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a Department of Cardiothoracic Surgery, Sheba Medical Center, Tel Hashomer, Israel
b Cardiac Rehabilitation Institute, Sheba Medical Center, Tel Hashomer, Israel
c Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Accepted for publication October 1, 2007.
* Address correspondence to Dr Kogan, Department of Cardiothoracic Surgery, Sheba Medical Center, Tel Hashomer, 52621; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, 69978, Israel (Email: alexander.kogan{at}sheba.gov.il).
| Abstract |
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| Introduction |
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We describe the occurrence of Takotsubo syndrome in a patient after open heart surgery. We have not found any such previous report.
A 62-year-old woman with a history of rheumatic heart disease and congestive heart failure (New York Heart Association functional class II) was admitted for elective mitral valve replacement and tricuspid valve repair. Preoperative transesophageal echocardiography demonstrated normal LV function, moderate-to-severe mitral regurgitation, and moderate-to-severe tricuspid regurgitation. A coronary angiography was normal. Through a median sternotomy on standard cardiopulmonary bypass and cardiac arrest, the degenerative native mitral valve was replaced with a Hancock II 29-mm bioprosthesis (Medtronic Inc, Minneapolis, MN), preserving posterior mitral leaflet and papillary muscle integrity. The tricuspid valve was repaired with a 33-mm Carpentier annuloplasty ring (Edwards Lifesciences, Irvine, CA). Cardiopulmonary bypass time was 153 minutes and aortic cross-clamp time was 101 minutes. After uneventful weaning off cardiopulmonary bypass, transesophageal echocardiography was repeated and revealed good mitral prosthetic function, minimal tricuspid regurgitation, normal global and regional left ventricular contractions, and normal right ventricular contractions. The patient was transferred to the intensive care unit and was extubated 8 hours later. Her condition deteriorated on the first postoperative day. She became dyspneic, hypotensive, and oliguric. An electrocardiogram showed atrial fibrillation (prior to surgery sinus rhythm), with a ventricular rate of 130 to 136 bpm, negative T-waves in leads I, II, aVL and in the precordial leads, and troponin T of 0.83 ng/mL (upper normal limit, 0.1 ng/mL). An echocardiography showed a significantly depressed LV function with extensive akinesis and dyskinesis of all apical and midventricular segments, sparing the basal segments, which were contracting vigorously. The LV ejection fraction of the patient was estimated to be at 35%. Based on the typical shape of the dysfunctioning left ventricle, the fact that the extensive wall motion abnormalities did not follow a coronary distribution pattern, and the coronary arteries were known to be angiographically normal, Takotsubo syndrome was diagnosed (Fig 1). Despite the concern of catecholamine-induced worsening of LV function, intravenous dobutamine, noradrenaline, and adrenaline therapy were started to maintain an adequate arterial perfusion pressure. The patient received warfarin (Taro Pharmaceutical Industries Ltd, Yakum, Israel), furosemide (Teva Pharmaceutical Industries Ltd, Petach Tikva, Israel), amiodarone (Sanofi-Aventis, Paris, France), and levothyroxine sodium (Glaxo Wellcome, Burgwedel, Germany) daily. She was gradually weaned from inotropic support by postoperative day 6, and she was started on carvedilol (Teva Pharmaceutical Industries Ltd). Daily transthoracic echocardiography demonstrated gradual improvement of LV function with LV ejection fraction returning to 50%, absence of systolic anterior motion of the mitral valve, and a decrease in systolic pulmonary artery pressure from an initial 50 to 55 mm HG to a 30 to 35 mm Hg. On postoperative day 7, the patient was transferred to a regular ward. On postoperative day 11, successful electrical cardioversion to sinus rhythm was performed. She was discharged home the next day. Follow-up echocardiography at 4 weeks revealed a completely normal LV function with a LV ejection fraction of 55% (Fig 2). Her exercise tolerance was excellent.
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Despite the characteristic, near pathognomonic pattern of LV wall motion abnormalities and the typical course of the syndrome, three potential differential diagnoses should be discussed. First, suboptimal myocardial protection, which may lead to potentially fully recoverable myocardial microcirculatory disturbance, yet highly unlikely, given the course of the surgery, the absence of predisposing factors (ie, LV hypertrophy or coronary artery disease), and the normal LV function after weaning off cardiopulmonary bypass. Second, impairment of LV function with LV sphericalization due to loss of the mitral papillo-annular continuity, described in the past after conventional mitral valve replacement with excision of both leaflets and papillary muscles. Such impairment may occur transiently, but this has been described much more frequently as a cause for permanent postoperative LV dysfunction. In this case, the posterior subvalvular apparatus was preserved. One may wonder whether at least some of the cases of postsurgical transient LV sphericalization described in the past were in fact cases of the Takatsubo syndrome, not yet known at that time. Intriguingly, some of the cases of postmitral valve replacement transient LV sphericalization described in the past have occurred in postmenopausal women, who seem to be more susceptible to this syndrome. Third, tachycardiomyopathy, another cause of transient LV dysfunction, can occur in patients with atrial fibrillation with a fast ventricular response over a prolonged period of time, neither of which was the case in this patient. We therefore believe that the diagnosis of Takatsubo syndrome is well established.
The precise mechanism of the syndrome remains unknown [4]. The suggested causes include direct toxic myocardial damage from catecholamine overload on cardiac adrenergic receptors, and an inadequate inotropic response or a subtype of neurogenic stunning of the myocardium [4] due to acute autonomic dysfunction during or after emotional or physical stress.
Remarkably, more than 60% of reported patients experienced an identifiable stressful event just prior to the onset of symptoms [5], psychological and emotional (26.8%) or physical stress (37.8%) [6]. A wide variety of additional triggering factors have been described. Emotional stress appears to be the key to the development of Takotsubo syndrome. This syndrome has also been described in the setting of anesthesia and noncardiac procedures such as tooth extraction, preparation for colonoscopy, laparotomy, thoracotomy, pulmonary lobectomy, and so forth.
Characteristically, the postmenopausal women are as much as 12 times more likely to be affected than men. In the recently established national registry on Takotsubo cardiomyopathy at Brown University in Rhode Island, 93.5% of all patients were women [5]. Far East Asians are the largest group reported with 57.2%, followed by Caucasians with 40%, but the disease has also been reported in African-Americans and native Hawaiians, apparently occurring across all ethnic and geographical lines.
In conclusion, enhanced awareness may lead to increasing recognition of this new nosological entity as a possible complication of cardiac surgery.
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This article has been cited by other articles:
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J. W. Heitz Takotsubo syndrome and the cardiac surgery patient. Ann. Thorac. Surg., February 1, 2009; 87(2): 674 - 674. [Full Text] [PDF] |
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A. Kogan, P. Ghosh, E. Schwammenthal, and E. Raanani Reply. Ann. Thorac. Surg., February 1, 2009; 87(2): 674 - 675. [Full Text] [PDF] |
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P. K. Ghosh, A. Kogan, and E. Raanani Mitral valve replacement and Takotsubo syndrome. Eur. J. Cardiothorac. Surg., August 1, 2008; 34(2): 466 - 466. [Full Text] [PDF] |
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C. Rao and T. Athanasiou Reply to ghosh et Al. Eur. J. Cardiothorac. Surg., August 1, 2008; 34(2): 467 - 467. [Full Text] [PDF] |
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