John P. Boineau

Modification of the maze procedure for atrial flutter and atrial fibrillation ☆ ☆☆ ★ ★★ ♢: I. Rationale and surgical results

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.

Five-year experience with the maze procedure for atrial fibrillation

Between September 25, 1987, and December 31, 1992, 75 patients (53 men, 22 women; average age, 52 years) underwent the maze procedure for the treatment of atrial fibrillation. Six patients had undergone a previous cardiac operation and 28% underwent concomitant cardiac procedures in addition to the maze procedure. One patient (1.3%) died 10 days after undergoing a combined maze procedure and Morrow procedure for the management of chronic atrial fibrillation and hypertrophic obstructive cardiomyopathy. Postoperative atrial pacemakers were required in 40%: 26% for preoperative sick sinus syndrome and 6% for iatrogenic injury of the sinus node, and 8% had pacemakers in place preoperatively. As of December 31, 1992, 65 patients had been followed up for at least 3 months after operation (range, 3 to 63 months). The maze procedure cured atrial fibrillation, restored atrioventricular synchrony, and preserved atrial transport function in 64 of 65 patients (98%). The procedure has been curative without the need for medications in 58 of 65 patients (89%) and with the need for medications in 6 of 65 (9%), with medications failing in only 1 of the 65 patients (2%). The results support the maze procedure as the treatment of choice in patients with medically refractory symptomatic atrial fibrillation.

The Cox maze III procedure for atrial fibrillation: long-term efficacy in patients undergoing lone versus concomitant procedures

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.

Modification of the maze procedure for atrial flutter and atrial fibrillation: II. surgical technique of the maze III procedure

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.

Slow Ventricular Activation in Acute Myocardial Infarction A Source of Re-entrant Premature Ventricular Contractions

The evolution of premature ventricular contractions (PVCs) in acute myocardial infarction was studied by recording bipolar potentials from the left ventricle before and after coronary artery occlusion in dogs. The potentials were recorded from 154 locations in the left ventricular wall as well as at the endocardial and epicardial surfaces. Desynchronization and marked slowing of previously uniform activation was noted and resembled abbreviated, local fibrillation. The dissociation of excitation was either simple, characterized by fragmentation into single delayed spikes, or complex, characterized by numerous spikes. Sustained, desynchronized activity, confined to local myocardial areas, was observed up to 215 msec after the onset of activation. These local areas of sustained excitation functioned as a source of re-entrant activity and were associated with PVCs. Histochemical stains of myocardium indicated a relationship between the inhomogeneous distribution of ischemia (stain) and the desynchronization of the electrical activity.

Successful Surgical Interruption of the Bundle of Kent in a Patient with Wolff-Parkinson-White Syndrome

Recurrent supraventricular tachycardia is a frequent complication in patients with the Wolff-Parkinson-White (WPW) syndrome. Our patient was unusual in that the arrhythmia was the predominant rhythm, and it was felt that the sustained tachycardia was responsible for signs and symptoms of congestive heart failure. The arrhythmia could not be controlled adequately with digitalis, quinidine, diphenylhydantoin, or propranolol. Atrial or ventricular pacing also failed to prevent recurrent episodes of tachycardia.Physiological and pharmacological studies suggested that an anomalous pathway was responsible for the WPW abnormality and participated in a re-entrant circuit which sustained the episodes of tachycardia. Isopotential body surface mapping suggested anomalous ventricular excitation at the lateral aspect of the right atrioventricular groove. Epicardial mapping at the time of surgery was used to localize the earliest area of anomalous ventricular activation, and surgical transection of the atrioventricular junction at that point abolished the electrocardiographic features of WPW and the recurrent tachycardia. Five months after surgery neither the ECG features of WPW nor the tachycardia has recurred. The signs and symptoms of congestive heart failure have subsided, and the patient has returned to work.

Demonstration of a widely distributed atrial pacemaker complex in the human heart.

