Author + information
- Received September 2, 1997
- Revision received May 21, 1998
- Accepted June 3, 1998
- Published online October 1, 1998.
- Miralem Pasic, MD, PhDa,* (, )
- Michele Musci, MDa,
- Henryk Siniawski, MDa,
- Barbara Edelmanna,
- Takeo Tedoriya, MDa and
- Roland Hetzer, MD, PhDa
- ↵*Address for correspondence: Dr. Miralem Pasic, Deutsches Herzzentrum Berlin, Klinik für Herz-, Thorax- und Gefässchirurgie, Augustenburger Platz 1, D-13353 Berlin, Germany
Objectives. This prospective study examined types, frequency and time dependency of the electrophysiologic manifestation of the sinus node dysfunction after the Cox-maze III procedure—the technique of choice for the management of medically refractory atrial fibrillation—in patients with organic heart disease, chronic fixed atrial fibrillation and no preoperatively overt dysfunction of the sinus node.
Background. The original maze procedure was modified twice in order to reduce the high incidence of the sinus node inability to generate an appropriate sinus tachycardia in response to maximal exercise, and occasional left atrial dysfunction. Despite these modifications, postoperative disturbance of sinus node function can be frequently observed.
Methods. In 15 adult patients, standard electrocardiogram, 24-h Holter monitoring, power spectral analysis of heart variability, exercise testing, Valsalva maneuver and rapid positional changes were performed 3, 6 and 12 months after the Cox-maze III procedure and mitral valve surgery or closure of atrial septal defect.
Results. Electrocardiographic manifestations of sinus node dysfunction were identified in 12 patients at 3 months, in 6 patients at 6 months, and in 0 patients at 12 months after surgery. The heart rate response to exercise during the first 6 months was reduced in the maze group and became fully normal at 12 months. Power spectral analysis of heart rate variability showed very low power values at 1 month with inhibited cardiac autonomic activity and no response on sympathetic stress. A potential of recovery of cardiac autonomic activity was documented 12 months after surgery.
Conclusions. The manifestations of sinus node dysfunction following the Cox-maze III procedure were time dependent and their frequency and intensity progressively decreased and disappeared within 12 months after surgery.
Several surgical approaches have been used to treat patients with atrial fibrillation (1–5). The Cox-maze procedure is based on the principle to prevent the atria from fibrillation interrupting of all the potential pathways for atrial macro-reentrant circuits (3,4). Multiple atrial incisions are made to channel sinus impulses through a path or “maze,” to reach the atrioventricular node. This prevents a critical mass of contiguous atrial tissue from sustaining atrial fibrillation while maintaining atrial contractility (3,4,6). The procedure needs neither intraoperative mapping nor specific correction of the technique in a particular patient (3). It possesses substantial functional advantages over other surgical techniques by achieving in almost all patients the four main therapeutic goals: rate control, restoration and maintenance of sinus rhythm, risk reduction of thromboembolism and restoration of normal cardiac hemodynamics. Some atrial incisions of the original maze procedure (4)have been rerouted in order to reduce the high incidence of the inability to generate an appropriate sinus tachycardia in response to maximal exercise and occasional left atrial dysfunction (7,8). This modified technique also decreased substantially a number of patients who required implantation of a permanent pacemaker (7). The current modification—the Cox-maze III procedure (8)—is now the technique of choice for the management of medically refractory atrial fibrillation (7,9,10).
Since January 1995, we have routinely used the Cox-maze III procedure in conjunction with mitral valve surgery or repair of atrial septal defect in patients with chronic fixed atrial fibrillation. Despite the use of the modified technique of the original maze procedure, we have frequently noted disturbances of sinus node function in our patients which encompassed a wide range of electrophysiologic abnormalities. The observed electrocardiographic manifestations predominantly included characteristics of sinus node dysfunction such as severe sinus bradycardia, sinus pauses or sinus arrest, sinoatrial exit block, atrial tachyarrhythmias, alternating periods of atrial bradyarrhythmias and tachyarrhythmias and inappropriate heart rate responses during physical exercise or emotional stress.
