Reversal of left ventricular intracavitary gradient with intracavitary diastolic regurgitation in hypertrophic obstructive cardiomyopathy.

A 73 year old man presented with angina and nonsustained ventricular tachycardia. Cardiac catheterization revealed the dynamic systolic intracavitary gradient of hypertrophic obstructive cardiomyopathy. Abnormal isovolumetric relaxation resulted in the development of a diastolic gradient from the left ventricular outflow tract to the left ventricular apex accompanied by intracavitary regurgitation of contrast material from the outflow tract to the left ventricular body during left ventriculography. This case provides hemodynamic and angiographic confirmation of abnormal isovolumetric relaxation in this syndrome and insight into its mechanism.

Cardiac arrest in an adolescent with atrial fibrillation and hypertrophic cardiomyopathy.

A 15 year old youth, who presented with out-of-hospital cardiac arrest due to documented ventricular fibrillation, was found to have nonobstructive hypertrophic cardiomyopathy. Electrophysiologic study demonstrated inducible sustained atrial fibrillation with a rapid ventricular response. This rhythm, associated with hypotension and evidence of myocardial ischemia, spontaneously degenerated into ventricular fibrillation. No ventricular arrhythmias were inducible by programmed ventricular stimulation. Therapy with metoprolol and verapamil slowed the ventricular rate during atrial fibrillation and maintained hemodynamic stability, both during follow-up electrophysiologic study and during a subsequent spontaneous episode.

Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter.

The need for prophylactic anticoagulation to prevent embolism before direct current cardioversion is performed for atrial fibrillation or atrial flutter is controversial. To examine this issue further, a retrospective review was undertaken to assess the incidence of embolic complications after cardioversion. The review involved 454 elective direct current cardioversions performed for atrial fibrillation or atrial flutter over a 7 year period. The incidence rate of embolic complications was 1.32% (six patients); the complications ranged from minor visual disturbances to a fatal cerebrovascular event. All six patients had atrial fibrillation, and none had been on anticoagulant therapy (p = 0.026). The duration of atrial fibrillation was less than 1 week in five of the six patients who had embolic complications. Baseline characteristics of patients with a postcardioversion embolic event are compared with those of patients who did not have an embolic event. There was no difference in the prevalence of hypertension, diabetes mellitus or prior stroke between the two groups, and there was no difference in the number of patients who were postoperative or had poor left ventricular function. Left atrial size was similar between the two groups. No patient in the embolic group had valvular disease. No patient with atrial flutter had an embolic event regardless of anticoagulant status; therefore, anticoagulation is not recommended for patients with atrial flutter undergoing cardioversion. Prophylactic anticoagulation is pivotal in patients undergoing elective direct current cardioversion for atrial fibrillation, even those with atrial fibrillation of less than 1 week's duration.

Right ventricular outflow tract ventricular tachycardia: detection of previously unrecognized anatomic abnormalities using cine magnetic resonance imaging.

OBJECTIVES: This study attempted to determine whether cine magnetic resonance imaging (MRI), because of its unique ability to image the right ventricle, detects abnormalities in patients with right ventricular outflow tract ventricular tachycardia. BACKGROUND: Right ventricular outflow tract ventricular tachycardia occurs in the absence of apparent structural heart disease. METHODS: We compared cine MRI scans in 22 patients with right ventricular outflow tract ventricular tachycardia, 16 subjects without structural heart disease and 44 patients with other cardiovascular diseases. Echocardiography was performed in 21 patients with ventricular tachycardia. RESULTS: All 22 patients with ventricular tachycardia had normal left ventricular function and no evidence of coronary artery disease. Cine MRI revealed right ventricular structural and wall motion abnormalities more often in patients with ventricular tachycardia (21 [95%] of 22) than in normal subjects (2 [12.5%] of 16, p < 0.0001) or patients without arrhythmia (17 [39%] of 44, p < 0.0001). The abnormalities in patients with ventricular tachycardia (fixed focal wall thinning, excavation, decreased systolic thickening) were located in the right ventricular outflow tract, whereas those in patients without arrhythmia were confined to the free wall. Cine MRI demonstrated abnormalities in patients with ventricular tachycardia more often than did echocardiography (21 [95%] of 22 vs. 2 [9%] of 21, respectively, p < 0.0001). CONCLUSIONS: Right ventricular outflow tract ventricular tachycardia was associated with focal structural and wall motion abnormalities of the right ventricular outflow tract that were detected more often by cine MRI than by other imaging modalities and were not present in patients without arrhythmia or in normal subjects.

Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure.

Abnormal procainamide pharmacokinetics (prolonged half-life and decreased volume of distribution) and pharmacodynamics (decreased threshold for the suppression of premature ventricular complexes) have been suggested in patients with acute myocardial infarction or congestive heart failure, or both. To better define procainamide kinetics, 37 patients in the acute care setting received intravenous procainamide (25 mg/min, median dose 750 mg) with peak and hourly blood samples taken over 6 hours. Compared with the 10 control patients, the 12 patients with acute myocardial infarction and the 15 patients with congestive heart failure had normal procainamide pharmacokinetics with respect to half-life (2.3 +/- 1.0, 2.5 +/- 0.9 and 2.6 +/- 0.8 hours, respectively), volume of distribution (1.9 +/- 0.7, 1.8 +/- 0.4 and 1.8 +/- 0.5 liters/kg, respectively), clearance (11.3 +/- 7.5, 9.3 +/- 3.6 and 9.1 +/- 3.5 ml/min per kg, respectively) and unbound drug fraction (66 +/- 9, 66 +/- 9 and 69 +/- 4%, respectively). Low thresholds for greater than 85% premature ventricular complex suppression were confirmed in these patients (median 4.7 micrograms/ml in patients with acute myocardial infarction and 3.3 micrograms/ml in patients with congestive heart failure). Thus, differences in the response of premature ventricular complexes to procainamide reflect electropharmacologic differences dependent on clinical setting rather than pharmacokinetic abnormalities. Furthermore, the reduction of procainamide dosing in patients with acute myocardial infarction or congestive heart failure, based solely on prior kinetic data, may result in inappropriate antiarrhythmic therapy.

Outcome of resuscitation from bradyarrhythmic or asystolic prehospital cardiac arrest.

Previous studies of outcome as a function of the initial electrophysiologic mechanisms recorded at the scene of prehospital cardiac arrest have demonstrated that bradyarrhythmias and asystole have the worst prognosis. In this report, our observations in bradyarrhythmic and asystolic arrests occurring from 1980 to 1982 are compared with those from 1975 to 1978. From 1980 to 1982, 61 (27%) of 225 cardiac arrest events meeting entry criteria for the study were bradyarrhythmic or asystolic. Only 2 (8%) of 24 patients with asystole and 1 (20%) of 5 patients with sinus bradycardia survived prehospital intervention. Only 1 of these 29 patients was discharged from the hospital alive. In contrast, 15 (47%) of 32 patients who presented with idioventricular rhythm at initial contact survived prehospital intervention and were hospitalized, and 8 (25%) of these 32 were ultimately discharged alive. When compared with the 1975 to 1978 patients with bradyarrhythmia and asystole, both prehospital survival (8 versus 30%, p less than 0.001) and survival after hospitalization (0 versus 15%, p less than 0.05) significantly improved, but the improvement occurred predominantly in the subgroup with idioventricular rhythm. Survivors within this subgroup tended to have a prompt response to prehospital pharmacologic interventions that were not available to the 1975 to 1978 group. The response was manifested by return to a sinus mechanism or increase in the rate of idioventricular rhythm. In conclusion, outcome has improved for a specific subgroup of victims of prehospital cardiac arrest with bradyarrhythmia or asystole; the improved outcome may relate to field interventions by rescue personnel at the scene of arrest but the mortality rate is still high.

Radiofrequency catheter ablation for management of symptomatic ventricular ectopic activity.

