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Background Heart rate (HR) and rhythm disturbances are common after cardiac surgery. This study tests the hypothesis that the inflammation caused by cardiac surgery is an underlying mechanism for postoperative changes in HR, rhythm, and HR variability (HRV). Method And Results Normal canines (n = 6 per group) were divided into 4 groups: (1) anesthesia, (2) sternotomy and pericardiotomy, (3) atriotomy, and (4) corticosteroids combined with an atriotomy. Continuous electrocardiographic recordings were done preoperatively and for 3 postoperative days. Electrophysiologic testing was done at the initial and terminal surgeries. C-reactive protein level was assessed at each study day, and tissue myeloperoxidase activity was assessed at the terminal study. Measurements of HRV were determined daily to detect changes in autonomic tone. Postoperatively, the HR increased in the pericardiotomy ( P = .0005) and atriotomy ( P = .001) groups and HRV decreased in both the groups. No significant change occurred in either the HR or HRV in the anesthesia ( P = .52) and steroid ( P = .16) groups. HRV (triangular index) on postoperative day 3 was correlated with the tissue myeloperoxidase levels ( r = − .83; P = .0004). Autonomic blockade with atropine and esmolol resulted in an HR and HRV that were not significantly different between groups. Atrial premature beats occurred postoperatively in the all the groups except the anesthesia group and were independent of the degree of inflammation. Conclusion Cardiac surgery increases the postoperative HR by reducing HRV, mostly because of a reduction in vagal tone. Furthermore, the magnitude of these changes is dependent on the degree of inflammation and is normalized by corticosteroids.

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.

Isopotential maps during the QRS interval demonstrate complex, non-dipolar distributions of the cardiac electrical field as it is projected onto the body surface. Correlations have been made in which the cardiac generator distribution and torso-isopotential distribution were related. These correlations suggest the specific torso-isopotential distributions and their evolution can be related to specific local events in ventricular activation.

Although the ventricular muscle band (VMB) is formed by one continuous band of myocardium and there is some evidence to suggest that it may contract sequentially along its course from the right ventricle, through the septum, then along its basoapical left ventricular spiral, the structure is not activated in this sequence. Activation as programmed by the fully developed Purkinje system proceeds broadly and directly from endocardium to epicardium and from apex to base. Although not activated sequentially along its course, the band may still contract and relax sequentially if there is a progressive lengthening of the contraction duration in association with a nonuniform lengthening of the cardiac fiber action potential (repolarization) duration. Also, the systolic and diastolic functions of the band should be considered as part of a complex, integrated electromechanical system in which the activation is programmed to ensure optimal function.

Background— Atrial fibrillation (AF) is common after cardiac surgery. Abnormal conduction is an important substrate for AF. We hypothesized that atrial inflammation alters atrial conduction properties. Methods and Results— Normal mongrel canines (n=24) were divided into 4 groups consisting of anesthesia alone (control group); pericardiotomy (pericardiotomy group); lateral right atriotomy (atriotomy group); and lateral right atriotomy with antiinflammatory therapy (methylprednisolone 2 mg/kg per day) (antiinflammatory group). Right atrial activation was examined 3 days after surgery. Inhomogeneity of conduction was quantified by the variation of maximum local activation phase difference. To initiate AF, burst pacing was performed. Myeloperoxidase activity and neutrophil cell infiltration in the atrial myocardium were measured to quantify the degree of inflammation. The inhomogeneity of atrial conduction of the atriotomy and pericardiotomy groups was higher than that of the control group (2.02±0.10, 1.51±0.03 versus 0.96±0.08, respectively; P P P =0.012). There also were significant differences in myeloperoxidase activity between the atriotomy and pericardiotomy groups and the control group (0.72±0.09, 0.41±0.08 versus 0.18±0.03 ΔOD/min per milligram protein, respectively; P P r =0.851, P Conclusions— The degree of atrial inflammation was associated with a proportional increase in the inhomogeneity of atrial conduction and AF duration. This may be a factor in the pathogenesis of early postoperative AF. Antiinflammatory therapy has the potential to decrease the incidence of AF after cardiac surgery.

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.

This study reports the comparative quantitative, morphological, and electrophysiological properties of two pacemaker cell types, spider and spindle-shaped cells, isolated from the rabbit sinoatrial node. Isolated nodal cells were studied with perforated and ruptured patch whole cell recording techniques. The basic spontaneous cycle length of the spider cells was 381 ± 12 ms, and the basic spontaneous cycle length of the spindle cells was 456 ± 17 ms ( n = 12, P < 0.05). The spider cells had a more positive maximum diastolic potential (−54 ± 1 mV) compared with the spindle cells (−68 ± 1mV, P < 0.05). The overshoot and action potential amplitudes were also smaller in the spider cells. The hyperpolarization-activated inward ( I f) current density, measured from their tail currents, was 15 ± 1.3 pA/pF for the spider cells and 9 ± 0.7 pA/pF for the spindle cells ( P < 0.01). I f current activation voltage was more positive in the spider cells than the spindle cells. Isoproterenol (1 μM) decreased the spontaneous cycle length of the spider cells by 28 ± 3% and the spindle cells by 20 ± 1.5% ( P < 0.05). Acetylcholine (0.5 μM) hyperpolarized the membrane potential of the spider cells to −86 ± 0.7mV and the spindle cells to −76 ± 0.8 mV ( P < 0.05). In summary, there are at least two distinct pacemaker cell types in the sinus node with different electrophysiological characteristics.

