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CASE REPORT OHKI ET AL AVR WITH LEFT VENTRICULAR NONCOMPACTION
FEATURE ARTICLES
would be unethical [1]. What is less clear is whether the decision to operate could equally be considered unethical. Acute type A IMH is generally treated with urgent or emergency surgical repair, but stability of the lesion [2] and even regression [3] have also been noted anecdotally. Thus, the determination to watch the patient with a type A IMH might be justified within the context of nonmaleficence. In some patient populations, surgical intervention might not even be offered. In octogenarians, for example, medical management of type A IMH has what are considered “acceptable” levels of morbidity and mortality [4]. Repair of a type A IMH is not without the risk of morbidity and mortality; such a risk would be considerable in a reoperation on a Jehovah’s Witness with renal failure and coronary artery disease. This patient demonstrated the relative stability of the disease, with 4 weeks elapsing from the onset of the IMH to the progression to frank dissection. Immediate harm was thus avoided, but would the outcome have been better with earlier intervention? The International Registry of Acute Aortic Dissection data would suggest that in those patients treated for chronic rather than acute dissections, the outcome appears to be unhampered by the wait [5]. Shinfeld and Raanami [6] also note that for a select group of patients with a type A dissection after CABG, nonoperative therapy appears to be as effective as surgical correction. Beneficence is the principle of goodness in action or deed, rather than the avoidance of the harmful action or deed. Conflict arises in the high-risk patient where the potential gain is overshadowed by the realistic risk of morbidity or death. This conflict could be mitigated by evidence-based data, consensus statements, or input from colleagues, but the true risk/benefit ratio may remain unknown. It would not be unreasonable to turn down the described patient under the assumption that the risks were extremely high, but we would also predict from previous experience that without an operation, the patient’s long-term survival would be directly challenged. Given the high probability of death with medical management, it would be rational to accept the surgical option despite the operative risks. But although most patients can grasp the concept of death, the idea of significant morbidity may come as a shock. The experience of Hata and colleagues [7] in their series of octogenarians with acute type A dissections treated surgically or medically is sobering. Surgical intervention provided an immediate benefit, with a postoperative mortality of 13.3% vs 60.7% for nonsurgical patients, but complications were burdensome to the families. McKneally’s [8] accompanying editorial summarized this burden. This case presentation involved three dilemmas: (1) the conflict felt by the surgical team regarding the ethics of proceeding with a high-risk procedure, (2) the conflict felt by the patient regarding his desire to live but within the confines of his religious beliefs, and (3) the conflict felt by the nursing staff and ancillary personnel who were asked to participate in the care of the patient without a priori involvement in the decision making. This patient was deemed nonoperable by two different surgical teams, first for the CABG and later for the type A © 2009 by The Society of Thoracic Surgeons Published by Elsevier Inc
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IMH. He survived both procedures to discharge, and yet died soon after the second procedure. Was this a foreseeable event? Given his multiple comorbidities, should medical management alone have been undertaken? In the final analysis, this might be the greatest benefit gained from this operation—a chance to reflect not only on the technical wizardry of the operation but also on the ethical considerations of such procedures.
References 1. Nuland S. How we die. New York: Knopf; 1993:250 –3. 2. Tittle SL, Lynch RJ, Cole PE, et al. Midterm follow-up of penetrating ulcer and intramural hematoma of the aorta. J Thorac Cardiovasc Surg 2002;123:1051–9. 3. Ohmi M, Tabayashi K, Moizumi Y, Komatsu T, Sekino Y, Goko C. Extremely rapid regression of aortic intramural hematoma. J Thorac Cardiovasc Surg 1999;118:968 –9. 4. Porcellini M, Elia S, Camera L, Bracale G. Intramural hematoma of the thoracic aorta in octogenarians: is non operation justified? Eur J Cardiothorac Surg 1999;16:414 –7. 5. Trimarchi S, Nienaber CA, Rampoli V, et al. Contemporary results of surgery in acute type A aortic dissection: The International Registry of Acute Aortic Dissection experience. J Thorac Cardiovasc Surg 2005;129:112–22. 6. Shinfeld A, Raanani E. Late acute aortic dissection after coronary artery bypass. Langenbecks Arch Surg 2008 (epublished April 2008). 7. Hata M, Sezai A, Niino T, et al. Should emergency surgical intervention be performed for an octogenarian with type A acute aortic dissection? J Thorac Cardiovasc Surg 2008;135: 1042– 6. 8. McKneally MF. “We didn’t expect dementia and diapers”: reflections on the Nihon experience with type A aortic dissection in octogenarians. J Thorac Cardiovasc Surg 2008;135:984 –5.