The aims of this prospective longitudinal study were (1) to identify types and frequency of the postoperative electrophysiologic manifestations of the sinus node dysfunction; (2) to detect their time-dependency during the first 12 postoperative months; and (3) to evaluate possible causes for these pathologic findings following the maze procedure in patients with organic heart disease and no preoperative evidence of underlying sinus node dysfunction.
Fifteen adult patients (13 females and 2 males) with chronic fixed atrial fibrillation and organic heart disease underwent combined Cox-maze III procedure and mitral valve surgery (n = 13) or closure of atrial septal defect type II (n = 2). The mean age was 62 years ranging between 52 and 72 years. The duration of chronic atrial fibrillation was between 6 months and 12 years with a mean of 5 years. Preoperative chronic atrial fibrillation was not associated with a slow ventricular response or alternating periods of atrial bradyarrhythmias and tachyarrhythmias. Mitral valve pathology was predominantly stenosis in 6 patients and incompetence in 7 patients. Three patients underwent mitral valve repair and 5 received mechanical and 5 biological valves. In 2 patients atrial septal defect type II was closed with autologous pericardial patch. The mean left ventricular ejection fraction was 50% ranging from 40% to 80%. All patients were preoperatively in New York Heart Association functional class III or IV. A routine battery of preoperative tests was performed to exclude major disorders such as hematological, thyroid, renal and hepatic abnormalities. Significant concomitant coronary artery disease was excluded by coronary angiography in all patients. No patient had had evident or suspected dysfunction of the sinus node before operation. No electrophysiologic studies had been performed preoperatively. All patients signed written informed consent.
The second modification of the maze technique, the Cox-maze III procedure (8), was applied with some minor modifications in all patients. Operation is carried out via median sternotomy using separate caval cannulation, total cardiopulmonary bypass and mild systemic hypothermia of 32°C. Generally, the Cox-maze procedure encompasses excision of the both atrial appendages, multiple incisions with consecutive continuous sutures of the left and right atria and cryoablation of the dissected coronary sinus as well as mitral and tricuspid anuli at the standard points. Briefly, the procedure starts with complete mobilization of the venae cavae, aorta, pulmonary artery and the posterior wall of the left atrium, and then the heart is arrested using a current cardioplegic technique. The left-side part of the procedure includes opening of the left atrium through the standard left-atrial, right-side mitral-valve approach, and isolation of the pulmonary veins using a pulmonary-veins-encircling incision, excision of the left atrial appendage, and connecting incisions between the pulmonary-veins-encircling incision and the left appendicular incision as well as between the pulmonary-veins-encircling incision and to the mitral anulus (Fig. 1). The right-side incisions are placed across the free anterior wall of the right atrium between the venae cavae, above the inferior vena cava towards the tricuspid valve anulus and into the interatrial septum (Fig. 2). In patients with atrial septal defect, the defects are closed with autologous pericardial patch at this time point. After closing all incisions (Fig. 3), the heart is deaired and the aortic crossclamp is removed. Four temporary atrial and four temporary ventricular wires are placed intraoperatively for future pacing. A regular rhythm typically with a possibility to perform atrial pacing, either sinus rhythm or mostly junctional rhythm, is characteristical for the reperfusion phase.
The postoperative recovery was uneventful in all patients. Two patients developed fluid retention with left-side pleural effusion which was treated by diuretics. The patients stayed at our institution for 3 to 7 days until stabilization of the rhythm. The sinus rhythm was confirmed by clearly visible P wave in surface electrocardiogram and/or by atrial electrocardiogram. Cardiac rhythm was continuously monitored after surgery until stable rhythm returned. Thereafter, patients were transferred back to a referral cardiology department. All patients were prospectively followed-up by their cardiologists or family physicians for adjustment of medication and control of anticoagulation and rhythm. All patients received peroral phenprocoumon (Marcumar) as anticoagulation medication. There was no bleeding or thromboembolic event in the study group during the follow-up. Regular surveillance at our institution was scheduled for 1, 3, 6, and 12 months after surgery. All patients were followed-up at least 12 months postoperatively. Standard and right precordial electrocardiogram, 24-h Holter monitoring, exercise testing, power spectral analysis of heart variability, Valsalva maneuver and rapid positional changes were performed 3, 6, and 12 months after surgery. The heart function was assessed by transesophageal echocardiography which demonstrated contractility and atrial transport of different grade of both atria in all patients which improved over time (data not reported). Transesophageal echocardiography was performed on a regular basis (at 1, 3, 6 and 12 months postoperatively) the same day as most of the other examinations. Anticoagulation with phenprocoumon (Marcumar) was discontinued and replaced with aspirin in patients without mechanical heart valves as early as 6 months postoperatively if a patient has had stable sinus rhythm in 24-h Holter monitoring and documented normal atrial contractions in TEE examinations (data not shown).
