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Objectives The effects of ablation lines on myocardial innervation and response to autonomic stimuli are unclear. This study examined the effects of radiofrequency ablation on atrial autonomic innervation and compared pulmonary vein isolation and the biatrial Cox maze procedure. Methods In 12 acute canines right and left vagosympathetic trunks and right and left stellate ganglia were isolated. Each nerve was stimulated before bipolar ablation, after pulmonary vein isolation, and after the Cox maze procedure. Nadolol (n = 6) and atropine (n = 6) were administered to block sympathetic and parasympathetic responses, respectively. Changes in heart rate and atrioventricular interval were compared. Changes in QRST area relative to an isoelectric baseline (index of local innervation) were calculated. Results Sympathetic stimulation of each nerve and parasympathetic stimulation of the vagosympathetic trunks caused significant changes in heart rate and atrioventricular interval. After pulmonary vein isolation, the effect of 33% of the nerves on heart rate changes was eliminated. The Cox maze procedure eliminated right stellate sympathetic effects on heart rate. Fifty percent of the nerves caused heart rate changes after the Cox maze procedure. There was no significant effect of either lesion set on atrioventricular interval changes. Stimulation of 50% of nerves after pulmonary vein isolation produced local area changes significantly different from control area. After the Cox maze procedure, a different 50% of the nerves produced local changes different from those seen after pulmonary vein isolation. Conclusions Surgical ablation procedures disrupted innervation, affecting heart rate but not atrioventricular interval. Autonomic innervation affecting the atria was changed by pulmonary vein isolation and additionally by the Cox maze procedure. Residual autonomic effects were present even after the complete Cox maze procedure.

Objective The Cox maze procedure was introduced in 1987 for the treatment of atrial fibrillation. This study evaluated the predictors of late atrial fibrillation recurrence in 276 consecutive patients who underwent this procedure at our institution. Methods From 1987 through June 2003, 276 patients (79 female and 197 male patients; mean age, 55 ± 11 years) underwent the Cox maze procedure. Thirty-three patients had Cox maze procedure I, 16 patients had Cox maze procedure II, and 197 patients had Cox maze procedure III. The last 30 patients underwent a modified procedure (Cox maze procedure IV) with bipolar radiofrequency ablation. There were 113 (41%) patients who had a concomitant operation, most commonly either a mitral valve procedure (19%) or coronary artery bypass grafting (20%). Data were analyzed by means of univariate analysis, with preoperative and perioperative variables used as covariates. Patient follow-up was conducted by means of questionnaire, physician examination, and electrocardiographic documentation. All patients had a minimum of 6 months of follow-up. Results Patient follow-up was achieved in 92.8% of cases, with a mean follow-up time of 5.8 ± 3.6 years. Risk factors for late atrial fibrillation recurrence were duration of preoperative atrial fibrillation ( P = .01) and Cox maze procedure version ( P = .001). There was no difference in actuarial 10-year survival between the Cox maze procedure versions. Conclusion The Cox maze procedure remains the gold standard for the treatment of atrial fibrillation and has excellent long-term efficacy. The most significant predictor of late recurrence was duration of preoperative atrial fibrillation, suggesting that earlier surgical intervention would further increase efficacy.

Background For the last decade, the Cox maze III procedure has been available for the treatment of atrial fibrillation. It is unknown whether the operation has similar efficacy in patients with lone atrial fibrillation compared with that in patients with atrial fibrillation associated with coronary, valve, or congenital heart disease. This study examined the long-term outcome of patients who underwent this procedure either as a lone operation or as a concomitant procedure. Methods From 1988 to 2001, 198 patients underwent a Cox maze III procedure; 112 were lone operations, and 86 were concomitant procedures. Major complications included renal failure, reoperation for bleeding, mediastinitis, stroke, and balloon pump insertion. Follow-up was performed by means of mail and telephone questionnaires with both the patients and their cardiologists. All patients who had any history of arrhythmia or who were taking medication had their rhythm documented by means of electrocardiography. Results The lone operation group was significantly younger (51.3 ± 10.5 vs 58.8 ± 9.9 years) and had a higher male/female ratio (4:1 vs 2:1). There was no difference in operative mortality between groups (1.8% vs 1.2%). At a follow-up of 5.4 ± 2.9 years, 96.6% (172/178) of all patients were free of atrial fibrillation. There was no difference between the lone operation and concomitant procedure groups (95.9% vs 97.5%). Conclusion The Cox maze III procedure has equivalent operative risk and long-term efficacy in patients undergoing both lone operations and concomitant procedures. The Cox maze III procedure remains the standard against which alternative procedures for atrial fibrillation must be judged.