Aortic Valve Replacement for Aortic Regurgitation in a Patient With Left Ventricular Noncompaction Satoshi Ohki, MD, Yukinori Moriyama, MD, Jun Mohara, MD, Chieri Kimura, MD, Naoyuki Sata, MD, and Kenkichi Miyahara, MD Department of Cardiovascular Surgery and Cardiology, Shinkyo Hospital, Kagoshima, Japan
We present a case of a 61-year-old man who underwent aortic valve replacement for aortic regurgitation complicated with left ventricular noncompaction. The pathogenesis of this condition remains unknown. In advanced form, left ventricular noncompaction produces marked disability and carries a poor prognosis. We underscore that familiarity with this disease entity will help to stimulate early diagnosis and timely treatment when necessary. (Ann Thorac Surg 2009;87:290 –2) © 2009 by The Society of Thoracic Surgeons Accepted for publication May 21, 2008. Address correspondence to Dr Ohki, Department of Cardiovascular Surgery, Shinkyo Hospital, 3-41-1 Usuki, Kagoshima, 890-0073, Japan; e-mail:
[email protected].
0003-4975/09/$36.00 doi:10.1016/j.athoracsur.2008.05.057
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CASE REPORT OHKI ET AL AVR WITH LEFT VENTRICULAR NONCOMPACTION
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Fig 1. Echocardiographic appearance of the patient: in the short-axis view of the left ventricle. Arrows denote noncompacted area showing prominent trabeculations and deep intertrabecular recesses.
L
eft ventricular noncompaction (LVNC) is a rare form of cardiomyopathy believed to be a result of an arrest in cardiac development in early embryogenesis. With the recent progress and spread of cardiac imaging technique, the chance to diagnose this disease entity is apparently increasing [1]. In pediatric patients, LVNC is often associated with other cardiac and extracardiac abnormalities and
A 61-year-old man came to our institution because of increasing shortness of breath. He had no family history of cardiovascular disease or sudden cardiac death. An echocardiogram and subsequent left heart catheterization demonstrated severe degree of aortic regurgitation with a bicuspid aortic valve. Characteristically, left ventricular trabeculations and intertrabecular recesses were prominent. There was thin, compacted myocardium on the epicardial side of the left ventricular wall and thicker, noncompacted myocardium on the endocardial side (Fig 1). The ratio of noncompacted to compacted thickness was approximately 2.0 to 3.0, which met the diagnostic criteria of LVNC [4]. Left ventricular end-diastolic diameter was 61 mm, and left ventricular ejection fraction was 55%. There was no other associated congenital anomaly. Thallium-201 myocardial imaging performed at rest disclosed a hypoperfusion area in the left ventricle corresponding to the zones where noncompacted ventricular myocardium can be localized. No significant disease was detected by a preoperative coronary angiography. Left ventricular dysfunction was deemed secondary to aortic valve regurgitation in addition to LVNC. The patient was referred for surgical management of his bicuspid aortic valve. Fig 2. Intraoperative endoscopic view of prominent trabeculations through the left ventricular outflow tract.
FEATURE ARTICLES
carries a high mortality as a result of heart failure or sudden cardiac death [2]. On the other hand, the prognosis of adult patients with LVNC is still controversial [3]. A morphological distinction between them is still unclear. Herein we report a case of aortic valve replacement for aortic regurgitation in a patient with LVNC.
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CASE REPORT NEHRA ET AL PULMONARY VENOUS OCCLUSION AFTER RADIOFREQUENCY ABLATION
The aortic valve was replaced with an ATS 23-mm mechanical valve (ATS Medical Inc, Minneapolis, MN) in a supra-annular position. After excision of the bicuspid aortic leaflets, prominent left ventricular trabeculations and intertrabecular recesses were observed through an endoscope (Fig 2). The patient’s postoperative course was straightforward, and he was discharged home on postoperative day 18. A follow-up echocardiogram 1 year after surgery showed almost normal cardiac function with a left ventricular end-diastolic diameter of 55 mm and an ejection fraction of 60%.