Background . The maze procedure cures atrial fibrillation; however, it isolates the pulmonary vein area and results in discordant activation in certain adjacent left atrial segments, which affects left atrial function. To preserve a more physiologic atrial transport function, we developed a new concept of surgical treatment for atrial fibrillation—the radial approach. The atrial incisions radiate from the sinus node toward the atrioventricular annular margins to allow a more physiologic atrial activation sequence and parallel the atrial coronary arteries to preserve blood supply to most atrial segments. Methods . We examined the atrial coronary arteries and the activation sequence during sinus rhythm in normal canine hearts to design the atrial incisions according to the concept of a radial approach. Results . The pattern of coronary artery distribution was centripetal, branching from the right coronary or left circumflex coronary artery at the right or left atrioventricular groove and spreading toward the sinus node. The endocardial mapping of the atria disclosed some important findings in designing the atrial incisions of the radial approach: the activation sequence at the left atrial septum and at the posterior left atrium between the pulmonary vein orifices. The atrial incisions were designed according to these findings. Conclusions . The radial approach may represent a more physiologic atrial transport function.

Abstract —Electrical coupling of pacemaker cells at gap junctions appears to play an important role in sinus node function. Although the major cardiac gap junction protein, connexin43 (Cx43), is expressed abundantly in atrial and ventricular muscle, its expression in the sinus node has been a subject of controversy. The objectives of the present study were to determine whether Cx43 is expressed by sinus node myocytes, to characterize the spectrum of connexin expression phenotypes in sinus node pacemaker cells, and to define the spatial distribution of different connexin phenotypes in the intact sinus node. To fulfill these objectives, we performed high-resolution immunohistochemical analysis of disaggregated adult canine sinus node preparations. Using enhanced tissue preservation and antigen retrieval techniques, we also performed immunohistochemical studies on sections of intact canine sinus node tissue. Analysis of disaggregated sinus node preparations revealed three populations of pacemaker cells distinguished on the basis of connexin immunohistochemical phenotype: ≈55% of cells expressed only connexin40 (Cx40); 30% to 35% of cells expressed Cx43, connexin45 (Cx45), and Cx40; and the remaining cells had no detectable connexin expression. In immunostained sections of intact sinus node, Cx43- and Cx45-positive cells were limited in their distribution and were observed in discrete bundles that appeared to abut atrial myocytes. In contrast, Cx40 immunoreactive signal was widely distributed in the sinus node region. These results indicate that subsets of pacemaker cells express distinct connexin phenotypes. Differential expression of connexins could create regions within the sinus node with different conduction properties, thereby contributing to the nonuniform conduction properties seen in this tissue.

Atrial flutter (AFL) is a common problem in children who have undergone a Fontan operation for single ventricle physiology. Although this has been attributed to the atrial stretch inherent in the earlier forms of this operation, AFL has persisted in spite of a modification that minimizes atrial distension. Therefore, it was hypothesized that AFL following the modified Fontan procedure may result from anatomic barriers related to suture lines rather than from atrial stretch or hypertension. In a series of experiments performed in dogs under general anesthesia, the modified Fontan repair was simulated by placing only the suture line of the intra-atrial repair. No baffle was placed, thus avoiding any hemodynamic alterations. After closure of the atriotomy, 253 point unipolar atrial endocardial form-fitting electrodes were inserted through the mitral and tricuspid valves via bilateral ventriculotomies. Induction of AFL was attempted with atrial burst pacing and programmed extrastimulation, and activation sequence maps of subsequent reentry were generated from the endocardial electrodes. Atrial flutter was induced in all of 17 dogs, with a median cycle length of 177 +/- 31 ms. Activation sequence maps demonstrated conduction block along the crista terminalis corresponding to the free wall portion of the suture line. This created an isthmus between the suture line and tricuspid annulus, which appeared critical for sustaining AFL, although the circuit used both the septal and free wall surfaces of the right atrium. In seven dogs, a cryolesion was placed from the tricuspid annulus to the free wall segment of the suture line, terminating the AFL, in all seven. When the free wall segment of the suture line was moved 5 mm medial to the crista terminalis, AFL was induced in four of five dogs, but only in the presence of isoproterenol and at a shorter cycle length (136 +/- 8 ms, P < .001). Atrial flutter was not inducible, even with the addition of isoproterenol, in any of five dogs in which the suture line was placed 10 mm anterior to the crista terminalis and incorporated into closure of the atriotomy. This acute canine model of the modified Fontan operation demonstrates that conduction block from the free wall portion of the suture line creates an isthmus of tissue between the suture line and the tricuspid annulus. This is a sufficient substrate to produce AFL; no hemodynamic alteration is required. Injury to the crista terminalis is a significant risk factor in this model, which suggests that a modification of the suture line might reduce the incidence of AFL in patients following this operation.

