J Interv Card Electrophysiol (2008) 21:219–222 DOI 10.1007/s10840-007-9196-8
CASE REPORT
Intra day ECG variation after general anesthesia in Brugada syndrome Natale Daniele Brunetti & Luisa De Gennaro & Pier Luigi Pellegrino & Riccardo Ieva & Francesco Di Nardo & Andrea Cuculo & Giulio Campanale & Matteo Di Biase
Received: 30 October 2007 / Accepted: 4 December 2007 / Published online: 22 February 2008 # Springer Science + Business Media, LLC 2007
Abstract ECG variations of characteristic coved-type patterns are a common finding in subjects with Brugada syndrome. Few data are available about patients with Brugada syndrome undergoing major surgery and requiring general anesthesia. We reported ECG serial variations in a patient with Brugada syndrome who underwent surgery for tibial fracture. Relevant variations of ST patterns in V1–V2 leads over 24-h ECG monitoring were detectable, albeit these modifications were not associated with incidence of arrhythmias. Keywords Brugada Syndrome . General Anesthesia . ECG Variations
1 Background Brugada syndrome (BS) is characterized by electrocardiographic (ECG) changes consisting of ST elevation in the anterior chest leads (V1–V3) and incomplete right bundlebranch block (RBBB). It often gives syncope or sudden death (SD) [1]. The syndrome is genetically determined and caused by mutations in gene SCN5A on chromosome 3, encoding the human cardiac sodium channel [2]. Although the ECG changes are characteristic, they are often intermittent and may be triggered by fever, increased vagal tone relative to N. D. Brunetti (*) : L. De Gennaro : P. L. Pellegrino : R. Ieva : A. Cuculo : G. Campanale : M. Di Biase Cardiology Department, University of Foggia, Viale Pinto 1, 71100 Foggia, Italy e-mail:
[email protected] F. Di Nardo Anesthesiology Department, University of Foggia, Foggia, Italy
sympathetic tone, and many pharmacological agents that have an effect on ion channel flux [3]. The potential pharmacological and physiological changes that accompany anesthesia might increase the risk of these patients developing a significant arrhythmia or cardiac dysfunction.
2 Case report We report the case of a 38-year-old male with a Brugada ECG pattern. The patient had a history of eight episodes of syncope, usually associated with emotive stress. One son suddenly died during delivery. The patient refused AICD implantation during a previous evaluation. Physical examination and biology did not reveal any abnormal finding. The patient suffered from both left tibia and fibula fracture after a car crash, and was scheduled for surgical osteo-synthesis with metallic plaque under general anesthesia. Anesthesia protocol included induction with propofol 2 mg/kg followed by remifentanyl 0.20 mcg/kg/m’ and cisatracurium 14 mg for neuromuscular block (followed by cisatracurium 2 mg boli); anesthesia was maintained with sevoflurane (1.5–2%). Continuous ECG monitoring during surgery did not show any arrhythmias, tachycardia or premature ventricular beats. The patient promptly recovered after anesthesia and underwent analgesia with morphine 30 mg/48 h. Serial 12-leads ECG recording was scheduled in order to evaluate sequential changes in ECG Brugada pattern over orthopedic surgery and general anesthesia. Precordial leads position was accurately marked in order to ensure reproducibility of registrations. Basal ECG showed characteristic coved-type Brugada pattern in precordial lead V1 and saddle-back aspect in V2 with ST elevation of about 2 mm (Figs. 1 and 2). The second ECG was recorded about 1 h
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after surgery: a change in ST anomalies was detectable in both V1 and V2 leads. V1 assumed a saddle back aspect and ST elevation increased up to 3 mm. At third ECG, 6 h later, V1 lead recovered coved-type aspect whilst ST elevation in V2 lead remained of about 3 mm. At fourth recording, ECG reassumed initial aspect as before surgery with coved-type pattern in V1 and 2 mm saddle-back ST elevation in V2. Unexpectedly, the last ECG recording 24 h after surgery showed a saddle back minimal (1 mm) ST elevation in V1 lead and a pseudo-normal ST aspect in V2. ECG monitoring was ended after 24 h. Postoperative recovery was uneventful. Serial ECGs were recorded 1 month later in concomitance with a period of rehabilitation: ECGs were held for five consecutive days as controls (Fig. 3). Typical Brugada anomalies shown soon after surgery were not more clearly evident. ST in V2–V3 lead was quite normal and a coved-type pattern was seldom detectable in V1.
