Ann Thorac Surg 2001;71:717-719
© 2001 The Society of Thoracic Surgeons
Case report
Infant partial left ventriculectomy for failure to wean from cardiopulmonary bypass
Stephen Westaby, FRCSa,
Pedro A. Catarino, FRCSa,
Takahiro Katsumata, MD, PhDa
a Department of Cardiac Surgery, Oxford Heart Centre, John Radcliffe Hospital, Oxford, United Kingdom
Accepted for publication March 20, 2000.
Address reprint requests to Dr Westaby, Oxford Heart Centre, John Radcliffe Hospital, Headley Way, Headington, Oxford OX3 9DU, UK
e-mail: swestaby{at}ahf.org.uk
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Abstract
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Following aortic reimplantation of anomalous left coronary artery from the pulmonary artery in a 6-month-old infant, the heart failed to wean after prolonged supportive cardiopulmonary bypass and maximal inotropic support. We performed partial left ventriculectomy (Batista procedure) that halved left atrial pressure and enabled discontinuation of bypass. Postoperative recovery was then uneventful.
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Introduction
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Infants with anomalous left coronary artery from the pulmonary artery (ALCAPA) usually present with ischemic cardiomyopathy and severe impairment of left ventricular function. Failure to wean from cardiopulmonary bypass is a frequent sequel to surgical correction of ALCAPA [1]. Mechanical circulatory assist devices have been used pending improvement in left ventricular function in the short term [2]. Partial left ventriculectomy (PLV) is a radical but controversial operation that aims to improve long-term global left ventricular function in chronic heart failure patients [3, 4]. Although reserved about the long-term outcome in our adult patients [5], we had employed the method successfully in an infant with cardiomyopathy. When a second infant could not be weaned from cardiopulmonary bypass after correction of ALCAPA, we employed PLV as a last resort in an attempt to avoid mortality.
A 6-month-old female infant presented with congestive cardiac failure and cardiomegaly (New York Heart Association functional class IV). The left lung was hypoplastic secondary to chronic cardiomegaly. Echocardiography showed a grossly dilated left ventricle with ejection fraction 20% and minimal mitral regurgitation (Fig 1A). Left heart catheterization demonstrated ALCAPA. Surgery was planned to follow an intensive 3-week period of antifailure medical treatment. At operation, she underwent aortic implantation of the left main coronary artery. Myocardial protection was achieved with intermittent cold crystalloid cardioplegia infused into both coronary ostia. The repair proceeded uneventfully with an ischemic time of 55 minutes after which the heart resumed beating in sinus rhythm. Right ventricular contraction was vigorous, but repeated attempts at weaning from bypass failed with left ventricular distension and high left atrial pressure (35 mm Hg). Despite 90 minutes of supportive perfusion and an electrocardiogram that did not suggest acute myocardial ischemia, further attempts at weaning with maximal inotropic support were unsuccessful.

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Fig 1. End-diastolic echocardiographic images from long axis view before (A) and 3 weeks after (B) partial left ventriculectomy. Note the grossly dilated spherical left ventricle preoperatively.
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Given the dimensions of the left ventricle with homogenous myocardial fibrosis (endocardial fibroelastosis) and no localized full thickness scarring, we decided to perform PLV. The technique followed that of standard PLV as described in adults by Batista and colleagues [3]. This was undertaken during supportive normothermic cardiopulmonary bypass with the heart beating without an aortic cross-clamp. A 14 g wedge of muscle was excised from the lateral wall of the left ventricle excising the circumflex marginal territory between (but not including) the bases of the papillary muscles. Circumferential subendocardial fibrosis was noted (Fig 2). An Alfieri suture approximation of the anterior and posterior mitral valve leaflets was carried out through the ventriculotomy. After double layer direct closure of the ventriculotomy, a further 30 minutes of supportive perfusion was employed before attempting to discontinue cardiopulmonary bypass. Weaning was then achieved with a left atrial pressure of 18 mm Hg, a systemic pressure of 70 mm Hg, and heart rate of 130 beats per minute with only moderate inotropic support. In effect, the left atrial pressure was halved by PLV and mitral repair.

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Fig 2. Partial left ventriculectomy. (A) At resection, the endocardium showed extensive fibroelastosis. (B) Surgically remodeled left ventricle.
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Over the next 48 hours, inotropes were discontinued progressively and she was extubated uneventfully. Left atrial pressure fell further to between 12 and 15 mm Hg, and the heart rate fell to 100 per minute with a systolic blood pressure varying between 70 and 100 mm Hg. She was discharged home after 3 weeks, before which echocardiography showed reduction of the left ventricular end diastolic dimension from 4.1 cm preoperatively to 2.8 cm (Fig 1B). Ejection fraction improved to 45%. Six months later, echocardiography showed the smaller cardiac size was well maintained as was ejection fraction. She is New York Heart Association functional class I.
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Comment
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There are few documented cases of PLV in the pediatric age group [5, 6]. Our previous (unreported) success was in an infant with dilated cardiomyopathy first discovered in utero, whose ventricle continued to deteriorate after delivery. This patient remains well 1 year after PLV. Others have applied elective PLV for neonate or infant dilated cardiomyopathy with encouraging results but not as an intraoperative salvage procedure for postcardiotomy acute left ventricular failure [5, 6]. In this case, PLV halved the left atrial pressure and prompted survival in the absence of a suitable left ventricular support system. The role of the Alfieri suture is poorly defined but we have found this simple method to be useful for pediatric patients where conventional repair and use of annuloplasty ring would be detrimental to growth potential. For adults with dilated cardiomyopathy, and particularly ischemic cardiomyopathy, the long-term outcome after PLV has proved disappointing.
Without mechanical circulatory support, hospital mortality is substantial (about 15%) [7]. The small number of cases of infant PLV make it difficult to assess both short- and long-term outcome. However, in the pediatric setting, the myocardial physiologic responses are not the same as those in the adult population. Myocyte mitotic activity is thought to persist for 3 to 6 months after birth [8], conveying the potential for myocyte division, growth, and extensive cardiac remodeling in infancy.
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References
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