There was a significant correlationbetween the atrial natriuretic peptide levels in the left atrium and thosein the peripheral radial artery, and the decreased levels of atrial natriureticpeptide in the radial artery continued for 7 days after the Cox maze procedure.There were no differences in the atrial natriuretic peptide levels betweenthe patients with transient recurrence of atrial fibrillation (n = 6) and those without recurrence(n = 13) afterthe Cox maze procedure. In the coronary artery bypass grafting group, theatrial natriuretic peptide levels in the right atrium were 115 ±37, 124 ± 48, 154 ± 54, and 156 ± 36 pg/mlbefore and 1, 2, and 3 days after the operation, respectively. No change wasseen after the operation.
Conclusions: We observed a significant decrease in atrial natriuretic peptidelevels after the Cox maze procedure. This may be one of the possible causesof fluid retention after this procedure. These decreased atrial natriureticpeptide levels after the Cox maze procedure may result from the multiple atriotomyincisions and excision of both atrial auricles performed during the procedure,rather than from the conversion of atrial fibrillation to normal sinus rhythm.(J Thorac Cardiovasc Surg 1998;115:139–47

	Introduction

Top Abstract Introduction Patients and methods Results Discussion Conclusions Discussion References

 
The Cox maze procedure (CMP), developed by Cox and associates, ^1,2 has become a safe and efficient surgical treatment for medically refractoryatrial fibrillation (AF). It has been widely performed as a concomitant procedurein patients with organic cardiac diseases and chronic AF. ^3,4 Despite thebeneficial midterm results of the CMP for AF, postoperative fluid retentionwith pulmonary edema and symptomatic pleural effusion has been observed asone of the early postoperative complications in 12% to 36% of the patients. ^5,6 Cox and associates ¹suggested that this may be the result of a postoperative decrease in the atrialnatriuretic peptide (ANP) level that is triggered by the multiple atriotomyincisions and the excision of both atrial auricles that are performed duringthe CMP. However, few reports have demonstrated a decrease in ANP levels afterthe CMP.

Several reports have shown a relationship between ANP levels and AFby demonstrating that ANP levels decrease in response to the conversion ofAF to normal sinus rhythm. ^7,9 Therefore, there are two possible explanations forthe postoperative decrease of ANP levels after the CMP, the surgical incisionsthat include multiple atriotomies and excision of both atrial auricles andpostoperative conversion of AF to normal sinus rhythm. The aims of this studywere (1) to examine the serial changes in ANP levels after the CMP and comparethem with those after coronary artery bypass grafting (CABG) and (2) to elucidateany differences between ANP levels in patients with transient recurrence ofAF after the CMP and those in patients without recurrence of AF.

	Patients and methods

Top Abstract Introduction Patients and methods Results Discussion Conclusions Discussion References

 
The CMP was performed in 19 patients with various organic heart diseasescombined with AF. Our indications to perform the concomitant CMP were chronicAF, presence of left atrial (LA) thrombus, or medical history of previousthromboembolic events. There were 11 men and 8 women, with a mean age of 46 ±8 years. The mean duration of AF before the operation was 68 ±54 months (4 to 180 months), and the mean size of the LA on preoperative transthoracicechocardiography was 57 ± 7 mm (37 to 70 mm). Most of the patientsin the CMP group had been treated before the operation with diuretics anddigitalis for congestive heart failure and AF. Eighteen patients, all butthe one patient with a ruptured sinus of Valsalva, underwent mitral valveoperations. Additional concomitant procedures involved aortic valve operationsin nine patients, tricuspid valve surgery in four, closure of atrial septaldefect in two, and CABG in one. The CMP III, as described elsewhere by Coxand coworkers, ¹⁰ was performed.After the CMP, six patients (32%) had transient recurrence of AF during theearly postoperative period. The recurrent AF continued from the operativeday until at least the third day after the operation, with conversion to normalsinus rhythm some days later. For comparison with the CMP group, seven patientswith ischemic heart disease who were undergoing CABG were studied. These patientswere all male, with a mean age of 54 ± 8 years, and were in sinusrhythm before and after the operation.

This study was approved by the hospital ethics committee. Written, informedconsent was obtained from each participating patient.

