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Combined maze procedure and septal myectomy in a septuagenarian
Combined Maze Procedure and Septa1 Myectomy in a Septuagenarian Arie Blitz, MD, David McLoughlin, MD, Jay Gross, MD, Daniel S. Schwartz, MD, John D. Fisher, MD, So0 G. Kim, MD, Rosemary Frame, RN, and Richard F. Brodman, MD Departments of Cardiothoracic Surgery, Surgery, and Medicine, Montefiore Medical Center, Moses Division, and the Albert Einstein College of Medicine, Bronx, New York
A 75-year-old woman with refractory paroxysmal atrial fibrillation and hypertrophic obstructive cardiomyopathy underwent a successful combined maze procedure and septal myectomy. Postoperative episodes of atrial fibrillation and flutter occurred only during periods of bradyarrhythmia and did not recur with atrial inhibited pacing. (Ann Thorac Surg 1992;54:364-5)
A
trial fibrillation is relatively common in patients with hypertrophic obstructive cardiomyopathy. Five percent of patients with hypertrophic obstructive cardiomyopathy have atrial fibrillation at the time of diagnosis; it develops in an additional 10% in the following 5 years [l]. Patients who rely on atrial augmentation for adequate filling of a noncompliant left ventricle tolerate atrial fibrillation poorly [2]. Surgical therapy is ideally directed toward correction of left ventricular outflow tract obstruction and atrial fibrillation. Left ventricular outflow tract obstruction is effectively treated with a septal myectomy. Atrial fibrillation may be cured by the maze procedure, as developed by Cox and associates [3-61. This operation is performed on total cardiopulmonary bypass, with cardioplegic arrest used for the left atrial portions of the procedure. Several strategically located incisions are placed in the atria and are subsequently closed. These incisions serve to interrupt the macroreentrant pathways believed to be critical in the pathogenesis of atrial fibrillation [4]. Unlike previously described procedures for atrial fibrillation [5], the maze procedure abolishes atrial fibrillation while preserving atrioventricular synchrony and atrial transport function; it may reduce the risk of thromboembolism. We report a case of symptomatic hypertrophic obstructive cardiomyopathy and refractory paroxysmal atrial fibrillation successfully treated with a combined maze procedure and septal myectomy. Paroxysmal atrial fibrillation and flutter with a rapid ventricular response developed after an open cholecystecAccepted for publication Nov 27, 1991. Address reprint requests to Dr Brodman, Department of Cardiothoracic Surgery, Montefiore Medical Center, 111 East 210th St, Bronx, NY 10467.
0 1992 by The Society of Thoracic Surgeons
tomy in a 75-year-old woman with hypertrophic obstructive cardiomyopathy previously controlled with metoprolol. These arrhythmias were accompanied by chest pain, dyspnea, syncope, and hypoxia requiring ventilatory support. Trials of digoxin, procainamide, and disopyramide were ineffective or were discontinued due to side effects. An echocardiogram revealed an asymmetrically hypertrophied septum, normal cardiac contractility, mild left atrial enlargement, moderate mitral regurgitation, and systolic anterior motion of the anterior leaflet of the mitral valve. After amyl nitrate inhalation, the patient’s left ventricular outflow tract gradient increased from 16 to 100 mm Hg. Cardiac catheterization demonstrated a gradient of 90 mm Hg at rest, a left ventricular end-diastolic pressure of 15 mm Hg, an ejection fraction of 0.76, and a cardiac index of 1.7 L * min-’ * mp2. The coronary arteries were normal. A combined maze procedure (approved by the human research committee in February 1991) and septal myectomy were performed. Temporary and permanent atrial and ventricular epicardial pacing wires (Medtronic 10130 in-line bipolar epicardial leads; Medtronic, Minneapolis, MN) were placed. Postoperative fluid retention required the use of mannitol, Aldactone (spironolactone with hydrochlorothiazide; G.D. Searle & Co, Chicago, IL), Zaroxolyn (metolazone; Fisons Corp, Rochester, NY), and furosemide. After 5 weeks of therapy, diuretic administration was discontinued. A repeat echocardiogram 2 weeks postoperatively demonstrated no residual left ventricular outflow tract gradient, a normal ejection fraction, and minimal mitral regurgitation. Her temporary pacemaker was initially set at a rate of 70 beatslmin. A decrease in the rate or transient discontinuation of pacing resulted in recurrent junctional bradycardia followed by bursts of atrial fibrillation and flutter with ventricular response rates of 120 to 150 beats/min (Figs 1, 2). Subsequently, a permanent (DDDR) pacemaker was implanted and set at a rate of 85 beats/min to suppress her atrial arrhythmias. Her digoxin regimen was discontinued. On week 7, the patient was discharged receiving warfarin sodium (Coumadin; DuPont Pharmaceuticals, Wilmington, DE). A subsequent Holter monitor showed atrioventricular sequential pacing and no recurrence of atrial fibrillation/flutter (Fig 3). 0003-4975/92/$5.00
Ann Thorac Surg 1992:54:3645
365
CASE REPORT BLITZ ET AL MAZE PROCEDURE AND SEPTAL MYECTOMY
L"""""""""1
I
I
1s
Fig 1 . Electrocardiograni showing sinus bradycardia followed 6y atrial fibrillation. Paper speed is 25 mmls.