All patients received angiotensin-converting enzyme inhibitors postoperatively. Antiarrhythmics were given in patients with episodes of postoperative supraventricular tachyarrhythmias and were tapered if the rhythm became stable. The patients were told to discontinue cardiovascular medications except angiotensin-converting enzyme inhibitors a week before postoperative studies and the patients were maintained without these drugs during the examinations.
Ambulatory 24-h Holter monitoring
performed during usual daily activities was used to assess occurrence of atrial fibrillation and sinus node dysfunction.
Power spectral analysis of heart rate variability
was analyzed under head-up tilt test (0° and 60°). Electrocardiographic documentation was continuously registered with a two-channel ambulatory recorder on supine and 60° head-up tilt position for 10 min each. The last 512 consecutive heart beats in each position were processed by the maximal entropy method. The spectral power of both low-frequency (LF: 0.04 to 0.15 Hz) and high frequency (HF: 0.15 to 0.40 Hz) components, as well as LF/HF were calculated. This examination was performed in 6 patients after the maze procedure.
Exercise stress testing
was used to assess the ability of the sinus node to accelerate in response to internal physiologic chronotropic stimuli. Ergometer bicycle study started at 25 W workload (150 kpm/min), increasing by 25 W every 3 min until peak exercise was reached as defined by development of fatigue and/or dyspnea. To assess possible dysfunction of the autonomic nervous system, autonomic activity was tested by control of the heart rate changes induced by Valsalva maneuver and by rapid positional changes. The heart rate was calculated from continuous standard 12 lead electrocardiogram monitoring at rest, at the end of each 3-min workload, and at peak exercise.
Definition of sinus node dysfunction
Sinus node dysfunction encompasses a wide range of electrophysiologic abnormalities, including disorders of the generation and subsequent emergence of the sinus impulse into atria, abnormal impulse transmission within the atria and specialized cardiac conduction system, failure of physiological subsidiary pacemaker function, and increased susceptibility to paroxysmal or chronic primary atrial tachycardias (11,12). Electrocardiographic manifestations of sinus node dysfunction included severe sinus bradycardia with a rate less than 50 beat per min, sinus arrest or sinus pauses longer than 3 s, sinoatrial exit block, atrial tachyarrhythmias, alternating periods of atrial bradyarrhythmias and tachyarrhythmias and inappropriate heart rate responses during physical exercise or emotional stress (11,13). Junctional rhythm early after surgery by the possibility to perform atrial pacing was considered as sinus node dysfunction (3).
All data are reported as mean ± standard error except where noted otherwise. Data were analyzed with use of a nonpaired or paired ttest as appropriate. Multiple comparisons within a group over time were made by use of univariate repeated measures of a one-way analysis of variance (ANOVA). Statistical significance was defined as a probability value of 0.05 or less.