Measurement.
In the CMP group, a median sternotomy was performed and the pericardiumwas opened with the patient under general anesthesia. The pressures were thenmeasured in and blood samples were obtained from both atria. Postoperativeblood sampling and pressure measurement of the right atrium (RA) were carriedout through a thermodilution catheter, and those of the LA were performedthrough a pressure line inserted in the right upper pulmonary vein. Postoperativeblood sampling and pressure measurements were continued on the first, second,and third postoperative days. Blood samples were also obtained from the radialartery on the first, second, third, fifth, and seventh postoperative daysin six cases among the CMP group for comparison with the atrial samples andto examine the serial changes after the operation. In the CABG group, bloodsamples from the RA and RA pressure measurements were obtained througha thermodilution catheter on the first, second, and third postoperative days.

Specimens of blood from each atrium and the radial artery (10 ml each)were collected into ethylenedi­aminetetraacetic acid–treated tubes,stored in ice, and immediately centrifuged at 3000 rpm for 10 minutes at 4°C to separate the plasma. The plasma samples were preserved at –70°C until the assay.

ANP concentration was determined by radioimmunoassay with rabbit anti-ANPserum (K-625 Radioimmunoassay kit for Atrial Natriuretic Peptide; Research& Diagnostic Antibodies, Berkeley, Calif.). ANP levels were measured twicefor each sample, and a mean was calculated as a representative value.

Statistics.
Statistical analysis was performed with the Statistical Analysis Systemsoftware package (version 6.04; SAS Institute, Cary, N.C.). The significanceof changes was assessed by Student's paired t test. Linear regression analysiswas used to determine any correlations between the ANP levels in each atriumand independent hemodynamic variables, and also between the ANP levels ofboth atria and those of the radial artery. Repeated-measures analysis of variancewas also performed to investigate the influence of postoperative recurrentAF on the ANP levels. All results were expressed as mean ± standarddeviation, and a value of p less than 0.05 was considered statistically significant.

	Results

Top Abstract Introduction Patients and methods Results Discussion Conclusions Discussion References

 
CMP group.
The ANP levels in the RA were 629 ± 366, 154 ±112, 162 ± 112, and 183 ± 97 pg/ml and those in theLA were 276 ± 168, 152 ± 91, 162 ± 111,and 145 ± 80 pg/ml just after induction of anesthesia and 1, 2,and 3 days after the operation, respectively. There was a statistically significantdecrease in ANP levels in both atria after the CMP (p < 0.001; Fig. 1). RA pressures were 8 ± 4,13 ± 3, 15 ± 3, and 17 ± 4 mm Hg and LApressures were 18 ± 9, 17 ± 4, 18 ± 4,and 21 ± 4 mm Hg just after induction of anesthesia and 1, 2,and 3 days after the operation, respectively. The LA pressure was about twotimes higher than the RA pressure before the operation; however, the preoperativeANP level was about two times higher in the RA than in the LA. There was nosignificant correlation between the preoperative ANP levels and preoperativepressures in each atrium, or between LA preoperative ANP levels and LA sizeas measured by preoperative transthoracic echocardiography. Furthermore, therewere no significant correlations between the ANP levels and the pressuresof each atrium after the CMP.

View larger version (20K): [in this window] [in a new window]   Figure 1. Changes in atrial ANP levelsand pressures in the CMP group. Statistically significant decreases in ANPlevels in both RA (A) and LA (B) were seen after the CMP (p <0.001). RAANP, RA ANP levels; RAP, RA pressure; Preop, just afterinduction of anesthesia; POD, postoperativeday; LAANP, LA ANP levels; LAP, LA pressure.

View larger version (13K): [in this window] [in a new window]   Figure 2. Changes in the ANP levels ofthe radial artery (ARTANP) in comparison withthose of RA (RAANP) and LA (LAANP) in the CMP group. ARTANP showed a close correlation withLAANP, and the decreased ARTANP continued for 7 days after the CMP. Preop, just after induction of anesthesia; POD, postoperative day.

View larger version (20K): [in this window] [in a new window]   Figure 3. Comparison of the RA (A) and LA (B) ANP levelsbetween patients with recurrence of AF (POSTAF(+))and patients without recurrence of AF (POSTAF(–)). There were no significant differences in ANP levels of eachatrium between the two groups with time. Preop,just after induction of anesthesia; POD, postoperativeday.