OBJECTIVES: This study assessed the useful role of intracardiac mapping and radiofrequency catheter ablation in eliminating drug-refractory monomorphic ventricular ectopic beats in severely symptomatic patients. BACKGROUND: Ventricular ectopic activity is commonly encountered in clinical practice. Usually, it is not associated with life-threatening consequences in the absence of significant structural heart disease. However, frequent ventricular ectopic beats can be extremely symptomatic and even incapacitating in some patients. Currently, reassurance and pharmacologic therapy are the mainstays of treatment. There has been little information on the use of catheter ablation in such patients. METHODS: Ten patients with frequent and severely symptomatic monomorphic ventricular ectopic beats were selected from three tertiary care centers. The mean frequency +/- SD of ventricular ectopic activity was 1,065 +/- 631 beats/h (range 280 to 2,094) as documented by baseline 24-h ambulatory electrocardiographic (ECG) monitoring. No other spontaneous arrhythmias were documented. These patients had previously been unable to tolerate or had been unsuccessfully treated with a mean of 5 +/- 3 antiarrhythmic drugs. The site of origin of ventricular ectopic activity was accurately mapped by using earliest endocardial activation time during ectopic activity or pace mapping, or both. RESULTS: During electrophysiologic study, no patient had inducible ventricular tachycardia. The ectopic focus was located in the right ventricular outflow tract in nine patients and in the left ventricular posteroseptal region in one patient. Frequent ventricular ectopic beats were successfully eliminated by catheter-delivered radiofrequency energy in all 10 patients. The mean number of radiofrequency applications was 2.6 +/- 1.3 (range 1 to 5). No complications were encountered. During a mean follow-up period of 10 +/- 4 months, no patient had a recurrence of symptomatic ectopic activity, and 24-h ambulatory ECG monitoring showed that the frequency of ventricular ectopic activity was 0 beat/h in seven patients, 1 beat/h in two patients and 2 beats/h in one patient. CONCLUSIONS: Radiofrequency catheter ablation can be successfully used to eliminate monomorphic ventricular ectopic activity. It may therefore be a reasonable alternative for the treatment of severely symptomatic, drug-resistant monomorphic ventricular ectopic activity in patients without significant structural heart disease.

Is hospital admission for initiation of antiarrhythmic therapy with sotalol for atrial arrhythmias required? Yield of in-hospital monitoring and prediction of risk for significant arrhythmia complications.

OBJECTIVES: We sought to determine the yield of in-hospital monitoring for detection of significant arrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might predict safe outpatient initiation. BACKGROUND: The need for hospital admission during initiation of antiarrhythmic therapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related. METHODS: The records of 120 patients admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determine the incidence of significant arrhythmia complications, defined as new or increased ventricular arrhythmias, significant bradycardia or excessive corrected QT (QTc) interval prolongation. RESULTS: Twenty-five patients (20.8%) experienced 35 complications, triggering therapy changes during the hospital period in 21 (17.5%). New or increased ventricular arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20 (16.7%) (rate <40 beats/min in 13, pause >3.0 s in 4, third-degree atrioventricular block in 1, permanent pacemaker implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinued in 6). Time to the earliest detection of complications was 2.1 +/- 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for complications within 3 days of monitoring. Baseline electrocardiographic intervals or absence of heart disease failed to distinguish a low risk group. Multivariate analysis identified absence of a pacemaker as the only significant predictor of arrhythmia complications (p = 0.022). CONCLUSIONS: Because clinically significant complications can be detected with in-hospital monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for initiation of sotalol. Patients without pacemakers are at higher risk for these complications.

Incidence and electrocardiographic localization of safe right bundle branch block configurations during permanent ventricular pacing.