Background A significant number of patients presenting for coronary revascularization have chronic atrial fibrillation. Although the Cox maze III procedure is the gold standard for the surgical treatment of this arrhythmia, few of these patients undergo atrial fibrillation operations at the time of their coronary bypass grafting. This study examined the long-term outcome of patients with ischemic heart disease who underwent the Cox maze procedure at our institution. Methods From 1990 to 2002, 47 patients undergoing operations for ischemic heart disease underwent a concomitant Cox maze III procedure. All patients underwent coronary bypass grafting, and 7 (15%) patients underwent coronary bypass grafting plus a mitral valve repair. Follow-up was performed by means of mail and telephone questionnaires with both the patients and their cardiologists. All patients who had any history of arrhythmia or who were taking medications had their rhythm documented by electrocardiogram. Results The mean age of these patients was 62 ± 8 years, with a marked male predominance (45 men and 2 women). Twenty-eight (60%) of the patients had paroxysmal atrial fibrillation, and the remainder had persistent arrhythmias. The mean duration of atrial fibrillation was 7.6 ± 6.5 years. The operative mortality in this series was 2%. Nine (19%) patients required postoperative pacemakers. At last follow-up (mean of 5.7 ± 3.3 years), 98% of patients were free of atrial fibrillation. Conclusion The Cox maze III procedure has a low operative mortality and excellent long-term efficacy in patients with ischemic heart disease. These data suggest a more widespread use of this procedure in these patients.

Background: Postoperative atrial flutter has been observed in approximately 10% of children undergoing lung transplantation at our institution. We hypothesized that the left atrial anastomoses made to establish pulmonary venous continuity provide the primary electrophysiologic substrates for atrial flutter. Objectives: Our objectives were (1) to determine whether the left atrial suture lines alone are sufficient to produce atrial flutter in an acute canine model of lung transplantation and (2) to characterize any resulting reentrant circuits to surgically ablate the atrial flutter. Methods: Supported by cardiopulmonary bypass, adult dogs ( n = 10) underwent bilateral pneumonectomies. The left atrial anastomotic suture lines were simulated by dividing the tissue between the ostia of the transected superior and inferior pulmonary veins and closing the resulting defects. Bilateral suture lines were placed in group 1 ( n = 6) to simulate bilateral lung transplantation. In group 2 ( n = 4), only a left-sided suture line was placed to represent single lung transplantation. Unipolar 253-point biatrial endocardial mapping electrodes were inserted via bilateral ventriculotomies. Atrial flutter was induced by atrial burst pacing, and activation sequence maps were generated. In five of six cases in group 1, a T-incision connecting the two suture lines and the mitral anulus was then made. In group 2, a single incision from the suture line to the mitral anulus was performed in each case. Burst pacing was subsequently repeated. Results: Atrial flutter could not be induced after bypass alone in any case. After simulated lung transplantation, sustained atrial flutter was reproducibly induced in 10 of 10 dogs. The mean cycle length in all dogs was 133 ± 7 msec. There was no significant difference in mean cycle length or activation sequence patterns between groups 1 and 2. The reentrant circuit was confined to the left atrium. Each simulated left atrial anastomosis created a zone of conduction block around which circus movement could occur. In group 1, either suture line functioned as the central obstacle. Atrial flutter was terminated in five of five dogs in group 1 by means of the T-incision and in all four dogs in group 2 with the incision connecting the suture line to the mitral anulus. Conclusions: (1) In an acute canine model of lung transplantation, each left atrial suture line alone provides an electrophysiologic substrate for atrial flutter by creating a zone of conduction block around which circus movement can occur. (2) Extending this zone of block to the mitral anulus, together with interruption of the isthmus of tissue between the two suture linespresent after bilateral lung transplantation, terminates the atrial flutter in this model and may have an application prophylactically at the time of lung transplantation in children to prevent postoperative atrial flutter. (J Thorac Cardiovasc Surg 1996;112:992-1001)