View larger version (19K): [in this window] [in a new window]   Figure 4. Changes in the RA ANP levels(RAANP) and RA pressures (RAP) in the CABG group. There were insignificant changes in theRAANP and RAP after the operation. Preop,just after induction of anesthesia; POD, postoperativeday.

	Discussion

Top Abstract Introduction Patients and methods Results Discussion Conclusions Discussion References

This study reveals four main findings. First, the ANP levels in bothatria decrease significantly after the CMP, and this may be one of the causesof postoperative fluid retention. Second, there is no significant correlationbetween the ANP levels and pressures in each atrium after the CMP, suggestingthat the secretion of ANP from the atria is impaired. Third, the decreasedANP levels in the radial artery continue until the seventh postoperative day,which suggests that the restoration of atrial mechanical function is delayedat least 1 week after the CMP. Fourth, there are no differences in the ANPlevels between patients with transient recurrence of AF after the CMP andthose without recurrence; this suggests that the decreased ANP levels afterthe CMP may result from the multiple atriotomy incisions and excision of bothatrial auricles, rather than from the conversion of AF to normal sinus rhythm.

ANP levels at different sites and the relationship between the ANPlevels and atrial pressures.
Most of our patients had mitral valvular disease, and the LA pressurewas about two times higher than the RA pressure before the operation; however,the preoperative ANP levels were about two times higher in the RA than inthe LA. A highly significant increase in ANP levels in the RA was also foundin a previous study, reflecting secretion of ANP into the coronary sinus andextraction of ANP by the lungs. ¹² Northridge and associates ¹³ showed a higher ANP level in the LA than in the pulmonary veins anddemonstrated secretion of the ANP into the LA as well as the RA. Our studydemonstrates that there is a significant correlation between the ANP levelsof the LA and those of the radial artery, and that the decreased levels ofANP continue until the seventh postoperative day. This close relationshipbetween LA and radial artery levels of ANP was also found previously. ^12,13 The radial artery ANP levels are therefore indicative of thoseof the central cardiac chambers.

The search for a mechanism that results in a release of ANP from theatria has produced several demonstrations of a relationship between atrialpressures and plasma ANP levels. ^7,14,15 Another study ¹⁶emphasized the role of the atrial stretch, rather than atrial pressure, inthe release of ANP. Our study shows an insignificant correlation between ANPlevels and atrial pressures in the CMP group, suggesting that the secretionof ANP from the atria was impaired.

Postoperative changes in ANP levels.
Ashcroft and associates ¹⁷ demonstrated that the postoperative ANP levels in their group ofpatients undergoing valve replacement showed a smaller increase in postoperativeANP response. They suggested that those findings were the result of a combinationof atrial damage and reduced atrial pressure caused by valve replacement oradaptation to chronic fluid overload; thus the valve-replacement group mighthave been more prone to fluid and salt retention. Our study demonstrates asignificant decrease in postoperative ANP levels in comparison with the preoperativeANP levels in both atria of the CMP group. As suggested previously, ¹ this finding may be the result ofa postoperative decrease in the ANP levels triggered by the multiple atriotomyincisions and excision of both atrial auricles. In patients with chronic AF,chronically elevated levels of ANP may lead to a resetting of the specificrenal receptors ⁷; the abruptpostoperative decrease of ANP levels therefore has a high possibility of beingthe cause of fluid retention. Cox and associates ⁶administered spironolactone to all patients after theoperation to prevent postoperative fluid retention, and Perera and associates ¹⁸ suggested the use of ANP afterthe CMP as a therapeutic possibility. The patients in our study did not haveany postoperative fluid retention despite the significant decrease in ANPlevels. We believe this is related to preoperative treatment of the patientswith diuretics because of some degree of congestive heart failure and postoperativetreatment with diuretics to maintain adequate urine output. There were nosignificant changes in the postoperative ANP levels in the CABG group. Fujiwaraand associates ⁹ showed agradual increase in ANP levels in patients with AF from the fourth hour to5 days after cardioversion, concomitant with an increase in atrial fillingfraction. They suggested recovery of atrial mechanical function as the mechanism.In our study, the ANP levels in the radial artery remained decreased untilthe seventh postoperative day. This suggests that atrial mechanical functionafter the CMP may need more time to recover.