Comment The maze procedure has been recently described as a curative procedure for atrial fibrillation [3-61. Although the surgical incisions are somewhat formidable, the clinical results have been exceptional [5]. This case is unusual in regard to the age of the patient and the presence of hypertrophic obstructive cardiomyopathy. It is conceivable that a septa1 myectomy alone would have ameliorated the atrial fibrillation; however, immediate failure might have necessitated a repeat operative procedure, which would have been daunting. In the experience of Cox and associates [5], the predominant rhythm in the early postoperative period was junctional, with sinus rhythm returning between 4 days and 3 weeks postoperatively. Thereafter, all patients had either sinus rhythm or an atrially generated rhythm. Not surprisingly, the 2 patients in their series with preoperative sick sinus syndrome also had sinus node dysfunction postoperatively. The patient reported here was pacemaker-dependent immediately after operation. Subsequently, when pacing was discontinued, the patient's rhythm revealed junctional bradycardia interrupted by paroxysms of atrial fibrillation and flutter (see Figs 1, 2). Both were suppressed with pacing rates greater than 70 beats/min. In our patient, sinus node dysfunction was either present preoperatively or was caused by the incisions in the superior vena cava-high right atrial junction that are a part of the maze procedure [6]. The question arises as to why a patient undergoing a properly performed maze procedure should have devel-
Fig 3 . Holter recording after DDDR pacemaker implantation showing atrioventricular sequential pacing rhythm. (A = electrocardiogram; B = pacer artifact channel; C = atrial pacer artifact; D = ventricular pacer artifact.)
opment of atrial fibrillation and flutter postoperatively. Theoretically, all possible macroreentrant circuits should have been obliterated by the procedure. The answer may lie in the existence of microreentrant circuits that are not extinguished [7]. Moreover, these arrhythmias may reflect a transient postoperative phenomenon distinct from spontaneously occurring atrial arrhythmias. In view of the patient's satisfactory postoperative course, surgical intervention should be considered for patients with atrial fibrillation and hypertrophic obstructive cardiomyopathy whose symptoms are not controlled by medical therapy.
Addendum
As of May 20, 1992, the patient continues to be atrially paced and has had no further recurrence of atrial arrhythmias. She is receiving no medications. We thank Dr Ira Rubin for the referral of this patient.
References 1. Robinson K, Frenneaux MP, Stockins B, et al. Atrial fibrillation in hypertrophic cardiomyopathy: a longitudinal study. J Am Coll Cardiol 1990;15:1279-85. 2. Glancy DL, OBrien KP, Gold HK, Epstein SE. Atrial fibrilla-
B
C
Fig 2. Electrophysiologic data demonstrating the development of atrial flutter after pacing was discontinued. (A = atrial electrogram; B = electrocardiogram; C = atrial stimulus.)
tion in patients with idiopathic hypertrophic subaortic stenosis. Br Heart J 1970;32:652-9. 3. Cox JL, Schuessler RB, Stone CM, et al. The surgical treatment of atrial fibrillation: I. Summary of the current concepts of the mechanisms of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:402-5. 4. Cox JL, Canavan TE, Schuessler RB, et al. The surgical treatment of atrial fibrillation: 11. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:406-26. 5. Cox JL, Schuessler RB, DAgostino HJ, et al. The surgical treatment of atrial fibrillation: 111. Development of a definitive surgical procedure. J Thorac Cardiovasc Surg 1991;101:569-83. 6. Cox JL. The surgical treatment of atrial fibrillation:IV. Surgical technique. J Thorac Cardiovasc Surg 1991;101:584-92. 7. Cox JL, Boineau JP, Schuessler RB, et al. Successful surgical treatment of atrial fibrillation: review and clinical update. JAMA 1991;266:197&80.