Objectives. This study sought to 1) establish whether the atrial flutter (AFL) inducible acutely occurs spontaneously in a chronic canine model, and 2) characterize any reentrant circuits present chronically. Background. We previously demonstrated, in an acute canine model of the modified Fontan operation, that the lateral tunnel suture line creates a sufficient electrophysiologic substrate for AFL. Methods. Using cardiopulmonary bypass, a suture line was placed through a right atriotomy in adult dogs (n = 7) to simulate the lateral tunnel of the Fontan operation. Holter recordings were made preoperatively, on the first postoperative day and 2, 4 and 6 weeks postoperatively. At 6 to 8 weeks, through bilateral ventriculotomies, 253-point unipolar atrial electrodes were inserted. AFL was induced using atrial burst pacing, and endocardial activation sequence maps were created. Results. Preoperatively, all dogs were in sinus rhythm. Spontaneous AFL occurred in all dogs postoperatively, with a mean (±SD) cycle length of 192 ± 22 ms. At 6 weeks postoperatively, of six dogs that survived, four had intermittent AFL, and two had incessant AFL. At reoperation, sustained AFL was inducible in six of six dogs, with a mean cycle length of 194 ± 17 ms. Activation sequence maps demonstrated conduction block at the lateral tunnel suture line, which facilitated unidirectional conduction critical for propagation of the reentrant circuit. The AFL circuit was similar to that observed acutely. Conclusions. In a chronic canine model of the modified Fontan operation, the lateral tunnel suture line alone, in the absence of atrial stretch or hypertension, provides an electrophysiologic substrate that promotes spontaneous AFL. This model may be useful for evaluating various forms of treatment and prevention of AFL after the Fontan operation.

The atria are anatomically complex three-dimensional (3-D) structures. Impulse propagation is dynamic and complex during both normal conduction and arrhythmia. Atria activation has traditionally been represented on two-dimensional surface maps, which have inherent inaccuracies and are difficult to interpret. Interactive computerized 3-D display facilitates interpretation of complex atrial activation sequence data obtained from form-fitting multipoint electrodes. Accordingly, the purpose of this article is to describe the application of 3-D form-fitting electrode molds to the 3-D mapping and display system developed in this laboratory for the study of complex cardiac arrhythmias. Computer generated 3-D surface models are created from a database of serial cross-sectional anatomical images. Points chosen on endocardial and epicardial surfaces in each cross-sectional image are processed to create polygons defining myocardial wall boundaries. The polygons from adjacent serial images are then combined, to create a 3-D surface model. The discrete anatomical locations of unit electrodes on multipoint electrode templates are then assigned in the proper position on the surface model. Computer analysis of simultaneous activation data from each unit electrode is performed based on parameters set by the user. Activation data from each unit electrode site are displayed on the computer surface model in a color spectrum correlating with a user-defined time scale. Activation sequence maps can be visualized as static isochrone maps, interval maps, or as dynamic maps at variable speeds, from any 3-D perspective. Thus, an interactive computerized 3-D display system is described, which allows anatomically superior analysis and interpretation of complex atrial arrhythmias.

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)

Objective The authors analyzed the clinical results during the first 8 1/2 years' experience with the Maze procedure for the surgical treatment of atrial fibrillation. Summary Background Data Atrial fibrillation occurs in 0.4% to 2% of the general population and in approximately 10% of patients older than 60 years of age. It is associated with significant morbidity and mortality. The irregular heartbeat causes discomfort, the loss of synchronous atrioventricular contraction compromises hemodynamics, and the stasis of blood flow increases the vulnerability to thromboembolism. Methods From September 25, 1987 to March 1, 1996, 178 patients underwent the Maze procedure. Thirty-two patients underwent the Maze-I procedure, 15 underwent the Maze-II procedure, and 118 underwent the Maze-III procedure. Patients were analyzed for recurrence of atrial flutter and atrial fibrillation between 3 months and 8 1/2 years after surgery (n = 164). Patients were analyzed for atrial transport function, sinus nodule function, and postoperative pacemaker requirements. Results Ninety-three percent of all patients were arrhythmia free without any antiarrhythmic medication. Of the remaining patients with arrhythmia recurrence, all were converted to sinus rhythm with medical therapy. All patients were documented to have atrial transport function by either direct visualization, transesophageal echocardiography, or atrioventricular versus ventricular pacing at the same rate. Ninety-eight percent had documented right atrial function, and 94% had left atrial function. Of the 107 patients in this series who were documented to have a normal sinus node preoperatively, only 1 patient required a permanent pacemaker. Conclusion The Maze procedure is an effective treatment for medically refractory atrial fibrillation in properly selected patients.

It was generally accepted that the site of normal impulse origin within the atria was a single static focus within the sinus node. This review will examine how this model of impulse origin came about and has evolved. Early on, conflicting data suggested that the sinus node focus was not static and changed with interventions that changed heart rate, such as vagal stimulation. Furthermore, even with removal of the sinus node, a normal atrial rhythm was generated. High-resolution mapping in humans and dogs showed that the initiation of the impulse was dynamic and could be multicentric, with more than one focus initiating a single beat. Shifts in the site of origin correlated with changes in rate and were consistent with P wave changes routinely observed in the standard ECG. These studies suggested multiple pacemakers were responsible for impulse initiation. However, it was not clear how these widespread pacemakers were coordinated to function synchronously. Recent canine data suggest that the node may be partially insulated from the surrounding atrium, resulting in multicentric origin starting from a single site within the node. What has evolved is a model of impulse origin with a sinus node having discrete exit sites and a dominant pacemaker within the node that can shift to other nodal sites. Complex and changing conduction out of the node, coupled with extranodal pacemakers, which can assume dominance over the node, combine with the autonomic nervous system to control heart rate and the pattern of impulse origin within the atria.