Background: Lateral tunnel total cavopulmonary connection, also called the modified Fontan operation, uses a baffle through the right atrium. We established, in an acute canine model, that atrial flutter after total cavopulmonary connection revolves around a line of conduction block imposed by the free wall lateral tunnel suture line. We hypothesized that a line of conduction block between the free wall total cavopulmonary connection suture line and the tricuspid anulus would interrupt atrial flutter in this model. Objective: Our objective was to determine whether a cryolesion placed between the free wall total cavopulmonary connection suture line and the tricuspid anulus would terminate atrial flutter in an acute canine model. Methods: Seven adult dogs underwent median sternotomy and institution of cardiopulmonary bypass. A suture line was placed through a right atriotomy to simulate total cavopulmonary connection lateral tunnel construction. Form-fitting 253-point biatrial endocardial mapping electrodes were placed via bilateral ventriculotomies. Atrial flutter was induced by atrial burst pacing. A cryothermal lesion was then placed between the free wall total cavopulmonary connection suture line and the tricuspid anulus in the low lateral right atrium (i.e., CRYO 1 procedure), and reinduction of atrial flutter was attempted. If atrial flutter was reinduced, the cryolesion was modified superiorly to include the caudal portion of the atriotomy (i.e., CRYO 2 procedure). Activation sequence maps were generated for sinus rhythms before and after the cryolesions were placed and for induced arrhythmias. Results: In all seven cases, atrial flutter was inducible after suture line placement, before placement of a cryolesion. The reentrant circuit incorporated both caval orifices in five of seven cases and was successfully ablated by the CRYO 1 approach in each case. Atrial flutter was not inducible after placement of the CRYO 2 lesion in the remaining two cases, in which breakthrough of the wave front occurred across the lateral tunnel suture line in the intercaval region. Activation sequence maps of sinus rhythm after placement of the cryolesions demonstrated a conduction block at the site of the lesion. Conclusions: A linear cryothermal lesion placed between the free wall aspect of the total cavopulmonary connection suture line and the tricuspid anulus created a line of conduction block that successfully ablates atrial flutter in the canine model. (J T HORAC C ARDIOVASC S URG 1996;112:898-907)

Intraatrial reentrant tachycardia, or atrial flutter, is a common postoperative problem after Fontan repair, which involves an atriopulmonary connection. A modification of Fontan repair, total cavopulmonary connection, minimizes the portion of the right atrium exposed to stretch and hypertension; however, atrial flutter continues to occur after this procedure. We postulated that the intraatrial lateral tunnel suture line of total cavopulmonary connection, in the absence of physiologic alterations such as atrial hypertension or stretch, provides the necessary electrophysiologic substrate for atrial flutter. The purpose of this study was to produce a canine model of total cavopulmonary connection (1) to establish that the intraatrial suture line alone is sufficient to permit sustained atrial flutter and (2) to characterize the pathways of resulting reentrant arrhythmias. After induction of general anesthesia, 25 to 30 kg dogs ( n = 17) underwent median sternotomy, cradling of the pericardium, and placement of a pacing electrode on the right atrial appendage. Normothermic cardiopulmonary bypass was initiated. The total cavopulmonary connection suture line was placed through a standard right atriotomy, simulating construction of the lateral tunnel. After closure of the atriotomy, 253 point unipolar atrial endocardial form-fitting electrodes were placed through bilateral ventriculotomies. By means of atrial burst pacing and programmed extrastimulation, induction of atrial flutter was attempted. If atrial flutter could not be induced, isoproterenol was infused and the stimulation protocol was repeated. After induction of atrial flutter, mapping of the activation sequence was performed. Before suture line placement, no dog had inducible atrial flutter. After placement of the suture line, sustained atrial flutter was reproducibly induced in every dog, although isoproterenol was required for this in three (17.6%). The mean flutter cycle length was 177 ± 30 msec. In each case, the atrial flutter circuit was limited to the right atrium, with the left atrium being passively activated. The atrial flutter circuit was dependent on a corridor of myocardium that resulted from conduction block on the free wall, created by the lateral margin of the total cavopulmonary connection. In no case was the atriotomy integral to the atrial flutter circuit. This study establishes that the total cavopulmonary connection baffle suture line alone, without alteration in circulatory physiology, creates a sufficient anatomic substrate for atrial flutter in a short-term canine model. Delineation of the anatomic boundaries of the reentrant circuit raises the possibility of targeting areas within the circuit that could be modified, potentially reducing the incidence of postoperative atrial flutter after total cavopulmonary connection. (J T HORAC C ARDIOVASC S URG 1996;111:514-26)