A 75-year-old woman with refractory paroxysmal atrial fibrillation and hypertrophic obstructive cardiomyopathy underwent a successful combined maze procedure and septal myectomy. Postoperative episodes of atrial fibrillation and flutter occurred only during periods of bradyarrhythmia and did not recur with atrial inhibited pacing. (Ann Thorac Surg 1992;54:364-5)
A
trial fibrillation is relatively common in patients with hypertrophic obstructive cardiomyopathy. Five percent of patients with hypertrophic obstructive cardiomyopathy have atrial fibrillation at the time of diagnosis; it develops in an additional 10% in the following 5 years [l]. Patients who rely on atrial augmentation for adequate filling of a noncompliant left ventricle tolerate atrial fibrillation poorly [2]. Surgical therapy is ideally directed toward correction of left ventricular outflow tract obstruction and atrial fibrillation. Left ventricular outflow tract obstruction is effectively treated with a septal myectomy. Atrial fibrillation may be cured by the maze procedure, as developed by Cox and associates [3-61. This operation is performed on total cardiopulmonary bypass, with cardioplegic arrest used for the left atrial portions of the procedure. Several strategically located incisions are placed in the atria and are subsequently closed. These incisions serve to interrupt the macroreentrant pathways believed to be critical in the pathogenesis of atrial fibrillation [4]. Unlike previously described procedures for atrial fibrillation [5], the maze procedure abolishes atrial fibrillation while preserving atrioventricular synchrony and atrial transport function; it may reduce the risk of thromboembolism. We report a case of symptomatic hypertrophic obstructive cardiomyopathy and refractory paroxysmal atrial fibrillation successfully treated with a combined maze procedure and septal myectomy. Paroxysmal atrial fibrillation and flutter with a rapid ventricular response developed after an open cholecystecAccepted for publication Nov 27, 1991. Address reprint requests to Dr Brodman, Department of Cardiothoracic Surgery, Montefiore Medical Center, 111 East 210th St, Bronx, NY 10467.
0 1992 by The Society of Thoracic Surgeons
tomy in a 75-year-old woman with hypertrophic obstructive cardiomyopathy previously controlled with metoprolol. These arrhythmias were accompanied by chest pain, dyspnea, syncope, and hypoxia requiring ventilatory support. Trials of digoxin, procainamide, and disopyramide were ineffective or were discontinued due to side effects. An echocardiogram revealed an asymmetrically hypertrophied septum, normal cardiac contractility, mild left atrial enlargement, moderate mitral regurgitation, and systolic anterior motion of the anterior leaflet of the mitral valve. After amyl nitrate inhalation, the patient’s left ventricular outflow tract gradient increased from 16 to 100 mm Hg. Cardiac catheterization demonstrated a gradient of 90 mm Hg at rest, a left ventricular end-diastolic pressure of 15 mm Hg, an ejection fraction of 0.76, and a cardiac index of 1.7 L * min-’ * mp2. The coronary arteries were normal. A combined maze procedure (approved by the human research committee in February 1991) and septal myectomy were performed. Temporary and permanent atrial and ventricular epicardial pacing wires (Medtronic 10130 in-line bipolar epicardial leads; Medtronic, Minneapolis, MN) were placed. Postoperative fluid retention required the use of mannitol, Aldactone (spironolactone with hydrochlorothiazide; G.D. Searle & Co, Chicago, IL), Zaroxolyn (metolazone; Fisons Corp, Rochester, NY), and furosemide. After 5 weeks of therapy, diuretic administration was discontinued. A repeat echocardiogram 2 weeks postoperatively demonstrated no residual left ventricular outflow tract gradient, a normal ejection fraction, and minimal mitral regurgitation. Her temporary pacemaker was initially set at a rate of 70 beatslmin. A decrease in the rate or transient discontinuation of pacing resulted in recurrent junctional bradycardia followed by bursts of atrial fibrillation and flutter with ventricular response rates of 120 to 150 beats/min (Figs 1, 2). Subsequently, a permanent (DDDR) pacemaker was implanted and set at a rate of 85 beats/min to suppress her atrial arrhythmias. Her digoxin regimen was discontinued. On week 7, the patient was discharged receiving warfarin sodium (Coumadin; DuPont Pharmaceuticals, Wilmington, DE). A subsequent Holter monitor showed atrioventricular sequential pacing and no recurrence of atrial fibrillation/flutter (Fig 3). 0003-4975/92/$5.00
Ann Thorac Surg 1992:54:3645
365
CASE REPORT BLITZ ET AL MAZE PROCEDURE AND SEPTAL MYECTOMY
L"""""""""1
I
I
1s
Fig 1 . Electrocardiograni showing sinus bradycardia followed 6y atrial fibrillation. Paper speed is 25 mmls.