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)

Abstract The site of earliest extracellular electrical activation in the sinoatrial node (SAN) is known to shift in response to autonomic stimuli, but the mechanisms underlying this phenomenon and the determinants of the location of dominant pacemaker activity have not been elucidated. The present study was designed to characterize the spatial distribution of muscarinic cholinergic and β-adrenergic receptors in the canine SAN and to determine whether a consistent relationship exists between autonomic receptor densities and the site of dominant pacemaker activity. We used quantitative light-microscopic autoradiography of radioligand binding sites to characterize the spatial distribution of muscarinic cholinergic and β-adrenergic receptor subtypes in tissue sections containing the SAN and adjacent right atrial muscle from 18 canine hearts. Muscarinic receptor density was 5.4 times greater in SAN cells than in atrial myocytes ( P P 1 -adrenergic receptors in the SAN. The region of dominant pacemaker activity, localized in 4 hearts with in vitro mapping, consistently exhibited greater densities of muscarinic and β 1 -adrenergic receptors than other SAN regions. Muscarinic receptor density in the dominant pacemaker region was 18±2% and 29±7% higher than in adjacent superior and inferior regions, respectively. β 1 -Receptor density in the dominant site was 53±5% and 26±4% higher than in adjacent superior and inferior SAN regions, respectively. Thus, the SAN is richly endowed with both muscarinic cholinergic and β 1 -adrenergic receptors. Differential responsiveness to autonomic inputs, related perhaps to regional differences in receptor density, may help determine the spatial localization of pacemaker activity.

Activation sequence maps derived during normal sinus rhythm from extracellular potentials in the canine right atrium exhibit widely separated sites of origin. The objectives of this study were to characterize the distribution of pacemakers within the right atrium and to determine the relationship of pacemaker action potentials to sites of earliest surface activation as well as to local extracellular electrograms. The right atria of six adult mongrel dogs were rapidly excised under deep pentobarbital sodium anesthesia and perfused with 95% O2-5% CO2 Krebs-Henseleit solution. Action potentials from the epicardial surface were recorded throughout the region bounded by the crista terminalis laterally and the atrial septum medially. Simultaneously, unipolar extracellular electrograms were recorded from 250 endocardial sites. The earliest pacemakers preceded the earliest electrogram by 63 +/- 34 ms; the latest pacemakers followed the earliest electrogram by 71 +/- 40 ms. Primary negativity in the extracellular electro gram did not predict the site of the earliest or dominant pace maker and in some cases was associated with the latest pace makers. We conclude that primary negativity and/or the sites of earliest activation reflect the point at which the impulse engages atrial myocardium, not the site of earliest pacemaker activity. As such, early extracellular activation appears to represent sites of exit from a relatively insulated sinus node.

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)

After over a decade of experimental and clinical research into the basic mechanisms underlying atrial fibrillation, we were able to develop a surgical procedure that appears to cure the arrhythmia. This surgical procedure has now been applied in 100 patients in our institution and in an aggregate total of approximately 130 patients by surgeons in other institutions, including Drs. McCarthy (Cleveland Clinic), Bonchek and Vazales (Lancaster, Pa.), Damiano (Medical College of Virginia), Laks (UCLA), Hammon (Bowman-Gray), Crawford (Medical University of South Carolina), Morris (Mayo Clinic), Brodman (Albert Einstein), Lawrie (Baylor), Johnson (Sydney), Kosakai and Jsobe (Tokyo), Cheung (Seoul), Landymore (Halifax), Bredikis (Kaunas), Bokeria (Moscow), Jatene (Sau Paulo), Large (London), and Yacoub (London). 37 The surgical results have been excellent, indicating that sophisticated electrophysiologic mapping systems are unnecessary and that the results are not surgeonspecific.

Cardiac pacing has undergone major changes in the areas of manpower, technology, and cost over the past 10 years. Arguments have been made to eliminate cardiac surgical involvement in pacing on the basis of these three areas of change: implantations are increasingly performed by nonsurgeons, surgeons have not kept up with the technologic advances in pacing, and consolidation of bradypacing resources is necessary during a time when reimbursement has declined significantly. This study examined two eras of pacing therapy at an institution where pacemaker implantation has always been performed by cardiothoracic surgeons. The purpose of the study was to critically analyze (1) the current role (if any) of cardiothoracic surgeons in delivery of pacemaker therapy and (2) the current results of cardiothoracic surgical involvement in pacemaker implantation. In 1,562 procedures performed between 1986 and 1992, the infection rate was 0.51% and the overall complication rate (both short-term and long-term) was 5.2%. During era 1 (1/1/86 to 6/30/89), 80% of implants were single-chamber and follow-up was incomplete and dependent in many instances on the referring cardiologist/internist. For the implantations performed in the second era (7/1/89 to 12/31/92) as part of an established Pacemaker Service, complete clinical and transtelephonic follow-up services were provided by this coordinated medical-surgical approach. During era 2, 53.9% of implants were dual-chamber (79% during 1992). Total and infectious complication rates remained low in era 2 despite this change in technology.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to develop a surgical treatment for atrial flutter using intraoperative activation sequence mapping to minimize the surgical procedure necessary to ablate the flutter. A canine model (n = 10) of left atrial enlargement was developed by creating a shunt from the left subclavian artery to the left superior pulmonary vein. Sustained atrial flutter was easily induced in this model. The flutter consisted of a single reentrant circuit that rotated around one or two anatomic obstacles linked by a region of functional block. Epicardial templates, consisting of 252 bipolar electrodes, were used to record activation time maps. After localization of the reentrant circuit, surgical incisions were placed to interrupt the pathways. In all 10 animals, flutter could be induced and intraoperative mapping localized the reentrant circuit. Seven circuits were in the right atrium and three were in the left atrium. The operation ablated all of the preoperative circuits. However, in 5 of the animals, flutter originating from a new circuit could be induced. Activation sequence mapping before and after operation demonstrates that there are multiple potential reentrant pathways in this canine model of atrial flutter. Therefore, all potential pathways must be surgically interrupted to prevent inducibility of atrial flutter.