The original maze procedure that was described for the treatment of patients with atrial fibrillation was followed by an unacceptable incidence of two problems: (1) the frequent inability to generate an appropriate sinus tachycardia in response to maximal exercise and (2) occasional left atrial dysfunction. In an effort to overcome these problems, we modified the original technique (maze I) twice. The results of these modifications culminated in the maze III procedure, which is associated with a higher incidence of postoperative sinus rhythm, improved long-term sinus node function, fewer pacemaker requirements, less arrhythmia recurrence, and improved long-term atrial transport function. In addition, the maze III procedure is technically less demanding than either the maze I or maze II procedure. Therefore, the maze III procedure is now the technique of choice for the management of medically refractory atrial fibrillation. (J T HORAC C ARDIOVASC S URG 1995;110:473-84)

The operative technique of the maze III procedure for the treatment of patients with medically refractory atrial flutter and atrial fibrillation is described in a sequential fashion. The accompanying diagrams of the procedure are illustrated from the view of the operating surgeon. (J THORAC CARDIOVASC SURG 1995;110:485-95)

The purpose of this study was to test the assumption that the cause for postoperative atrial flutter/fibrillation after cardiopulmonary bypass is inadequate atrial myocardial protection. Dogs were subjected to cardioplegic arrest for 60 minutes without augmented atrial hypothermia (seven dogs, control group) or augmented atrial hypothermia with topical atrial cooling (seven dogs, study group). Twenty-five electrodes (15 on the right atrium and 10 on the left atrium) were fixed on the atria to measure effective refractory period and conduction time. Data were taken before bypass, immediately after bypass, and 2 hours after bypass. During cardioplegic arrest the mean temperatures measured in the atria were significantly lower (p less than 0.001) in the study group (13.5 degrees +/- 7.0 degrees C) than in the control group (23.7 degrees +/- 3.2 degrees C). There was no significant change in the mean effective refractory period after bypass in the control or study groups or in the prevalence of inducibility of atrial flutter/fibrillation by extrastimulation (3/7 dogs in the control group and 2/7 in the study group). During right atrial pacing, total conduction times were significantly longer (p less than 0.025 at cycle lengths of 300 and 350 msec) in the control group (74 +/- 5 msec and 75 +/- 7 msec, respectively) than in the study group (65 +/- 9 msec and 64 +/- 8 msec, respectively) immediately after bypass. Two hours after bypass, however, there were no significant differences under the same conditions between the two groups. There were no significant differences in conduction during left atrial pacing after bypass. Comparing those atria that were inducible with those not inducible demonstrated a significantly increased dispersion of effective refractory period (90 +/- 23 msec versus 74 +/- 18 msec, p less than 0.05) and increased conduction time in the inducible group. We concluded that augmented atrial hypothermia during cardioplegic arrest had no effect on the inducibility of fibrillation, had no effect on repolarization, and had only a small effect on conduction, which resolved within 2 hours after bypass. However, the study demonstrates that when the atria are inducible the substrates are an increased dispersion of refractoriness and a prolongation of conduction time.

Discrete cryosurgical modification of atrioventricular conduction abolishes refractory atrioventricular node reentry tachycardia with preservation of antegrade atrioventricular nodal conduction. This procedure presently requires cardiopulmonary bypass. To modify atrioventricular conduction without cardiac surgery, we evaluated the electrophysiologic effects of cryolesions applied to the peri-nodal area in the closed heart in 16 dogs before operation, during cryothermic exposure, and at 1 hour and 3 hours after operation. The electrophysiologic effects were evaluated in 10 of the 16 dogs at 2 weeks postoperatively. The dogs were given general anesthetics, and a cryoprobe was introduced into the right atrial cavity through the right atrial appendage. Cryolesions (-60 degrees C) were placed at nine to eleven preselected points around the perinodal area guided by electrodes on the tip of the cryoprobe. Postoperatively, there were significant prolongations of the atrio-His interval, Wenckebach's point, effective refractory period, and functional refractory period of the atrioventricular node. Atrial echo beats were eliminated or decreased in frequency. There was also a significant increase in retrograde ventriculoatrial conduction time. In the long-term observation period the atrio-His intervals remained significantly prolonged in comparison with the preoperative values, the atrial echoes progressively decreased, and ventriculoatrial conduction was absent in five of seven animals. A serendipitous atrioventricular node reentry tachycardia that was inducible in one animal with dual atrioventricular node conduction pathways was successfully eliminated and was not inducible at 2 weeks postoperatively. Complete atrioventricular block occurred during attempts to produce greater atrio-His prolongation in three of the 16 animals and persisted in two for the 2-week period of observation. Closed heart intracardiac cryomodification of atrioventricular conduction is feasible, with the cryoprobe in normothermic blood, producing changes in atrioventricular conduction similar to the open cardiac procedure.