3 Discussion and literature review The finding of a typical Brugada ECG pattern might be difficult in some patients due to the presence of concealed and intermittent forms [4]. The autonomic changes and multiple pharmacological interactions commonly seen during anesthesia may exacerbate the underlying disease process and trigger Brugada ECG changes and arrhythmias [5]. Local anesthetics, because of their sodium channel blockade, may also exacerbate Brugada ECG changes. However, the class IB drugs mexiletine and lidocaine have never been shown to cause ST-segment elevation [6]. Use of a bupivacaine epidural infusion has been implicated in the evolution of a Brugada-type ECG [7]; however, a single-shot spinal anesthetic has been described without event by using 0.5% bupivacaine [8]. Fig. 1 Baseline ECG with typical Brugada pattern (covedtype in precordial lead V1 and saddle-back aspect in V2 with ST elevation of about 2 mm)
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Beta-adrenergic blockade and alpha-receptor stimulation have been repeatedly shown to aggravate the ST-segment changes in Brugada syndrome. The use of volatile anesthetic agents has also raised some concerns. Their use in patients with prolonged QT syndromes has been questioned because of their tendency to further prolong the QT interval [9]. This occurs with isoflurane but not with sevoflurane, while a significant shortening occurs with halothane [9]. Antagonism of the neuromuscular block with neostigmine and atropine has been reported as associated with an elevation of the ST segments on the ECG [10]. Changes in autonomic tone are considered as a contributory factor inducing tachy-arrhythmias in patients with BS [11–12]. To prevent postoperative sudden autonomic tone change, adequate postoperative analgesia is important. However, there are currently few data on the effects of anesthetic drugs on Brugada patients and BS, although it is not uncommon, is rarely mentioned in the latest anesthesia literature [12]. In a case report, continual monitoring of the ECG during epidural analgesia showed no abnormalities as a result of the anesthetic or the operation [10]. Controversy remains about duration of ECG monitoring after uneventful anesthesia, since no episodes of arrhythmias have been reported; observational times ranged from a few hours to a couple of days [8, 10, 13]. We describe for the first time ECG changes consecutive to general anesthesia. These findings are suitable with ECG variability previously reported as common in subjects with BS [4] and not associated with an increased risk of ventricular arrhythmias. Throughout a 10-year follow-up period, almost half of patients with BS enrolled showed changes in ST-segment elevation pattern and normalization of ST-segment elevation at least once [14]. Patients displaying transient normalization of the ECG pattern were shown as at a similar risk for ventricular
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Fig. 2 ECG variations during 24 h following surgery with general anesthesia
fibrillation (VF) and SD as those with persistent STelevation [3]. Priori et al. also reported that the morphology of ST-segment elevation (whether saddleback or coved) could not be an outcome predictor [15]. However, the rate of inducible VF was significantly higher in patients with more than 50% coved-type ECGs than in patients with less than 50% diagnostic ECGs [16]. Fig. 3 ECG variations during 24 h about 1 month after surgery with general anesthesia
The day-to-day and year-to-year variations of ST segment elevation have been reported in some previous studies [17, 18] and there was a correlation between the augmentation of ST-segment elevation and occurrence of ventricular extrasystoles or VF in symptomatic patients [5, 18]. About half of patients diagnosed with BS presented fluctuations between diagnostic and non-diagnostic ECGs
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[16]. A significant number of patients (47%) with a BS does not reveal a spontaneous diagnostic basal ECG during follow-up and only 1 out of 43 patients showed a continuously diagnostic coved-type ECG [16]. Further studies are needed to establish the real prognostic relevance of the ECG changes we reported; a close cooperation of the anesthetist with cardiologist is however essential both before and after surgery for patients with Brugada syndrome.
