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Ann Thorac Surg 2001;71:587-590
© 2001 The Society of Thoracic Surgeons
a Division of Cardiovascular Surgery, Keio University School of Medicine, Tokyo, Japan
Accepted for publication May 4, 2000.
Address reprint requests to Dr Shin, Division of Cardiovascular Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
e-mail: h-shin{at}med.keio.ac.jp
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Abstract |
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Methods. Forty-six patients underwent successful mitral valve surgery via the SSA. Preoperatively, 25 patients were in atrial fibrillation (AF), 20 were in normal sinus rhythm (SR), and 1 patient was paced. Thirteen patients who demonstrated no sinus node dysfunction preoperatively underwent postoperative electrophysiological studies. Peripostoperative cardiac rhythm was monitored using a portable four-lead electrocardiograph, and late cardiac rhythm was examined using standard 12-lead electrocardiography in the outpatient clinic.
Results. Twelve of 20 patients with preoperative SR experienced early postoperative supraventricular arrhythmias, but all spontaneously recovered SR. Electrophysiological studies revealed a basic cycle length of 767 ± 74 ms, sinoatrial conduction time of 72 ± 34 ms, sinus node recovery time of 1,119 ± 139 ms, and corrected sinus node recovery time of 349 ± 114 ms, thus demonstrating a lack of sinus node dysfunction. During the postoperative period (34 ± 24 months), 2 of the 20 patients with preoperative SR developed persistent AF, and 3 of the 25 patients with preoperative AF achieved normal SR.
Conclusions. The SSA does not appear to cause long-term adverse effects on sinus node function, although temporary effects may occur.
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Introduction |
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TopAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Material and methods |
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TopAbstractIntroductionMaterial and methodsResultsCommentReferences |
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The surgical approach used depended on the surgeon. One surgeon (H.S.) primarily used the SSA, whereas the others elected not to use this approach due to its uncertain effects on SA function. Among the 46 cases studied, three had acute mitral regurgitation (MR) due to active infective endocarditis, two had acute MR due to acute myocardial infarction, and three had undergone previous mitral valve surgery. Patient demographic data is shown in Table 1.
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To assess SN function, we measured the basic cycle length (BCL), sinoatrial conduction time (SACT) measured by Narula’s method [6], sinus node recovery time (SNRT) after overdrive pacing, and corrected sinus node recovery time (CSNRT). Atrial vulnerability was assessed based on the atrial effective refractory period (ERP) and responses to atrial extrastimuli. The internodal conduction time (INCT) was also measured.
Cardiac rhythm and follow-up
Early postoperative cardiac rhythm was monitored using a portable four-lead electrocardiograph until the rhythm stabilized. We defined early postoperative arrhythmias as continuous arrhythmias for at least 6 hours. Electrical cardioversion was not performed to restore SR in any of the patients. Late cardiac rhythm was determined using a standard 12-lead electrocardiogram recorded in the outpatient clinic. The follow-up was complete in all 46 patients. The duration of follow-up was ranged from 3 to 87 months (mean 34 ± 24 months). Follow-up was discontinued on April 30, 1999.
Surgical procedures
Moderate hypothermic cardiopulmonary bypass was utilized and myocardial protection was accomplished using intermittent cold blood cardioplegia, topical cooling, and terminal warm blood cardioplegia in all patients.
The surgical technique is described elsewhere [1–4]. Briefly, a right atrial incision was made parallel to the atrioventricular groove. Caution was paid to avoid injuring the crista terminalis, an important internodal conduction pathway. An atrial septal incision was started from the fossa ovalis and joined the right atrial incision cranially at the interatrial sulcus. The incision was extended to the left atrial roof behind the aorta. At this time, sufficient width of the atrial wall was retained on the atrioventricular sulcus side to avoid problems in closing the left atrial roof. After the cardiac lesions were corrected, in addition to right ventricular temporary pacing leads, two atrial pacing leads were placed in patients whose preoperative rhythm was SR. At this time, one of the atrial pacing leads was placed in Bachmann’s bundle to assure atrial capture [7].
Data analysis
Continuous variables are expressed as the mean ± standard deviation. Preoperative SR groups with and without early postoperative supraventricular arrhythmias were compared using Student’s t test for continuous variables and 
2 or Fisher’s exact test for categorical variables. Values of p less than 0.05 were considered statistically significant.