On the basis of the known electrophysiologic mechanisms of atrial fibrillation, multiple surgical procedures were designed and tested in dogs to determine the feasibility of developing a surgical cure for human atrial fibrillation. These experimental studies culminated in a surgical approach that effectively creates an electrical maze in the atrium. The atrial incisions prevent atrial reentry and allow sinus impulses to activate the entire atrial myocardium, thereby preserving atrial transport function postoperatively. Since September 1987, this surgical procedure has been applied in seven patients, five with paroxysmal atrial fibrillation of 2 to 9 years' duration and two with chronic atrial fibrillation of 3 and 10 years' duration. All seven patients have been cured of atrial fibrillation and none is receiving any postoperative antiarrhythmic medications.

Computerized mapping of atrial fibrillation was performed in animals and man. To study atrial fibrillation in a systematic manner, we developed a clinically relevant experimental model of atrial fibrillation. Chronic mitral regurgitation was created surgically in 25 dogs without opening the pericardium. After several months of chronic mitral regurgitation, the atria became enlarged and sustained atrial fibrillation could be induced by standard programmed electrical stimulation techniques. Computerized isochronous activation maps of the atria were recorded during atrial fibrillation from 208 bipolar electrodes simultaneously. In a parallel study, human atrial fibrillation was mapped with a separate 160-channel intraoperative mapping system in patients with paroxysmal atrial fibrillation who were undergoing surgical correction of the Wolff-Parkinson-White syndrome. The canine activation sequence maps demonstrated a spectrum of rhythm abnormalities ranging from simple atrial flutter to complex atrial fibrillation. They also showed that macroreentrant circuits within the atrial myocardium were responsible for the entire spectrum of arrhythmias. Atrial reentry was also documented during human atrial fibrillation. All patients had nonuniform conduction around regions of bidirectional block in both atria resulting in multiple discrete wave fronts. In addition, six patients had a single reentrant circuit in the right atrium in which bidirectional block of the activation wave front occurred along the sulcus terminals between the venae cavae. The left atrium in all patients demonstrated multiple wave fronts and conduction block, but left atrial reentry could not be detected. Both the experimental study and the clinical study demonstrated that multiple wave fronts, nonuniform conduction, bidirectional block, and large (macroreentrant) reentrant circuits occur during atrial fibrillation. The presence of macroreentrant circuits and the absence of either microreentrant circuits or evidence of atrial automaticity suggests that atrial fibrillation should be amenable to surgical ablation.

Atrial fibrillation is a common arrhythmia that is frequently resistant to medical therapy and has no satisfactory surgical therapy. The development of an effective surgical procedure to treat atrial fibrillation has been hampered by the paucity of clinically relevant information on the basic mechanisms responsible for the arrhythmia. This paper summarizes the current concepts of the electrophysiologic abnormalities in atrial flutter and fibrillation.