Effect of recurrent AF on ANP levels.
Roy and associates ⁷demonstrated a decrease in ANP levels in patients with chronic AF after restorationto sinus rhythm and a significant increase in ANP levels during laboratory-inducedsupraventricular tachycardia. Dussaule and associates ¹⁹ observed decreases in ANP levels as well as in LApressures after percutaneous balloon valvuloplasty in patients with mitralstenosis without AF; however, the plasma ANP levels remained elevated in patientswith AF despite the decrease in LA pressure. They suggested that the inappropriateresponse of ANP to the decrease in the LA pressure was caused by the highfiring rate of the atria, abnormal stretch of the atrial wall, and largeratrial volume. These observations imply that recovery from the high firingrate of the atria in AF may also be an important factor in the decrease inANP levels, in addition to the CMP's multiple atriotomy incisions and excisionof both atrial auricles. AF recurred transiently in 32% of our patients, similarto rates in other reports. ^3,4,6 A comparisonof patients with transient postoperative recurrence of AF with those withoutrecurrence showed that postoperative ANP levels in the AF recurrence groupdid not increase significantly despite the AF, and there was no significantdifference in the ANP levels between the two groups with time. Data from ourstudy suggest that decreased ANP levels after the CMP may result from themultiple atriotomy incisions and excision of both atrial auricles, ratherthan from the conversion of AF to normal sinus rhythm.

Limitations.
Several limitations of our study must be recognized. First, there isno accepted world standard for measuring human ANP. ²⁰ Normal levels of immunoreactive ANP are hard todefine, not only because of the lack of assay standardization but also becausethe condition of subjects in whom normal values are measured varies withinand between studied populations. Factors such as the sodium-volume status,systemic blood pressure, posture, age, heart and renal function, and timeof sampling all affect the measurement. Second, the perioperative measurementof hemodynamic parameters and blood sampling for the ANP levels were not performedunder uniform conditions. Measurements obtained before the operation wereperformed with patients under general anesthesia, whereas those obtained afterthe operation were performed with patients in an awake state. This may makeit more difficult to interpret the significance of changes in various hemodynamicparameters and ANP levels. Third, the CABG group was used as a control groupto compare the postoperative changes in ANP levels. Taking into considerationthe multiple factors that may affect ANP levels, a non-CMP group with valvularheart disease and chronic AF would have been more suitable as a control group,but such a group would have been extremely difficult to incorporate into thestudy. Fourth, the comparison of patients with transient recurrence of AFwith those without recurrence of AF used a small sample size for each group,which may preclude valid statistical comparison of the effect of recurrenceof AF on changes in ANP levels.

	Conclusions

Top Abstract Introduction Patients and methods Results Discussion Conclusions Discussion References

 
Despite several limitations in our study as a clinical approach, wedemonstrated a statistically significant decrease in the ANP levels of bothatria after the CMP. This may be one of the causes of postoperative fluidretention. This decrease in ANP levels after the CMP may result from the multipleatriotomy incisions and excision of both atrial auricles, rather than fromthe conversion of AF to normal sinus rhythm.

	Discussion

Top Abstract Introduction Patients and methods Results Discussion Conclusions Discussion References

 
Dr. Tirone E. David (Toronto, Ontario, Canada). Not all patients retain fluid afterthe CMP. In our experience, which is limited to about 40 cases, I would saythat fewer than one in five require long-term diuretic therapy. They do retainfluid for the first 2 or 3 days, but every patient undergoing cardiopulmonarybypass does so. So there must be factors other than the ANP. Do you thinkthat ANP is perhaps just one of several factors? Are there not more factorsthat may play a role on this problem of fluid retention?

Dr. Kim. Postoperative fluid retentionwith pulmonary edema has been observed as one of the early postoperative complicationsafter the CMP in 12% to 36% of the patients. This incidence is higher thanthat among the other patients undergoing cardiopulmonary bypass. In our study,we demonstrated a significant decrease in the ANP levels after the CMP. Thesesuggest that the decreased ANP levels after the CMP may play an importantrole in the problem of further fluid retention. Fortunately, the patientsin our study did not have any significant postoperative fluid retention despitethe significant decrease in the ANP levels. We believe this is because ofpreoperative treatment with diuretics in response to some degree of congestiveheart failure and postoperative treatment with diuretics to maintain adequateurine output.