The usual morphology for paced events originating from the right ventricle has a left bundle branch block (BBB) pattern. However, in a few patients, right BBB configurations are identified. It is important to differentiate safe right BBB patterns from those caused by septal or free wall perforation. Paced electrocardiograms were examined in 179 consecutive patients who underwent pacemaker placement. Fourteen patients (8%) were identified with right BBB configurations. Posteroanterior and lateral chest radiographs and echocardiograms were evaluated specifically to identify the pacing lead location in this group. In addition, 152 paced episodes from published reports were combined with our population to create an electrocardiographic algorithm differentiating right ventricular septum, right ventricular apex, coronary venous, and left ventricular pacing. Chest radiographs and echocardiographic lead locations correlated perfectly in the 11 patients available for echocardiograms. With use of a left superior axis and precordial transition by lead V3, right ventricular right BBB morphologies were correctly detected in 18 of 21 patients (86% sensitivity, 99% specificity) and appropriately separated from left ventricular pacing in 18 of 19 patients (95% positive predictive value). Therefore, 12-lead electrocardiograms are a rapid, reliable means of separating right and left ventricular right BBB pacing morphologies. Prudent use of these criteria will help eliminate unnecessary echocardiography, anticoagulation, and lead revision.

Lethal ventricular arrhythmias following one-step pacemaker reprogramming for rapid tracking of atrial tachyarrhythmias.

An abrupt decrease in the pacing rate in patients with dual-chamber pacemakers tracking atrial tachyarrhythmias carries a high risk of malignant ventricular arrhythmia. The pacing rate should be reduced by multistep programming over several days.

Paradoxical failure of QT prolongation during cardioinhibitory neurocardiogenic syncope.

QT modulation was explored in 31 patients with cardioinhibitory neurocardiogenic syncope. Despite a marked in increase in RR intervals, the QT interval remained stable.

Single-chamber ventricular pacing is not associated with worsening heart failure in sick sinus syndrome.

Ventricular pacing (with loss of normal atrioventricular synchrony) has been considered to have a role in the development or progression of congestive heart failure (CHF) in patients with sick sinus syndrome (SSS). No rigorous study has tested this hypothesis. Five hundred seven consecutive patients with SSS who received an initial pacemaker from January 1980 to December 1989 were studied. Atrial or dual-chamber pacemakers were implanted in 395 patients and ventricular pacemakers in 112. After a mean follow-up of 65 +/- 37 months, 97 patients (19%) developed new CHF or increased their New York Heart Association functional class. By univariate analysis, preimplant predictors for these events were left ventricular dysfunction (p < 0.001), valvular heart disease (p = 0.004), peripheral vascular disease (p = 0.005), diabetes (p = 0.02), coronary artery disease (p = 0.02), high New York Heart Association functional class (p = 0.03) and complex ventricular arrhythmia (p = 0.03). By multivariate analysis (logistic regression), the only predictors for CHF were valvular heart disease (p = 0.002; odds ratio [OR] 2.51), peripheral vascular disease (p = 0.003; OR 1.7) and complex ventricular arrhythmia (p = 0.027; OR 2.74). When the analysis was restricted to patients who had preimplant assessment of left ventricular function, independent predictors for CHF were left ventricular dysfunction (p < 0.001; OR 1.66), and complex ventricular arrhythmia (p < 0.001; OR 1.75). In conclusion, progressive or new-onset CHF is a consequence of the underlying cardiovascular disease. In the present population of patients with SSS, ventricular pacing mode was not associated with an increased incidence of CHF.

Cost effectiveness of administration of intravenous anesthetics for direct-current cardioversion by nonanesthesiologists.

Well-trained nonanesthesiologists can safely and effectively administer IV anesthetics for cardioversion. This practice results in considerable cost savings without compromising patient care.

QRS morphology-dependent pharmacodynamics in multiform ventricular ectopic activity.