Atrial depolarization was analyzed in 14 patients with the Wolff-Parkinson-White syndrome undergoing surgery to ablate accessory atrioventricular pathways associated with tachyarrhythmias. Bipolar potentials were recorded simultaneously from 156 atrial epicardial electrodes arranged in three templates to fit the anterior and posterior aspects of both atria. Spontaneous or sinus rhythms were recorded, as were atrial escape rhythms after overdrive pacing at rates of 150 and 200 beats/min. Atrial activation maps revealed different patterns of impulse initiation varying from typical unifocal sinus node impulse origin, unifocal extranodal impulse origin, and multicentric impulse origin from two to four widely distributed atrial pacemaker sites. In subjects demonstrating only unifocal impulse origin during control or sinus rhythm, other widely divergent pacemaker sites were recorded in other maps during subsequent rhythms. In addition to sites located at the upper superior vena cava-right atrium junction, pacemakers also dominated at sites anterior and inferior to the sinus node region during both control and escape depolarizations. Most of the subjects were found to have two or more pacemaker sites when maps of all control and postpacing conditions were analyzed. The right atrial pacemaker region encompassed a zone of 7.5 X 1.5 cm centered about the long axis of the sulcus terminalis posteriorly and the precaval band anteriorly. An unexpected finding was the participation of left atrial escape pacemakers. The functional behavior of both the control and escape pacemakers, as assessed by sinus node recovery time, was normal, indicating physiologic operation of the extranodal sites as part of an overall system of distributed pacemakers involved in the control of rate. Although functional assessment was limited in these initial patient studies, correspondence with similar observations in extensive previous canine studies supports the concept of a widely distributed atrial pacemaker complex in man.

Microfibrosis Produces Electrical Load Variations Due to Loss of Side‐to‐Side Cell Connections; A Major Mechanism of Structural Heart Disease Arrhythmias

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 hading; these increases result from changes in the normal distribution of the gap junctions. Recent studies indicate 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.

Cholinergically mediated tachyarrhythmias induced by a single extrastimulus in the isolated canine right atrium.

Cholinergic agonists and vagal stimulation potentiate the inducibility of atrial fibrillation. To describe the activation patterns and determine the mechanisms that sustain cholinergic fibrillation, tachyarrhythmias were induced with a single extrastimulus in the isolated Krebs-Henseleit-perfused canine right atrium (n = 11) at increasing concentrations of acetylcholine (from 10(-7.5) to 10(-4.5) M). Bipolar electrograms were recorded from 250 epicardial sites simultaneously during control conditions and during extrastimulation (S1S1, 300 msec; S1S2, effective refractory period+5 msec) with and without acetylcholine. Activation sequence maps were constructed from each recording. Without acetylcholine, no tachyarrhythmias were induced. With increasing concentrations of acetylcholine, the refractory period decreased, and nonsustained (< 2 seconds) rapid repetitive responses were induced. At higher concentrations, a sustained (> 2-minute) fibrillation was induced. Activation sequence maps revealed that the rapid repetitive responses were characterized by multiple reentrant circuits. The number of circuits and wavelets increased in a dose-dependent fashion. However, unexpectedly, this trend did not continue when the tachyarrhythmia became sustained. Instead, the reentry tended to stabilize to a small, single, relatively stable reentrant circuit. In conclusion, the data suggest that, in this model, below a critical level of refractory period (< 95 msec) atrial reentrant circuits, unassociated with anatomic obstacles, can become stable and dominate activation.

Inflammation of Atrium After Cardiac Surgery Is Associated With Inhomogeneity of Atrial Conduction and Atrial Fibrillation

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<0.005). Antiinflammatory therapy decreased the inhomogeneity of atrial conduction after atriotomy (1.16±0.10; P<0.001). AF duration was longer in the atriotomy and pericardiotomy groups than in the control and antiinflammatory groups (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 &Dgr;OD/min per milligram protein, respectively; P<0.001). Myeloperoxidase activity of the antiinflammatory group was lower than that of the atriotomy group (0.17±0.02; P<0.001). Inhomogeneity of conduction correlated with myeloperoxidase activity (r=0.851, P<0.001). 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.