Dr. Yoshio Kosakai (Osaka, Japan). We have done the CMP on 270 patients from February1992 to February 1997. Research similar to yours was performed by our colleague,Dr. Yoshibara. In our results, the ANP value in the CMP group did not increaseafter the operation. This result was almost the same as yours. However, theANP value in our control group increased after the operation, because theatrial appendages of the control group were not removed. I think that ourresult is more reasonable than yours. My question is, what do you think aboutthis difference?

Dr. Kim. Do you mean that the ANP levelsin your control group are higher than those in ours?

Dr. Kosakai. Yes, the ANP of our controlgroup increased more after operation than in your results.

Dr. Kim. Did you have the same controlgroup as ours?

Dr. Kosakai. No. All diagnoses in ourcontrol group were valvular disease.

Dr. Kim. In our CABG group, the ANP levelsin the RA showed no change after the operation. This finding is a little differentfrom those of others, including yours. As I indicated in my limitations, thereare a couple of possible explanations for this difference. First, there isno accepted world standard for measuring human ANP. Second, a CABG group withrelatively small sample size was used as a control group, and this may precludevalid statistical comparison.

Dr. David. Your control group consistedsolely of patients undergoing CABG?

Dr. Kim. Yes.

Dr. David. You did not have patientsundergoing valvular procedures with similar problems?

Dr. Kim. No. Most of our patients undergoingvalvular procedures have AF, and I am doing the CMP in all the patients withvalvular heart disease with chronic AF, thromboembolic events, or LA thrombusbecause the CMP can cure chronic AF. So it was extremely difficult to usea non-CMP group with valvular heart disease and chronic AF as a control group.

Dr. Chi-Ming Wei (Baltimore, Md.). What kind of mechanism do you think decreasesANP? Did you also measure coronary sinus concentrations of ANP and compareaortic position for ANP? In your slides, you show that the decreases in bothRA and LA concentrations of ANP differ somewhat from the degree of ANP plasmaconcentration.

Did you also measure another natriuretic peptide, such as a brain natriureticpeptide? We know that the brain natriuretic peptide is important for the cardiacrelease of a natriuretic peptide hormone and is also an important contributorto fluid balance.

Dr. Kim. In answer to your first question,we did not measure the ANP levels in coronary sinus or aortic positions. Wemeasured the ANP levels in the RA and the radial artery. The RA preoperativeANP levels were about two times higher than those in the LA or radial artery,reflecting secretion of ANP into the coronary sinus and extraction by thelungs. We suggest that the decreased ANP levels after the CMP may result fromthe multiple atriotomy incisions and excision of both atrial auricles. Inresponse to the second question, we did not measure the brain natriureticpeptide level.

Dr. Akira T. Kawaguchi (Kanagawa, Japan). I have been wondering about the relationshipbetween decrease in ANP and the denervation of the heart that occurs afterthe CMP. I also wonder whether you see the ANP level come back up as the heartbecomes innervated again. I would like to know the relationship between denervationand innervation of the heart and the level of ANP.

Dr. Kim. Fujiwara and associates, ⁹ in the Journal of the American Collegeof Cardiology, showed a gradual increase in the ANP levels in patients withAF from the fourth hour to 5 days after cardioversion, concomitant with anincrease in LA filling fraction. In our study, the ANP levels in the radialartery remained decreased until the seventh postoperative day. We are notsure when the ANP levels return to normal. However, if we follow the suggestionof Fujiwara and associates, recovery of ANP secretion after the CMP wouldbe expected to be delayed more than after the cardioversion, because we observedthe restoration of the LA function a few months after the operation in mostof our patients.

Dr. David. Dr. Cox, would you care to comment on the importanceof this hormone in fluid retention. What is the proportion of patients thatretain fluid?

Dr. James L. Cox (St. Louis, Mo.). Ourresults are a bit different, although I have never reported them because Iam not sure that I can make any sense out of them. Our actual numbers correlatemore with Dr. Kosakai's, in that the ANP levels are elevated on the firstpostoperative day. By the second or third day after the operation, they areback to control levels. Thereafter they go down, but not as dramatically asin this series.