The effect of an infusion of intravenous procainamide on the frequency of ventricular premature complexes (VCPs) of differing QRS morphologies was studied in 20 patients with multiform ectopic activity. In 17 of 20 patients, there was differential suppression of single VPCs with different QRS morphologies. VPCs of the most frequent QRS morphology and the second most frequent QRS morphology were compared with respect to the procainamide level at the escape of VPCs from 85% suppression and the duration of suppression measured from the onset of the procainamide infusion. In 8 patients, VPCs of the most frequent QRS morphology remained suppressed at lower procainamide concentrations and for longer times than did VPCs of the second most frequent QRS morphology (escape procainamide concentration = 2.8 +/- 1.7 versus 5.4 +/- 2.3 micrograms/ml, p less than 0.025; time to escape 244 +/- 138 versus 98 +/- 114 min; p less than 0.05). In 9 other patients, VPCs of the second most frequent QRS morphology remained suppressed at lower procainamide concentrations and for longer times than did VPCs of the most frequent QRS morphology (escape procainamide concentration 2.9 +/- 1.4 versus 8.3 +/- 6.3 micrograms/ml, p less than 0.025; time to escape 317 +/- 114 versus 63 +/- 80 min; p less than 0.001). Thus, in individual patients there are specific patterns of suppression of VPCs of different QRS morphologies which are independent of the frequency of each morphology. There is apparently a differential pharmacologic effect of procainamide on the foci or pathways responsible for the different QRS morphologies of multiform VPCs.

Cardiac arrhythmias associated with prophylactic pacing during coronary angiography.

Data from 518 consecutive cardiac catheterizations were analyzed to test the value of prophylactic pacemaker insertion during coronary angiography and to compare the incidence of arrhythmic complications in patients with and without pacemakers. In patients without pacing (n = 273), 1 episode of ventricular fibrillation occurred, which responded promptly to defibrillation. Sinus bradycardia (fewer than 30 beats/min for 10 seconds) was recorded in 74 patients (27%) and required treatment in 30 (11%). No patient required or would have benefited from pacemaker placement. Of the 245 patients with prophylactic pacemakers, there was an increased incidence of all ventricular (9 vs 1; p less than 0.013) and supraventricular (5 vs 0; p less than 0.046) arrhythmias. Pacemaker-associated induction of ventricular fibrillation occurred in 2 patients and was clearly related to electrical stimulation during a normally non-vulnerable period of the cardiac cycle. In conclusion, routine prophylactic pacemaker insertion during coronary angiography is not warranted in patients with normal sinus rhythm and normal atrioventricular conduction. More information is needed to determine if pacing is needed in patients with conduction system disease.

Significance of pacing cycle lengths in manifest entrainment of orthodromic circus movement tachycardia by ventricular pacing.

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 +/- 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 +/- 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 +/- 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 +/- 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 +/- 3% of the tachycardia CL, compared with 84 +/- 3% for retrograde AV nodal penetration (p less than 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.

Catheter ablation of the atrioventricular junction using radiofrequency energy and a bilateral cardiac approach.

Radiofrequency current catheter ablation was used successfully to create complete atrioventricular (AV) block in 60 of 61 patients (98%) with drug refractory supraventricular tachyarrhythmias. The remaining patient developed Mobitz I AV block and is clinically improved (clinical efficacy 100%). In 54 patients (89%), complete AV block was achieved using a right-sided approach. Patients aged > 60 years needed significantly fewer right-sided radiofrequency applications to produce complete AV block (5.3 +/- 5.3 vs 11.1 +/- 10.0; p = 0.009). In 6 of 7 patients with unsuccessful right-sided ablation, a left ventricular approach was used. In each case, 1 to 4 additional radiofrequency applications produced complete AV block. Patients with unsuccessful right-sided ablation were generally younger than those with successful ablation (50 +/- 16 vs 64 +/- 11; p = 0.007). It is concluded that catheter ablation using radiofrequency current is an extremely effective means of producing complete AV block. Older patients appear to be more susceptible to right-sided radiofrequency approaches. Left ventricular ablation easily produces complete AV block in patients refractory to right-sided attempts.

Annihilation, entrainment and modulation of ventricular parasystolic rhythms.