References 1. Brugada, P., & Brugada, J. (1992). Right bundle-branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. A multicenter report. Journal of the American College of Cardiology, 20, 1391–1396. 2. Chen, Q., Kirsch, G. E., Zhang, D., Brugada, R., Brugada, J., Brugada, P., et al. (1998). Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature, 392, 293–296. 3. Brugada, R., Brugada, J., Antzelevitch, C., Kirsch, G. E., Potenza, D., Towbin, J. A., et al. (2000). Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle-branch block but structurally normal hearts. Circulation, 101, 510–515. 4. Brugada, J., Brugada, P., & Brugada, R. (1999). The syndrome of right bundle branch block ST segment elevation in V1 to V3 and sudden death: the Brugada syndrome. Europace, 1, 156–166. 5. Miyazaki, T., Mitamura, H., Miyoshi, S., Soejima, K., Aizawa, Y., & Ogawa, S. (1996). Autonomic and antiarrhythmic drug modulation of ST-segment elevation in patients with Brugada syndrome. Journal of the American College of Cardiology, 27, 1061–1070. 6. Candiotti, K. A., & Mehta, V. (2004). Perioperative approach to a patient with brugada syndrome. Journal of Clinical Anesthesia, 16, 529–532. 7. Phillips, N., Priestley, M., Denniss, A. R., & Uther, J. B. (2003). Brugada-type electrocardiographic pattern induced by epidural bupivacaine. Anesthesia and Analgesia, 97, 264–267.
J Interv Card Electrophysiol (2008) 21:219–222 8. Kim, J. S., Park, S. Y., Min, S. K., Kim, J. H., Lee, S. Y., Moon, B. K., et al. (2004). Anaesthesia in patients with Brugada syndrome. Acta Anaesthesiologica Scandinavica, 48, 1058–1061. 9. Guler, N., Kati, I., Demirel, C. B., Bilge, M., Eryonucu, B., & Topal, C. (2001). The effects of volatile anesthetics on the Q-Tc interval. Journal of Cardiothoracic and Vascular Anesthesia, 15, 188–191. 10. Edge, C. J., Blackman, D. J., Gupta, K., & Sainsbury, M. (2002). General anaesthesia in a patient with Brugada syndrome. British Journal of Anaesthesia, 89, 788–791. 11. Kaneda, Y., Fujita, N., Ueda, K., et al. (2001). Surgically treated primary lung cancer associated with Brugada syndrome: report of a case. Surgery Today, 31, 817–819. 12. Gussak, I., Antzelevitch, C., Bjerregaard, P., Towbin, J. A., & Chaitman, B. R. (1999). The Brugada syndrome: Clinical, electrophysiologic and genetic aspects. Journal of the American College of Cardiology, 33, 5–15. 13. Candiotti, K. A., & Mehta, V. (2004). Perioperative approach to a patient with Brugada syndrome. Journal of Clinical Anesthesia, 16, 529–532. 14. Sakabe, M., Fujiki, A., Tani, M., Nishida, K., Mizumaki, K., & Inoue, H. (2003). Proportion and prognosis of healthy people with coved or saddle-back type ST segment elevation in the right precordial leads during 10 years follow-up. European Heart Journal, 24, 1488–1493. 15. Priori, S. G., Napolitano, C., Gasparini, M., Pappone, C., Della Bella, P., Giordano, U., et al. (2002). Natural history of Brugada syndrome: Insights for risk stratification and management. Circulation, 105, 1342–1347. 16. Veltmann, C., Schimpf, R., Echternach, C., Eckardt, L., Kuschyk, J., Streitner, F., et al. (2006). A prospective study on spontaneous fluctuations between diagnostic and non-diagnostic ECGs in Brugada syndrome: implications for correct phenotyping and risk stratification. European Heart Journal, 27, 2544–2552. 17. Bjerregaard, P., Gussak, I., Kotar, S. L., Gessler, J. E., & Janosik, D. (1994). Recurrent syncope in a patient with prominent J wave. American Heart Journal, 127, 1426–1430. 18. Sumiyoshi, M., Nakata, Y., Hisaoka, T., Ogura, S., Nakazato, Y., Kawai, S., et al. (1993). A case of idiopathic ventricular fibrillation with incomplete right bundle branch block and persistent ST segment elevation. Japanese Heart Journal, 34, 661–666.