Ten patients (67%) left the operating room with stable sinus rhythm and 5 (33%) with junctional rhythm that required faster atrial pacing. Three of the 10 patients with initial stable sinus rhythm changed to junctional rhythm on the second and third postoperative days, respectively. After continuous intravenous administration of orciprenaline sulfate (Alupent), it converted to sinus rhythm within the following 3 days; orciprenaline sulfate administration was stopped after sinus rhythm returned. During the early postoperative course, 5 patients had had junctional rhythm continuously after operation that changed to sinus rhythm within the first 3 postoperative days in 2 patients. The other 3 junctional rhythm patients that had not converted to sinus rhythm within the first 3 postoperative days were put on a regimen of orciprenaline sulfate (Alupent) intravenously; sinus rhythm appeared in all patients following 2–3 days. Continuous monitoring of the rhythm was necessary because 2 patients with junctional rhythm and atrial pacing were intermittently asystole after their pacemakers were temporarily turned off. Episodes of atrial fibrillation were observed in 8 (53%) patients during their hospital stay. All were treated with digoxin in combination with verapamil and all were in stable sinus rhythm when they were discharged from our institution. Intermittent episodes of atrial fibrillation were observed in 3 (20%) patients within 3 months after the operation. One patient was treated with digoxin alone, 1 patient in combination with verapamil, and 1 patient with digoxin in combination with sotalol. Twelve months after surgery—at the end of the study period—all patients were in stable sinus rhythm as assessed by 24-h Holter monitoring, standard and right precordial electrocardiogram and patients’ subjective judgment of absence of arrhythmia.
Electrocardiographic manifestations of sinus node dysfunction
Severe sinus bradycardia, sinus pauses or sinus arrest, sinoatrial exit block, atrial tachyarrhythmias, alternating periods of atrial bradyarrhythmias and tachyarrhythmias were identified in 12 patients during the first 3 months, in 6 patients at 6 months, and in 0 patients at 12 months after surgery. Subjective symptoms that might be associated with dysfunction of the sinus node were easy fatigue in 9 patients, palpitations in 6 patients, nausea in 1 patient, dizziness in 1 patient, and faintness in another patient. These complaints were mild and transient in all symptomatic patients and disappeared completely within 6 months after surgery. Syncope or congestive heart failure occurred in no instances.
Heart rate at rest and exercise
Heart rate at rest was higher during the early months after surgery than 12 months after surgery (Table 1). Serial exercise studies found lower resting heart rates and higher maximal exercise heart rates over time in the maze patients. Inappropriate heart rate responses during physical exercise were clearly evident during the first 6 months and normalization of its physiologic functions can be seen at 12 months (Table 1). Thus, the heart rate response to exercise of the maze patients were pathologically low from 1 through 6 months and with normal values at 12 months postoperatively.
Power spectral analysis of heart rate variability
showed very low power values 1 month after the maze procedure with inhibited cardiac autonomic activity and no response on sympathetic stress (LF, HF, LF/HF: at 0°, 12.5, 32.5, 0.38; at 60°, 1.2, 16.4, 0.07, respectively). A potential of recovery of cardiac autonomic activity was documented in the later paired at the 1-year-follow-up (LF, HF, LF/HF: at 0°, 206.7, 403.4, 051; at 60°, 9.6, 25.6, 037, respectively).
In patients with the maze procedure there was no increase in heart rate within 30 s of standing up during the first 6 postoperative months. Valsalva maneuver did not affect the rate in our patients and they failed to show normal responses with an early reflex tachycardia followed by a reflex bradycardia during the Valsalva maneuver. At 12 months, the heart rate increased in the maze group by 5 to 10 beats within 30 s of standing up and during early exercise.
Our study showed that transient disturbances of sinus node function occurred postoperatively in all patients with chronic fixed atrial fibrillation and organic heart disease undergoing combined the Cox-maze III procedure and mitral valve surgery or atrial septal defect closure. Duration of sinus node dysfunction and intensity and frequency of manifestations were time dependent and successively decreased during the postoperative follow-up. The physiologic effects of sinus node dysfunction in changes in heart rate and other manifestations were clearly evident during the first 6 months after the procedure. Thereafter, between 6 and 12 months following surgery, a continuous improvement of the sinus node physiologic functions was documented. One year after surgery normal sinus node function was noted in all patients. Therefore, we concluded that sinus node dysfunction following the Cox-maze III procedure is a transient process in patients with chronic fixed atrial fibrillation and organic heart disease.