Annihilation and one-to-one entrainment of modulated parasystolic rhythms in humans has not been previously discussed. In 9 nonmedicated patients, it was possible to measure the intrinsic, parasystolic ectopic cycle length given by the intervals between 2 consecutive parasystolic beats without any interposed nonparasystolic beat. The corresponding values varied between 960 and 2,350 ms (corresponding to rates between 62 and 26 beats/min). In addition, modulation could be determined, because nonparasystolic beats falling during the initial 59% of the cycle prolonged the parasystolic cycle length (by 12 to 37.5%), whereas those that fell later in the cycle shortened it (by 9 to 25%). Plotting this prolongation or shortening as a function of the temporal position of the nonparasystolic beats in the cycle yielded biphasic response curves, of which 7 were symmetric and 2 asymmetric. In 2 patients, episodes of concealed one-to-one entrainment were initiated by late nonparasystolic (sinus) beats and, later on, terminated by early ventricular extrasystoles. In 2 other patients (and in 2 separate occasions) nonparasystolic beats, falling in part of the cycle located in between those of maximal delay and acceleration, produced pacemaker annihilation (cessation of automatic activity for the remaining monitoring time). Parasystolic annihilation and concealed entrainment may be one of the causes that can explain the large, spontaneous, day-to-day variability in the incidence of ectopic ventricular beats reported in Holter recordings. Nevertheless, future prospective studies performing interventions that can change the sinus and ectopic rates are required to corroborate our finding.

Selection bias in electrophysiologically-guided therapy of sustained ventricular tachyarrhythmias.

To analyze if patient selection bias could contribute to the improved prognosis reported for ventricular tachycardia (VT) and ventricular fibrillation (VF) when therapy is guided by electrophysiologic studies (EPS), we studied 90 consecutive patients admitted to a tertiary referral center with recent VT/VF who were candidates for EPS. Seventeen patients (19%) died during the initial hospital admission, and 30 (33%) died after discharge. Survival probability was 0.83 (95% confidence interval [CI], 0.74-0.90); 0.67 (95% CI, 0.56-0.75); and 0.53 (95% CI, 0.42-0.63) at 1 month, 1 year, and 3 years, respectively. Of the 56 patients (62%) who underwent EPS during their initial hospitalization, only 1 died during that admission. Patients in whom EPS could not be performed had characteristics associated with a poorer prognosis. NYHA functional class (p = 0.005), inability to perform baseline EPS (p = 0.003) and use of digoxin (p = 0.016) were independent predictors of death. Early in-hospital mortality in patients with VT/VF remains high. Thus, omission of these deaths in reports of EPS-guided therapy creates incomplete, biased cohorts. Furthermore, there may be a bias toward a healthier population among hospital survivors undergoing EPS. These findings may contribute to better outcomes in current series compared to historical controls.

Initial experience with the maze procedure for atrial fibrillation.

From January 1991 until May 1992, a total of 14 patients (mean age 48 years) underwent the maze procedure for refractory atrial fibrillation (mean duration, 7 years; mean number of antiarrhythmic medications, six). Three patients had had embolic events, one patient had had a cardiac arrest from flecainide, one had pulmonary fibrosis from amiodarone, and six of ten who were employed were temporarily disabled. Two patients underwent successful mitral valve repair in which the maze procedure was added as a secondary goal of the operation. Postoperative fluid retention was a problem in five patients (36%). Six patients (43%) were temporarily treated with an antiarrhythmic medication. Two patients (14%) with preoperative sick sinus syndrome required pacemakers. One patient was discharged from the hospital but died suddenly less than 1 month after the operation (7% operative mortality) of hyperkalemia caused by acute renal failure. All patients beyond 3 postoperative months (100% "cure") are receiving no antiarrhythmic medications, have sinus rhythm, or have p-wave tracking with ventricular pacing. Atrial contraction has been documented by cinegraphic magnetic resonance imaging studies and by Doppler echocardiography performed when sinus rhythm had resumed. The maze procedure is an extensive operation but is indicated for selected patients who have the severe sequelae of atrial fibrillation.