BACKGROUND Since the atria are thin-walled structures, most studies that have examined the spread of activation in the atria have assumed that they behave electrophysiologically as a two-dimensional surface. It was the objective of this study to determine whether or not this assumption is true by simultaneously mapping the epicardial and endocardial activation sequences in the right atrium. METHODS AND RESULTS Identical precisely superpositioned epicardial and endocardial electrode templates with 250 unipolar electrodes each were used to map the isolated canine right atrium (n = 8) during continuous perfusion and superfusion with Krebs-Henseleit buffer. Data were recorded during control conditions (normal sinus rhythm), continuous pacing (S1S1 = 300 msec), and premature stimulation (S1S2 = effective refractory period + 5 msec). Pacing was performed at two sites, one located on the inferior crista terminalis and one lateral to the crista terminalis on a pectinate muscle. Tachyarrhythmias were induced by a single extrastimulus during the continuous perfusion of acetylcholine (10(-3.5) mol/L). Individual electrode sites were correlated with the gross anatomy and histology. Activation time differences were calculated between each two corresponding epicardial and endocardial sites. There were differences in the activation times between the epicardium and endocardium during all experimental conditions. However, the average difference for each condition was < 1 msec, suggesting that overall activation did not spread faster on either the epicardium or the endocardium, even though in certain regions one surface could lead the other. The dispersion of time differences was smallest during normal sinus rhythm and continuous pacing (SD = 5.6-5.8 msec) and largest after premature stimulation (SD = 6.3 msec for crista pacing, p < 0.05; SD = 8.1 msec for pacing lateral to the crista, p < 0.001). Differences in the activation sequence correlated with the underlying anatomic architecture. The largest differences in activation times between the epicardium and endocardium were associated with those regions of the atrium where pectinate muscles ran below the epicardial surface. The pectinate muscles in those areas were often discontinuous with the epicardial surface and facilitated the discordant epicardial-endocardial activation. The discordant activation was also found in regions where the atrial wall thickness was < 0.5 mm and correlated with transmural differences in fiber orientation. A tachyarrhythmia induced in the presence of acetylcholine, which demonstrated a focal activation pattern, was shown to have a reentrant loop that used free-running muscle bundles connecting the epicardial and endocardial surfaces, resulting in a three-dimensional pathway. CONCLUSIONS The findings of this study demonstrate that epicardial and endocardial activation can be discordant in specific regions and that discordance increases with abnormal activation sequences. Many of the differences in the epicardial and endocardial activation can be correlated with the heterogeneity of the anatomic architecture of the right atrium. The study also demonstrates that reentry can occur in a three-dimensional plane using the epicardial and endocardial surfaces connected by transmural muscle fibers.

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.

A Review of Surgery for Atrial Fibrillation. Atrial fibrillation is the most common of all sustained cardiac arrhythmias, yet it has no effective medical or surgical therapy. During the past decade, multipoint computerized electrophysiologic mapping systems were used to map both experimental and human atrial fibrillation. On the basis of these studies, a new surgical procedure was developed for atrial fibrillation. Between September 25, 1987, and July 1, 1991, this procedure was applied in 22 patients with paroxysmal atrial flutter (n = 2), paroxysmal atrial fibrillation (n = 11), or chronic atrial fibrillation (n = 9) of 2 to 21 years duration. All patients were refractory to all antiarrhythmic medications, and each patient failed to receive the desired therapeutic benefits of an average of five drugs administered preoperatively. There were no operative deaths and all perioperative morbidity resolved. All 22 patients have been successfully treated for atrial fibrillation with surgery alone. Preservation of atrial transport function has been documented in all patients postoperatively, and all have experienced marked clinical improvement.

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.