Surgical isolation of the body of the right atrium presents a unique hemodynamic situation in which the synchronous right atrial contraction (kick) is lost but the synchronous left atrial contraction is preserved. The hemodynamic effects of this procedure were evaluated by pacing at selected atrial sites postoperatively to simulate (1) sinus rhythm with a synchronous right atrial kick, (2) sinus rhythm without a synchronous right atrial kick, (3) right atrial tachycardia propagated to the entire heart (propagated right atrial tachycardia), and (4) right atrial tachycardia confined to the isolated right atrium with sinus rhythm in the rest of the heart (confined right atrial tachycardia). Hemodynamic data recorded under these four conditions showed that (1) during sinus rhythm, synchrony of right atrial contraction had no significant effect on any of the hemodynamic parameters studied and (2) conversion from propagated right atrial tachycardia to confined right atrial tachycardia resulted in an increase in mean arterial pressure (65 +/- 5 to 78 +/- 3 mm Hg, p less than 0.005) and stroke volume index (9 +/- 1 to 19 +/- 3 ml/beat/m2, p less than 0.005) with a decrease in left atrial pressure (9 +/- 2 to 5 +/- 1 mm Hg, p less than 0.05) and right atrial pressure (6 +/- 1 to 5 +/- 1 mm Hg, p less than 0.05). Moreover, cardiac hemodynamic performance remained within normal limits for up to 14 weeks. Thus the right atrial isolation procedure does not adversely affect cardiac hemodynamics despite the loss of synchronous right atrial contraction during sinus rhythm, and the procedure prevents hemodynamic deterioration during right atrial tachycardia.

This study describes the surgical technique and electrophysiologic effects of isolating the right atrium while preserving normal function and continuity of the sinoatrial node with the remainder of the heart. Thirteen adult mongrel dogs underwent normothermic cardiopulmonary bypass. A posterorlateral right atriotomy was performed that encircled the upper right atrium but excluded the atrial pacemaker complex. The incision was extended anteromedially to the tricuspid valve anulus just anterior to the membranous interatrial septum and inferiorly just posterior to the os of the coronary sinus and the tricuspid valve anulus. Postoperatively, electrophysiologic data confirmed (1) that the body of the right atrium was electrically isolated from the remainder of the heart, (2) that the sinoatrial node continued to function normally, and (3) that the sinoatrial node remained in continuity with the left atrium and ventricles. Right atrial tachycardia was simulated by rapid right atrial pacing and was confined to the isolated right atrium. Moreover, the simulated tachycardia did not affect normal sinus rhythm or normal atrioventricular conduction. It is concluded that isolation of the right atrium with preservation of normal sinoatrial node function and continuity is feasible. This technique offers an alternative to the current surgical approaches for management of refractory supraventricular tachycardias that arise in the right atrium.

Background: Although the implantable cardioverter-defibrillator effectively prevents sudden cardiac death, patients are still prone to recurrence of ventricular tachyarrhythmias. Electrophysiologically guided surgery is the most effective modality in abolishing ventricular tachycardia, having a lower recurrence rate than pharmacologic therapy or catheter ablation. Return cycle mapping after entrainment has been shown to localize the central common pathway, which is the target region for ablation, without pacing at the pathway or recording the potentials from the pathway. Methods: To determine the accuracy and usefulness of return cycle mapping in surgery for ventricular tachycardia, we cryoablated 8 morphologies of ventricular tachycardia induced in postinfarction dogs with the guidance of return cycle mapping. The ventricular tachycardia was entrained from 3 to 5 different epicardial sites at a paced cycle length 10 to 20 ms shorter than the ventricular tachycardia cycle length and the epicardium was mapped with 61 unipolar electrodes during cessation of entrainment to construct return cycle maps. The return cycle was determined by subtracting the first activation time from the second activation time after the last stimulus in each electrode location, and the maps were then displayed on a computer. Results: The total analysis process was completed within 3 minutes by means of a computer with custom-made programs. The activation map during ventricular tachycardia did not localize the central common pathway in any morphology of ventricular tachycardia, because the pattern of activation was concentric and diastolic potentials were not recorded. Cryoablation of the region where the isotemporal lines of the return cycle equal to the ventricular tachycardia cycle length intersected resulted in termination of ventricular tachycardia in all morphologies. The intersection was 26 ± 9 mm from the earliest activation site. Epicardial mapping with 253 electrodes during cryothermia showed that the region localized by return cycle mapping was the central common pathway sandwiched between the lines of conduction block and that the cryolesion connected the lines of block, blocked the rotating wave front, and resulted in termination of the ventricular tachycardia. Conclusion: Return cycle mapping provides an accurate and rapid means of localizing the central common pathway without the need for recording potentials from the pathway or pacing at the pathway in ablation for ventricular tachycardia. (J Thorac Cardiovasc Surg 2001;121:249-58)