Comment
FEATURE ARTICLES
Left ventricular noncompaction is assumed to have a higher prevalence than previously believed [1], although surgical cases have been rarely reported. We believe that there was only one surgical case previously reported in the English literature, in which left ventricular restoration surgery was effective for end-stage dilated cardiomyopathy caused by LVNC [5]. In our patient, LVNC was complicated with a severe degree of aortic regurgitation due to bicuspid aortic valve, but cardiac function was still good enough to receive a valve replacement. Hence, we performed an elective surgery on this patient without any complication. Left ventricular noncompaction is a rare congenital dysfunction of ventricular morphogenesis resulting from arrested muscle fiber compaction in early embryogenesis [1]. Initially, LVNC was reported to carry a high mortality [6, 7]. In the meantime, a fairly large number of cases have been published with much better prognosis [1]. Especially, asymptomatic patients had clearly better prognosis than symptomatic patients [3]. However, a morphological distinction of noncompacted myocardium among these patients is still unclear. Moreover, the pathogenesis of this condition remains unknown. In the present case, aortic valve regurgitation was diagnosed before cardiac function became deteriorated, and a valve replacement was performed according to the usual operative indication. In view of his improved cardiac performance after operation, even patients with LVNC should receive cardiac repair procedure while they are viable candidates for surgery. However, left ventricular dysfunction can occur any time after initial presentation, emphasizing that the patients with LVNC should have lifelong follow-up with at least an annual echocardiography.
References 1. Stöllberger C, Finsterer J. Left ventricular hypertrabeculation/ noncompaction. J Am Soc Echocardiogr 2004;17:91–100. 2. Burke A, Mont E, Kutys R, et al. Left ventricular noncompaction: a pathological study of 14 cases. Human Pathology 2005;36:403–11. 3. Ritter M, Oechslin EN, Sutsch G, et al. Isolated noncompaction of the myocardium in adults. Mayo Clin Proc 1997;72:26 – 31. 4. Jenni R, Oechslin E, Schneider J, et al. Echocardiographic and pathoanatomical characteristics of isolated noncompaction: a © 2009 by The Society of Thoracic Surgeons Published by Elsevier Inc
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step towards classification as a distinct cardiomyopathy. Heart 2001;86:666 –71. 5. Shimamoto T, Murai A, Yamanaka K, et al. Left ventricular restoration surgery for isolated left ventricular noncompaction: report of the first successful case. J Thorac Cardiovasc Surg 2007;134:246 –7. 6. Chin TK, Perloff JK, Williams RG, et al. Isolated noncompaction of left ventricular myocardium: a study of eight cases. Circulation 1990;82:507–13. 7. Oechslin EN, Attenhofer Jost CH, Rojas JR, et al. Long-term follow-up of 34 adults with isolated left ventricular noncompaction: a distinct cardiomyopathy with poor prognosis. J Am Coll Cardiol 2000;36:493–500.
Complete Pulmonary Venous Occlusion After Radiofrequency Ablation for Atrial Fibrillation Deepika Nehra, MD, Moishe Liberman, MD, Parsia A. Vagefi, MD, Nathaniel Evans, MD, Ignacio Inglessis, MD, Richard L. Kradin, MD, Jill Ono, MD, David J. Kanarek, MD, and Henning A. Gaissert, MD Divisions of Thoracic Surgery, Cardiology, Pathology, and Pulmonary Medicine, Massachusetts General Hospital, Boston, Massachusetts
Pulmonary vein stenosis is a known, yet under-recognized complication of radiofrequency ablation for atrial fibrillation. We present the case of a patient developing complete left-sided pulmonary venous occlusion following radiofrequency ablation. Recommendations are made to allow earlier diagnosis of this complication. (Ann Thorac Surg 2009;87:292–5) © 2009 by The Society of Thoracic Surgeons
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ulmonary vein stenosis is a known complication of radiofrequency ablation for atrial fibrillation with a reported incidence as high as 42% [1, 2]. We present a patient with complete occlusion of both left-sided pulmonary veins after radiofrequency ablation for atrial fibrillation. A 58-year-old woman presented 6 years earlier with atrial fibrillation and congestive heart failure. Echocardiography was normal. Normal sinus rhythm was restored with cardioversion, and medical treatment was instituted. Three years later, she experienced symptomatic, paroxysmal atrial fibrillation and underwent circumferential radiofrequency ablation of both left pulmonary veins. Paroxysmal atrial fibrillation refractory to medical therapy recurred after 5 weeks. A transesophageal echocardiogram 2 months after ablation showed a left atrial thrombus and anticoagulation with warfarin was begun.
Accepted for publication June 19, 2008. Address correspondence to Dr Gaissert, Division of Thoracic Surgery, Massachusetts General Hospital, Blake 1570, 55 Fruit St, Boston, MA 02114; e-mail:
[email protected].
0003-4975/09/$36.00 doi:10.1016/j.athoracsur.2008.06.060