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Results |
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Early postoperative cardiac rhythm
Of the 20 patients with preoperative SR, only 8 patients did not develop postoperative supraventricular arrhythmias during hospitalization. The other 12 patients experienced early postoperative supraventricular arrhythmias. Of these 12 patients, 7 had junctional bradycardia (JB), 2 suffered both JB and AF, and 3 developed AF. JB was managed using temporary atrial pacing. The duration of the supraventricular arrhythmias was from 1 to 19 days (mean 5.5 ± 6.4 days). The arrhythmias spontaneously reverted to normal SR before discharge from the hospital in all cases (Fig 1). No significant differences were seen between the two groups with and without early postoperative supraventricular arrhythmias in terms of age, gender, preoperative New York Heart Association functional class, or original mitral valve lesion.
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Electrophysiological study
Thirteen patients, including 6 with early postoperative supraventricular arrhythmias (4 with JB, 1 with AF, and 1 with both), underwent postoperative EPS with PAB. The SCL was 767 ± 74 ms (heart rate: 78 ± 8 beats/min), SACT was 72 ± 34 ms, SNRT was 1,119 ± 139 ms, and CSNRT was 349 ± 114 ms. These values were all within the normal ranges. The atrial ERP was 265 ± 37 ms, which was also within the normal range. Neither supraventricular arrhythmias nor repetitive atrial responses were induced by atrial extrastimuli in any of the patients. The INCT was increased in 10 patients and was within the normal range in 3 patients. The INCT was 65 ± 22 ms, which was slightly extended (Table 2).
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Comment |
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TopAbstractIntroductionMaterial and methodsResultsCommentReferences |
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SN function and atrial vulnerability after surgery remain important considerations with the SSA because the technique involves transecting the SN artery and the anterior internodal conduction pathway as well as making incisions in both atria. Consequently, there are concerns associated with the potential effect on postoperative SN function and atrial vulnerability. Thus, the technique has not gained widespread acceptance. Many surgeons have recommended caution in selecting this procedure [4, 8–10], while others have reported encouraging early results [1–3, 11–14]. In this series, 12 of the 20 patients with preoperative SR experienced supraventricular arrhythmias lasting more than 6 hours during the early postoperative period. This 60% incidence is quite high, suggesting that the SSA may cause transient SN dysfunction or may enhance atrial vulnerability.
Previous studies, including comparative studies between conventional approaches and the SSA, have examined electrocardiographic changes. Such evaluations may overlook latent SN dysfunction and increased atrial vulnerability. To determine the effects of the SSA on SN function and atrial vulnerability more accurately, electrophysiological evaluation is mandatory. Although comparison between preoperative and postoperative electrophysiological parameters of SN function is ideal, it is quite difficult to perform such a comparison given that preoperative EPS with PAB may be inadequate in patients whose cardiac performance is impaired, and also that certain patients cannot tolerate EPS. We therefore only conducted EPS after surgical treatment in patients without clinical evidence of preoperative SN dysfunction. Thirteen patients underwent postoperative EPS approximately 1 month after surgery. BCL, SACT, SNRT, and CSNRT under PAB, which reflect SN function, were all within the normal ranges. Atrial ERP was within the normal range, and supraventricular arrhythmias were not induced by atrial extrastimuli, nor were repetitive atrial responses to atrial extrastimuli. These findings suggest that SN function and atrial vulnerability after the SSA recover in the early postoperative period. Extended INCT was probably caused by transection of the anterior internodal conduction pathway, but INCT extension itself is not believed to be harmful.
In addition to the EPS results, the following findings strongly suggest that the SSA does not induce any permanent or serious damage: (1) most patients with preoperative SR maintained SR; (2) of the 25 patients with preoperative AF, 3 were in SR during the late phase; and (3) no patients required implantation of a permanent pacemaker. Additionally, postoperative JB was managed without difficulty by external pacing and the duration of intensive care unit stay was not influenced by the arrhythmias. However, impact of the arrhythmias after the SSA on hospital stay and medical costs should be assessed to determined whether widespread acceptance of the SSA is justified.
In conclusion, the SSA does not appear to cause long-term adverse effects on sinus node function or atrial vulnerability, although transient changes may be observed. Based on these results, the SSA can be viewed as an effective approach for mitral valve surgery and may be indicated for patients in whom unsatisfactory exposure through conventional approaches is anticipated.
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References |
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