Preoperative sinus node dysfunction
It should be emphasized that sinus node dysfunction may already exist in patients with chronic atrial fibrillation before they undergo the Cox-maze procedure. Latent concomitant dysfunction can be masked by atrial fibrillation being recognized postoperatively after establishing of stable sinus rhythm. Our patients did not have coronary artery disease which was excluded by preoperative angiography, and preoperative chronic atrial fibrillation was not associated with a slow ventricular response or alternating periods of atrial bradyarrhythmias and tachyarrhythmias. Although there had been no evidence of underlying dysfunction of the sinus node before operation in our patients, it could not be excluded only by electrocardiographic findings or anamnestical data. Preoperative exclusion of this abnormality in case of sustained atrial fibrillation is often difficult and not even possible without electrophysiologic studies which had not been performed in this group of patients. Etiology of preoperatively existed dysfunction of the sinus node in patients with chronic fixed atrial fibrillation and structural heart disease is multifactorial in nature. Common findings in these patients are atrial dilatation and patchy fibrosis that can range from scattered foci to diffuse involvement, including evidence of destruction of the sinus node (14). If fibrosis in the region of the sinus node is excessive, it may result in loss of central pacemaker cell nests and might result in more peripherally located pacemakers being responsible for the cardiac rhythm (11). Some of patients may have had preexisting coronary artery disease with subsequent impaired blood supply of the sinus node which also can cause its transient or permanent dysfunction (15). The possible role of antibodies to the human sinus node in sinus node dysfunction has not yet been well defined (16).
Possible causes of postoperative sinus node dysfunction
Mechanisms involved in disturbance of cardiac rhythm following the Cox-maze procedure occur either as 1) primary events of the maze procedure itself or 2) as general postoperative complications of open-heart surgery. In both instances the sinus node can be either a) directly damaged (intrinsic sinus node dysfunction) or b) its function can be impaired by remote causes without direct injury of the nodal tissue (extrinsic sinus node dysfunction). The surgical factors that directly alter the anatomy and functional integrity of the sinus node or surrounding atrium or both include mechanical trauma due to atrial incisions, surgically interruption of the nodal arterial supply, traction on the heart with retractors and manipulations during the operation, suture injury, placement of caval cannulas, inadequate atrial preservation during cardiopulmonary bypass especially when the sinus node artery is transected, hemorrhage, ischemia, or necrosis (3,6,9,17). The factors that impair sinus node function without evidence of structural sinoatrial injury itself have an important role not only in modulating normal function of the sinus node function but also as potential contributors to sinus node dysfunction (11). These factors extrinsic to the sinus node are disturbances of autonomic neural control, humoral and electrolyte imbalance and effect of cardiovascular drugs such as sympatholytic agents or antiarrhythmic drug. Each of these factors can modify the electrophysiologic characteristics of the sinus node independently from others or in interaction with them (12).
Surgical factors of sinus node dysfunction
The effects of currently used surgical incisions of the maze procedure on atrial innervation, humoral homeostasis, and consecutive rhythmogenic effects are still not known and not well understood. The main concerns are influences on integrity of functional sinus node region, autonomic neural regulation and arterial blood supply. The arterial supply to the sinus node may be more variable than had previously been appreciated, making the entire junctional area between the right atrium and the superior vena cava a critical zone. The sinus node artery is larger than expected considering the extent of the area that it supplies, probably due to its physiologic importance (12). A single sinus node artery originates from the proximal 2 to 3 cm of the right coronary artery in 55% of humans and from the proximal 1 cm of the left circumflex artery in 45% with a rich supply of collateral vessels, densest centrally and sparser peripherally of the sinus node region (12). Better preservation of the sinus node as well as its arterial blood supply during the Cox-maze procedure may reduce the incidence of sinus node dysfunction requiring pacemaker implantation and may enable earlier recovery of sinus rhythm (3,8). However, the disturbance in flow of the sinus node artery might contribute to sinus node dysfunction in a few cases but probably does not represent a substantial contribution to the pathogenesis, especially after the modifications of the arteriotomies of the Cox-maze III procedure that preserve sinus node arteries and possibly the sinus node itself (7). The maze incisions in the right atrial wall spare the anatomical region of the sinus node (8). However, pacemaker function within the atria is complex and not readily attributed to a single pacing site. Experimental and clinical evidence suggest that the functional sinus node region is less well defined than previously appreciated. For instance, in neonates and infants, the region of the sinus node may extend more caudally toward the inferior vena cava. Damage to this region during operative procedures may ultimately lead to abnormalities of sinoatrial function (11).