Comment The maze procedure has been recently described as a curative procedure for atrial fibrillation [3-61. Although the surgical incisions are somewhat formidable, the clinical results have been exceptional [5]. This case is unusual in regard to the age of the patient and the presence of hypertrophic obstructive cardiomyopathy. It is conceivable that a septa1 myectomy alone would have ameliorated the atrial fibrillation; however, immediate failure might have necessitated a repeat operative procedure, which would have been daunting. In the experience of Cox and associates [5], the predominant rhythm in the early postoperative period was junctional, with sinus rhythm returning between 4 days and 3 weeks postoperatively. Thereafter, all patients had either sinus rhythm or an atrially generated rhythm. Not surprisingly, the 2 patients in their series with preoperative sick sinus syndrome also had sinus node dysfunction postoperatively. The patient reported here was pacemaker-dependent immediately after operation. Subsequently, when pacing was discontinued, the patient's rhythm revealed junctional bradycardia interrupted by paroxysms of atrial fibrillation and flutter (see Figs 1, 2). Both were suppressed with pacing rates greater than 70 beats/min. In our patient, sinus node dysfunction was either present preoperatively or was caused by the incisions in the superior vena cava-high right atrial junction that are a part of the maze procedure [6]. The question arises as to why a patient undergoing a properly performed maze procedure should have devel-
Fig 3 . Holter recording after DDDR pacemaker implantation showing atrioventricular sequential pacing rhythm. (A = electrocardiogram; B = pacer artifact channel; C = atrial pacer artifact; D = ventricular pacer artifact.)
opment of atrial fibrillation and flutter postoperatively. Theoretically, all possible macroreentrant circuits should have been obliterated by the procedure. The answer may lie in the existence of microreentrant circuits that are not extinguished [7]. Moreover, these arrhythmias may reflect a transient postoperative phenomenon distinct from spontaneously occurring atrial arrhythmias. In view of the patient's satisfactory postoperative course, surgical intervention should be considered for patients with atrial fibrillation and hypertrophic obstructive cardiomyopathy whose symptoms are not controlled by medical therapy.
Addendum
As of May 20, 1992, the patient continues to be atrially paced and has had no further recurrence of atrial arrhythmias. She is receiving no medications. We thank Dr Ira Rubin for the referral of this patient.
References 1. Robinson K, Frenneaux MP, Stockins B, et al. Atrial fibrillation in hypertrophic cardiomyopathy: a longitudinal study. J Am Coll Cardiol 1990;15:1279-85. 2. Glancy DL, OBrien KP, Gold HK, Epstein SE. Atrial fibrilla-
B
C
Fig 2. Electrophysiologic data demonstrating the development of atrial flutter after pacing was discontinued. (A = atrial electrogram; B = electrocardiogram; C = atrial stimulus.)
tion in patients with idiopathic hypertrophic subaortic stenosis. Br Heart J 1970;32:652-9. 3. Cox JL, Schuessler RB, Stone CM, et al. The surgical treatment of atrial fibrillation: I. Summary of the current concepts of the mechanisms of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:402-5. 4. Cox JL, Canavan TE, Schuessler RB, et al. The surgical treatment of atrial fibrillation: 11. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:406-26. 5. Cox JL, Schuessler RB, DAgostino HJ, et al. The surgical treatment of atrial fibrillation: 111. Development of a definitive surgical procedure. J Thorac Cardiovasc Surg 1991;101:569-83. 6. Cox JL. The surgical treatment of atrial fibrillation:IV. Surgical technique. J Thorac Cardiovasc Surg 1991;101:584-92. 7. Cox JL, Boineau JP, Schuessler RB, et al. Successful surgical treatment of atrial fibrillation: review and clinical update. JAMA 1991;266:197&80.