Having said that, the standard errors of these numbers are similar,in that if you plot each individual result it looks like a scattergram. Ithink one problem is perhaps in sampling. One of Dr. Kim's initial statementswas that there is no worldwide standard for measuring ANP levels, and I believethat this is a key to the confusion of results. Some of the samples are takenfrom the radial artery, some from the RA, some from the LA, and so on. Dr.Kim is to be congratulated for his efforts to systematizing sampling in thehope of obtaining more meaningful results.

What we do know is that these patients do retain fluid more aggressivelyafter the operation than do patients undergoing CABG or valvular procedures.They are more comparable with the patients we used to operate on years agowho had severe mitral stenosis and retained a lot of fluid after the operation.Whether the tendency toward excessive fluid retention after the CMP is a problemwith ANP, some alteration in the renin-angiotensin system, or a problem withdenervation of the heart, I do not know. However, because of this tendency,we started routine use of spironolactone.

I would advise surgeons who are doing this procedure to be aggressiveabout putting these patients on some regimen to reverse their tendency toretain fluid. I generally leave patients on regimen of spironolactone for6 weeks and handle additional diuretic needs with furosemide (Lasix).

	References

Top Abstract Introduction Patients and methods Results Discussion Conclusions Discussion References

 

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				K. Tanaka, S. Satake, S. Saito, S. Takahashi, Y. Hiroe, Y. Miyashita, S. Tanaka, M. Tanaka, and Y. Watanabe A new radiofrequency thermal balloon catheter for pulmonary vein isolation J. Am. Coll. Cardiol., December 1, 2001; 38(7): 2079 - 2086. [Abstract] [Full Text] [PDF]

				A. Albage, J. van der Linden, L. Bengtsson, D. Lindblom, G. Kenneback, and H. Berglund Elevations in antidiuretic hormone and aldosterone as possible causes of fluid retention in the Maze procedure Ann. Thorac. Surg., July 1, 2001; 72(1): 58 - 64. [Abstract] [Full Text] [PDF]

				K.-B. Kim, J.-H. Huh, C. H. Kang, H. Ahn, and D.-W. Sohn Modifications of the Cox-Maze III procedure Ann. Thorac. Surg., March 1, 2001; 71(3): 816 - 822. [Abstract] [Full Text] [PDF]

				R. C. Millar, J. M. Arcidi Jr, and P. J.M. Alison The maze III procedure for atrial fibrillation: should the indications be expanded? Ann. Thorac. Surg., November 1, 2000; 70(5): 1580 - 1586. [Abstract] [Full Text] [PDF]

				N. Yoshimura, M. Yamaguchi, Y. Oshima, S. Oka, Y. Ootaki, T. Hasegawa, and C. Shimazu Suppression of the secretion of atrial and brain natriuretic peptide after total cavopulmonary connection J. Thorac. Cardiovasc. Surg., October 1, 2000; 120(4): 764 - 769. [Abstract] [Full Text] [PDF]

				A. Rossi, M. Enriquez-Sarano, J. C. Burnett Jr., A. Lerman, M. D. Abel, and J. B. Seward Natriuretic peptide levels in atrial fibrillation: A prospective hormonal and Doppler-echocardiographic study J. Am. Coll. Cardiol., April 1, 2000; 35(5): 1256 - 1262. [Abstract] [Full Text] [PDF]

				F. Yoshihara, T. Nishikimi, Y. Sasako, J. Kobayashi, Y. Kosakai, R. Hattori, T. Horio, S. Kitamura, H. Matsuo, T. Ohe, et al. PRESERVATION OF THE RIGHT ATRIAL APPENDAGE IMPROVES REDUCED PLASMA ATRIAL NATRIURETIC PEPTIDE LEVELS AFTER THE MAZE PROCEDURE J. Thorac. Cardiovasc. Surg., April 1, 2000; 119(4): 790 - 794. [Abstract] [Full Text] [PDF]

				T. Nitta, R. Lee, R. B. Schuessler, J. P. Boineau, and J. L. Cox Radial approach: a new concept in surgical treatment for atrial fibrillation I. Concept, anatomic and physiologic bases and development of a procedure Ann. Thorac. Surg., January 1, 1999; 67(1): 27 - 35. [Abstract] [Full Text] [PDF]

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