Possible roles of autonomic neural system on sinus node dysfunction
Autonomic nerves affect cardiac chronotropism, dromotropism and inotropism through their efferent projections to the sinus node, atrioventricular node and atrial musculature. Both blocking and stimulation of sympathetic or parasympathetic systems may cause sinus node dysfunction. Activation of the parasympathetic pathway increases transmembrane potential and reduces phase 4 slope; both effects tend to reduce pacemaker rate, prolonged refractoriness of sinus node cells, and further slow intranodal conduction velocity resulting in negative chronotropic, dromotropic, and inotropic changes in the heart. It causes electrocardiographic findings of marked sinus bradycardia, sinus arrest, and sinoatrial exit block, which are all consistent with sinus node dysfunction (11). Enhanced parasympathetic tone predisposes otherwise normal hearts to the onset of atrial fibrillation and, similarly, increased sympathetic tone may also lead to atrial fibrillation. Elevated sympathetic tone, decreased parasympathetic tone, or combination of both factors could lead to an immediate increase in heart rate. During simultaneous stimulation of the sympathetic and parasympathetic systems, deceleration of sinus rate predominates over the acceleratory effects of sympathetic stimulation with pacemaker shift from the superior part to the inferior part of the sinus node (18). In both health individuals and patients with sinus node dysfunction, influence of the autonomic nervous system on sinus node function changes during life with predominance of vagal tone in young adults and a preeminence of sympathetic activity in older (19,20). The age at which the parasympathetic predominance is replaced by a sympathetic predominance varies according to the state of the sinus node (normal or sick) beginning already at age less than 60 years (20). The form of autonomic neural influence that will dominate postoperatively is not uniform in patients undergoing the maze procedure. Occurrence of atrial fibrillation during the early postoperative course at night, during rest, and preceded by progressive bradycardia indicates a vagal form of atrial fibrillation in our patient. However, in some patients it appeared exclusively during the daytime and often preceded by exercise and emotional stress, typically with a specific sinus rate of near 90 beat/min indicates adrenergic (sympathetic dominance) type of atrial fibrillation (21).
Heart denervation after the maze procedure
It is very likely that some degree of both partial parasympathetic denervation (due to decentralization and the direct surgical injury of the ganglia) and partial sympathetic denervation (due to partial autotransplantation) can simultaneously occur in patients with the maze procedure. This partial denervation of the heart could be one of the causes for the transient sinus node dysfunction during the early postoperative course. Efferent parasympathetic innervation of the human heart consists of preganglionic neurons located in the brain stem that project by the vagus nerve to postganglionic neurons within the cardiac ganglia. The postganglionic neurons project to the sinoatrial and atrioventricular nodes, as well as to the atrial and ventricular musculature. The largest populations of cardiac ganglia are concentrated lateral to the right pulmonary veins and inferior to the superior vena cava, near but not within the sinus and atrioventricular nodes, and at the interatrial grove and coronary sulcus junction (22). The incisions in the right atrium between the superior and inferior caval veins as well as the classic approach to the mitral valve made through areas of high cardiac ganglia density are likely to alter parasympathetic innervation of the sinus node and the right atrial free wall, thereby resulting in partial or total parasympathetic denervation of the sinus node (23). Our results of power spectral analysis of heart rate variability showed inhibited cardiac autonomic activity and no response on sympathetic stress early postoperatively. A potential of recovery of cardiac autonomic activity was documented 12 months after surgery.