To delineate the propagation of electrical activation in the atrial septum, atrial epicardial and atrial septal maps were recorded intraoperatively using a 156-channel computerized mapping system in 12 patients during sinus rhythm (n = 10), supraventricular tachycardia associated with septal pathways in Wolff-Parkinson-White syndrome (n = 3), atrioventricular (AV) node reentrant tachycardia (n = 4), and atrial flutter (n = 5). The epicardial and septal data were recorded simultaneously from 156 atrial electrodes, digitized, analyzed, and displayed as isochronous maps on a two-dimensional diagram of the atria. During sinus rhythm, the activation wave fronts propagated most rapidly along the large muscle bundles of the atrial septum. During supraventricular tachycardia associated with Wolff-Parkinson-White syndrome, the earliest site of retrograde atrial activation usually corresponded to the position of atrial insertion of the septal pathways. However, the earliest site of activation during orthodromic supraventricular tachycardia was different from that during ventricular pacing in 1 patient with a posterior septal accessory pathway localized by the epicardial mapping study. The data document the rationale for dividing the ventricular end of the accessory pathways (ie, the endocardial technique) rather than the atrial end (ie, the epicardial technique) in patients with Wolff-Parkinson-White syndrome. During AV node reentrant tachycardia, aural activation data suggested that atrial tissue lying outside the confines of the anatomical AV node is a necessary link in this common arrhythmia. Thus, these atrial septal maps explain why surgical dissection, or properly positioned small cryolesions placed in the region of the AV node, can ablate AV node reentrant tachycardia without altering normal AV node function. The maps recorded during atrial flutter suggest the importance of the atrial septum as one limb of a macroreentrant circuit responsible for the arrhythmia, and imply that atrial flutter is arnenable to control by surgical techniques. These studies demonstrate the details of normal atrial septal activation, the importance of the atrial septum in a variety of different atrial arrhythmias, and the basis of and potential for surgical ablation of the most common types of supraventricular arrhythmias.

Nine adult mongrel dogs were subjected to cardiopulmonary bypass and both right and left atria were surgically isolated, exclusive of the sinoatrial (SA) node, crista terminalis, and interatrial septum. Thus, the SA node remained in continuity with the ventricles despite biatrial isolation. Moreover, of the right and left SA node arteries, the predominant one (right in 7 dogs, left in 2 dogs) was spared. Postoperatively, normal SA node function was preserved in 8 out of 9 dogs, with no difference in sinus rhythm cycle length (preop: 446 +/- 25, postop: 434 +/- 22 sec, p = NS) or sinus node recovery time (preop: 488 +/- 28, postop: 487 +/- 32 msec, p = NS). Simulated supraventricular tachycardia was confined in the isolated right or left atria did not affect sinus rhythm in the remainder of the heart. One out of 9 dogs developed junctional rhythm postoperatively, indicating exclusion of the SA node or a fast atrial pacemaker. In the 8 dogs with postoperative sinus rhythm, the spared SA node artery was occluded at the end of each study. All dogs developed rhythm deterioration including sinus rhythm slowing with prolonged sinus node recovery time (4 dogs), sinus bradyarrhythmia (2 dogs) and atrioventricular nodal rhythm (2 dogs). Thus, biatrial isolation is feasible for the treatment of supraventricular tachycardia, but it is essential to preserve SA node blood supply in order to maintain normal sinus rhythm in the remainder of the heart.

Electrocardiographers have frequently observed and commented upon the different morphologies of the P wave. This in spite of the fact that the gain and speed of the standard ECG were designed primarily to emphasize the higher-voltage QRS complex. Variations in the morphology of the P wave not apparent in the standard electrocardiogram are conspicuous in high-gain, high-speed tracings. Different P wave configurations, as well as cycle-to-cycle changes in P morphology with sinus arrhythmia, multifocal atrial rhythm, and tachycardia, ectopic left atrial rhythms, and tachycardias, are well described. Not commonly appreciated is progressive change in P morphology associated with progressively increasing heart rates during standard exercise stress tests. In addition, the tall, peaked, vertically oriented P wave associated with sinus tachycardia has frequently been commented upon. The first systematic study of the P wave was undertaken by Brody et al., in 1967.1 These investigators observed that no single P wave morphology existed for a normal individual. They determined that the P wave could not be signal averaged and thereby improve on the signal-to-noise ratio if one assumed a single basic morphology. They reported three or more different P waves in a single normal subject. These changes could not be related to differences in respiratory excursion and therefore different heart-lead interrelationships or to other extracardiac factors. They speculated that these different patterns might represent differences in the

A detailed description of the electrocardiogram of the early repolarization variant, including its most common morphological variations is presented. Included is a recently identified anomaly of the QRS complex, which has not previously been reported. Ventricular activation data is presented to explain the unique QRS changes. A comparison with Wolff-Parkinson-White (preexcitation) reveals certain similarities related to a premature completion of depolarization in early repolarization variant.

It has been hypothesized that atrial lesions must be transmural to successfully cure atrial fibrillation (AF). However, ablation lines often do not extend completely across the atrial wall.The purpose of this study was to determine the effect of residual gaps on conduction properties of atrial tissue.Canine right atria (n = 13) were isolated, perfused, and mounted on a 250-lead electrode plaque. The atria were divided with a bipolar radiofrequency ablation clamp, leaving a gap that was progressively narrowed. Conduction velocities at varying pacing rates and AF frequencies were measured before and after ablations. AF was induced with an extra stimulus and acetylcholine.Gap widths from 11.2 to 1.1 mm were examined. Conduction velocities through gaps were dependent cycle length (P = .002) and gap size (P.001). Overall, 253 (97%) of a total of 260 gaps allowed paced propagation; 51 (91%) of 56 gaps 1-3 mm in width permitted paced propagation, as did 202 (99%) of 204 gapsor=3.0 mm. Similarly, 253 (97%) of a total of 260 gaps allowed propagation of AF. For AF, 51 (93%) of 55 gaps 1-3 mm allowed AF to pass through, as did 202 (99%) of 205 gapsor=3.0 mm. Gaps as small as 1.1 mm conducted paced and AF impulses.Conduction velocities were slowed through residual gaps. However, propagation of wave fronts during pacing and AF occurred through the majority of residual gaps, down to sizes as small as 1.1 mm. Leaving viable tissue in ablation lines for the treatment of AF could account for failures.