Management of postoperative sinus node dysfunction
Treatment strategy of sinus node dysfunction after the maze procedure is largely dictated by patient’s symptoms and electrocardiographic findings. Continuous monitoring of the rhythm and stand by modus of ventricular pacing “on demand” are important during the early postoperative course after the maze procedure because some of the patients may be intermittently asystole. Sinus arrhythmia, sinus tachycardia, and nonphysiological sinus tachycardia do not need pacemaker implantation (11). Sinus pause or arrest longer than 3 s is rarely an indication for pacemaker implantation in patients with the maze procedure because they were uncommonly associated with symptoms in our patients. However, in patients other than those with the maze procedure, these electrocardiographic findings may be combined with the symptoms and therefore may require pacemaker implantation (24), although some found symptoms to be uncommon during such pauses, and prognosis was not altered by cardiac pacing (25). Nevertheless, pauses longer than 3 s warrant careful clinical assessment, with further attempts being made to detect symptomatic correlation or other evidence of sinus node dysfunction (11). Sinoatrial exit block (first-degree sinoatrial block, Mobitz I AV block, Wenckebach periodicity third-degree or complete sinoatrial exit block) implies either delay or failure of a normally generated sinus impulse to exit the nodal region. The clinical implications for pauses in cardiac rhythm resulting from sinoatrial exit block are essentially the same as those associated with sinus pauses or arrest. As a rule, high-grade sinoatrial exit block implies severe sinus node dysfunction and is usually associated with symptoms (12). In patients with persistent bradycardia (complete heart block, bradycardia with underlying sinus rhythm, nodal rhythm or atrial fibrillation) after operation, it should be determined whether to continue hospitalization with temporary pacing or to place a permanent pacemaker. A pacemaker is primarily indicated to treat documented symptomatic bradyarrhythmias resulting from sinus node dysfunction itself in order to decrease mortality and diminish the component of exercise intolerance related to chronotropic incompetence. Permanent pacemaker implantation for sinus node dysfunction after the maze procedure especially in asymptomatic or mildly symptomatic patients should be restrictively applied because of the transient nature of this disorder. However, some patients need a permanent pacemaker because symptomatic sinus node dysfunction existed already before the operation. It is well known from the clinical experience with cardioversion that some patients with sinus node dysfunction exhibit exceedingly long asystolic periods after cardioversion because of sinus node automaticity or because of high-grade sinoatrial exit block along with inadequate subsidiary pacemaker responsiveness. In some cases it is not possible to reinitiate sinus rhythm and, despite of termination of atrial fibrillation or flutter, the atria may remain silent, or a junctional or fascicular rhythm becomes dominant necessitating a permanent pacemaker implantation in most cases. If oral therapy with theophyline, a drug that exerts positive chronotropic and dromotropic effects on the sinus node and atrioventricular node cells (9,26), can be beneficial in this group of patients, it must first be determined.
Limitations of the study
A significant limitation of this study is the small group of patients. There were only 15 patients in the study group and all of them were without underlying sinus node dysfunction existing preoperatively. Therefore, this group of patients cannot be considered a representative group of general population with chronic atrial fibrillation. Thus, this study should be considered only as an observational study. Because of the small number of patients and the fact that the patients had been selected for the maze procedure, we were able to achieve an excellent postoperative result. In this group of patients there was no need for permanent pacemaker implantation. However, in a larger group of patients an optimal result should be expected with a success of about 85–90% of postoperative conversion in sinus rhythm and an incidence of about 5% of permanent pacemaker implantations (7,10). However, the aim of the study was to show that in selected patients the conversion is practically 100% with no late sequelae due to the surgical procedure itself.
Sinus node dysfunction following the Cox-maze III procedure in patients is transient in nature, mostly asymptomatic and incorporated into the picture of postoperative reconvalescence. In patients without underlying sinus node dysfunction before operation, this transient postoperative abnormality can be caused both by the operative procedure itself or by several processes not directly related to surgery. Permanent pacemaker implantation for sinus node dysfunction after the maze procedure—especially in asymptomatic or mildly symptomatic patients—should be restrictively applied because of the transient nature of this disorder.
We are indebted to Mrs. Diana Kendall for her secretarial work and Mr. Helge Haselbach for the illustrations.
- transesophageal echocardiography
- the spectral power of low-frequency of heart variability
- the spectral power of high-frequency of heart variability
- Received September 2, 1997.
- Revision received May 21, 1998.
- Accepted June 3, 1998.
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