Purpose Intraoperative activation sequence mapping during atrial fibrillation (AF) is difficult because of the complexity of the data. The data analysis is time consuming, and picking activation times can be ambiguous. The purpose of this study was to determine whether mapping in the frequency domain during AF can be used to rapidly locate the region and assess the stability of the dominant frequency. Methods In 33 patients, epicardial bipolar electrograms were intraoperatively recorded from 250 sites during AF. For each electrogram, a power spectrum was calculated using a fast Fourier transform. The peak frequency below 11 Hz was determined from the power spectrum for each electrogram. Results Isofrequency mapping demonstrated that 91% of the patients exhibited a distinct region of maximum (dominant) frequency at least once during the recording period. Nine percent had no distinct region of dominant frequency. A distinct region of stable dominant frequency was located in the left atrium 30% of the time and the right atrium 12% of the time for the entire recording period. The location of dominant frequency changed during the recording period in 48% of the patients. The dominant frequency was highest in patients with chronic AF (8.29 ± 1.0 Hz) compared to those with paroxysmal AF (PAF) (6.54 ± 0.62 Hz, P = .001). The dispersion of frequency was higher in the patients with persistent AF (1.03 ± 0.4 Hz) than in those with PAF (0.6 ± 0.3 Hz, P Conclusion Frequency mapping rapidly and accurately identifies the region of dominant activation frequency. The frequency is faster and more variable in persistent AF than in PAF. The location of the dominant frequency was unstable, changing during the recording period, in half the patients. The location of the dominant frequency was independent of the type of AF.

Background— The critical mass hypothesis for atrial fibrillation (AF) was proposed in 1914. There has never been a systematic investigation defining the relationship between tissue geometry and AF. The purpose of this study was to determine the association among the probability of maintaining AF and the width, area, weight, effective refractory period (ERP), and wavelength in atrial tissue. Methods and Results— Isolated canine atria (n=20) were perfused with Krebs-Henseleit solution. Baseline ERPs were obtained with and without acetylcholine (10E-3.5 mol/L) using single extra-stimulus pacing while unipolar electrograms were recorded from 250 sites. The tissue was then partitioned using bipolar radiofrequency ablation, and the ERPs were measured again with and without acetylcholine. Any section of tissue that maintained AF was divided until the arrhythmia was no longer inducible. ERPs and conduction velocities were measured in all of the sections after each ablation, and the wavelengths were calculated. The probability of AF was found to be correlated with increasing tissue areas, widths, and weights ( P P Conclusions— The probability of sustained AF was significantly associated with increasing tissue area, width, and weight and decreasing ERPs and wavelengths. These data may lead to a better understanding of the mechanism of AF and, thus, help to design more-effective interventional procedures in the future.

Background— The Maze procedure restores normal sinus rhythm in the majority of patients. However, atrial tachyarrhythmias (ATA) are a common early complication after the operation. The purpose of this study was to define the incidence and natural history of ATA after the Maze procedure. Methods— Complete medical records from 200 patients who underwent the Maze procedures (I, II, and III) from 1987 to 2002 were examined for all episodes of early postoperative ATA that occurred during the first 30 days after the procedure. Two electrophysiologists independently reviewed all postoperative 12-lead electrocardiograms. Results— ATA occurred in 86 patients (43%) after the Maze procedure. Of the patients with ATA, 59% had atrial fibrillation (AF), 14% had atrial flutter (AFL), and 27% had both AF and AFL. Of the patients with AF or AFL, 20% and 5%, respectively, also had episodes of atrial tachycardia and supraventricular tachyarrhythmia. The peak incidence of early postoperative ATA was on postoperative day 8. The average duration of ATA was 5.7±5.0 days. Late recurrence of AF (>1 year postoperatively) occurred in 7.0% of patients who had early postoperative ATA and 8.8% of patients without early postoperative ATA ( P =0.8). Conclusions— ATA occurred in 43% of patients after the Maze procedure. The tachyarrhythmias occurred primarily within 8 days after surgery and resolved within 3 weeks in almost all patients. There was no relationship between the incidence of early postoperative ATA and the late recurrence of AF.

The Maze procedure was developed for the treatment of atrial fibrillation over a period of several years. Extensive experimental and clinical studies of the underlying electrophysiology of the arrhythmia were performed, and numerous surgical techniques and principles were tried before the Maze procedure was conceived. Few cardiac surgical procedures have undergone more extensive research and experimental trials before being applied clinically. This article gives a brief summary of the work leading up to the eventual Maze-III procedure that is now in clinical use.

Background . The MAZE-III is the surgical treatment of choice for medically refractory atrial fibrillation. Although a number of nonsurgical techniques are evolving to duplicate the transmural atrial lesions of the MAZE-III, the surgical atriotomy remains the gold standard for conduction block. It was the objective of this study to surgically create the atrial incisions of the MAZE-III without the use of cardiopulmonary bypass. Methods . A technique was developed to create and intersect the linear incisions of the MAZE-III on 10 beating canine hearts without the use of cardiopulmonary bypass using a "tunnel" of atrial tissue. The effectiveness of the procedure was tested by atrial burst pacing. Results . This technique was successfully performed on 10 mongrel dogs without operative mortality. Preoperatively, sustained atrial fibrillation (>30 seconds) was induced in all animals. Postoperatively, all the animals remained in sinus rhythm even after burst pacing. Conclusions . In an experimental canine model, the MAZE-III can be performed on beating hearts without the assistance of cardiopulmonary bypass using a "tunnel" technique. This technique allows for the immediate assessment of electrophysiologic and mechanical function after the MAZE-III, or any other type of procedure using the "maze principle" and may find future application in the clinical arena.

The purpose of this study was to develop an animal model of atrial flutter (AFL) or fibrillation (AFB) and to determine precisely the pathway of atrial activation during arrhythmias induced by programmed stimulation. In 10 dogs, a shunt from the left subclavian artery to the left upper pulmonary vein was created to produce left atrial enlargement. Five months later, using programmed electrical stimulation, it was possible to induce 17 sustained atrial tachycardias in 9 of the 10 dogs, including 9 episodes of AFL caused by circus movement re-entry, 6 episodes of focal tachycardia, and 2 episodes of AFB. Short cycle length left atrial tachycardias caused by either circus movement or a focus did not propagate in a uniform 1:1 pattern to the right atrium (RA), resulting in RA dissociation. In these arrhythmias, complex wavefronts from both current and preceding left atrial cycles coexisted in the RA. Circus movement was associated with a spectrum of different re-entrant pathways with different path lengths. These differences in the path length were determined by various ways in which obstacles such as the superior vena cava and orifice of the right atrial appendage or pulmonary vein orifices were combined by contiguous areas of functional block. (Jpn Circ J 1998; 62: 201-210)

Background —The central common pathway, which is the target for ablation in reentrant ventricular tachycardia, can be localized by entrainment mapping techniques. However, localization of the pathway is not always possible because of the elevated pacing threshold and the low voltage and fractionated potentials at the pathway. We examined whether return cycle mapping after entrainment localizes the pathway without pacing at the pathway or recording the potentials from the pathway and determined the required electrode resolution to localize the pathway. Methods and Results —Epicardial mapping was performed with 253 unipolar electrodes during and after entrainment of 13 morphologies of ventricular tachycardia that were induced in dogs 4 days after infarction. The return cycle was calculated by subtracting the first activation time from the second activation time after the last stimulus and the return cycle distribution map was constructed for each stimulation site. The return cycle isochrones equal to the ventricular tachycardia cycle length converged on the lines of conduction block irrespective of the stimulation site, and the central common pathway was localized at the region between the intersections of the return cycle isochrones after entrainment from different stimulation sites. The potentials from the central common pathway were not required to localize the pathway, and the mapping accuracy did not change with or without analysis of the potentials from the pathway. According to the correlation between the electrode resolution and the mapping accuracy, an interelectrode distance of 8.5 mm was estimated as sufficient resolution for successful tachycardia termination during radiofrequency ablation guided by return cycle mapping. Conclusions —Return cycle mapping after entrainment localizes the central common pathway without pacing at the pathway or recording the potentials from the pathway. This new mapping technique could improve the success rate of the ablative procedures.

The purpose of this article is to demonstrate how adaptive changes in myocardial microstructure provide mechanisms for emergent new conduction disturbances that initiate reentrant arrhythmias. The mechanisms are based on discontinuous conduction phenomena produced by increases in cellular loading; these increases result from changes in the normal distribution of the gap junctions. Recent studies that at a microscopic level propagation in normal mature cardiac muscle is stochastic. For example, the nonuniform and irregular distribution of the gap junctions in such normal muscle produces load variations that are associated with changes in Vmax inside individual cells during both longitudinal and transverse propagation. The stochastic nature of normal propagation at a microscopic level offers considerable protection against arrhythmias by reestablishing the general trend of wavefront movement after small variations in excitation events occur. If such microscopic diversity is decreased, large fluctuations in load develop that are distributed over more cells than usual. The decrease in diversity may be caused by loss of side-to-side coupling between fibers, which produces relatively isolated groups of cells with microfibrosis. With loss of side-to-side fiber coupling, the myocardial architecture may fail to reestablish a smoothed wavefront at the macroscopic level. Spatial nonuniformities of electrical loading then give rise to conduction block and reentry.

Background Atrial refractory periods and their spatial distribution are important determinants of atrial reentrant arrhythmias. The objective of this study was to demonstrate a correlation between the local atrial fibrillation interval (AFI) and local effective refractory period (ERP). Methods and Results To measure the local ERP and local AFI under stable conditions without hemodynamic, autonomic, or reflex influences, isolated perfused canine whole atria were used (n=8). The isolated atria were mounted on two endocardial electrodes. Bipolar electrograms were simultaneously recorded from 253 endocardial sites, and 16 to 20 randomly distributed electrodes were used to measure the local ERP by the extrastimulus technique. In all studies, several episodes of AF were induced by a single extrastimulus. The ERP and minimum AFI converged with increasing duration of AF. The convergence was more rapid if the total duration of AF analyzed came from multiple episodes of AF. The correlation coefficient between the local ERP and minimum local AFI was .92 (n=119, P Conclusions The minimum local AFI measured from at least 10 seconds of AF approximates the local ERP. Construction of a minimum local AFI map during AF can be used to predict the distribution of refractoriness and can be used to predict sites of functional block. Contrary to studies done in intact animals and patients, the AFI were longer than the ERPs, suggesting that reflex changes may shorten ERP in the intact heart.