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Ann Thorac Surg 2007;83:1179-1181
© 2007 The Society of Thoracic Surgeons
a Division of Pediatric Cardiovascular Surgery, Montreal Children’s Hospital, Montréal, Québec
b Division of Pediatric Cardiology, Montreal Children’s Hospital, Montréal, Québec
c Division of Pediatric Anesthesia, Montreal Children’s Hospital, Montréal, Québec
d Division of Pediatric Critical Care Medicine, Montreal Children’s Hospital, Montréal, Québec
e Division of Cardiac Surgery, University of Western Ontario, London, Ontario
Accepted for publication August 9, 2006.
* Address correspondence to Dr Cecere, Montréal Children’s Hospital, 2300 Tupper St, Room C-829, Montréal, Québec H3H 1P3, Canada (Email: renzo.cecere{at}muhc.mcgill.ca).
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Introduction |
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A 4-year-old boy with hypoplastic left heart syndrome (HLHS) had been previously palliated with uncomplicated stage 1 Norwood and Glenn operations. A Fontan operation had been planned but never performed because of progressive tricuspid regurgitation, eventually requiring tricuspid valve repair at age 4. Two months later, he was readmitted for congestive heart failure with gross peripheral edema, hepatomegaly, and arterial oxygen desaturations (mid-60%).
Echocardiography showed a dilated, poorly functioning systemic right ventricle with moderate tricuspid regurgitation and thrombus in the rudimentary left ventricle. Cardiac catheterization identified an elevated right ventricular end-diastolic pressure of 12 to 14 mm Hg and a mean Glenn pressure of 16 mm Hg. The patient was listed for heart transplantation.
Despite inotropic support, his clinical status progressively deteriorated, with marked fatigue, anorexia, and profound arterial and venous oxygen desaturations, with a femoral venous oxygen saturation of 20%. At this time, we believed the patient was at high risk for sudden death and warranted a bridge to transplantation.
The Berlin Heart VAD (Berlin Heart AG, Berlin, Germany) is a pulsatile paracorporeal circulatory support device. A 30-mL VAD was selected for this 14.6-kg patient (body surface area, 0.64 m2), according to previously defined manufacturer recommendations based upon height and weight. With cardiopulmonary bypass on the beating heart, the inflow and outflow cannulas were implanted into the diaphragmatic surface of the systemic ventricle and the ascending neoaorta, respectively (Fig 1A). The VAD was set at a rate of 80 beats/min, while inflow suction and diastolic filling time were optimized to produce VAD flows of approximately 3.8 L/(min · m2).
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On postoperative day 10, the patient contracted influenza, a respiratory tract infection that resulted in significant fatigue and lethargy. Metabolic acidosis and diffuse peritonitis developed on postoperative day 13. Computed tomography imaging demonstrated pneumatosis intestinalis and laparotomy revealed diffuse bowel necrosis in the entire superior mesenteric artery (SMA) distribution. Although an SMA thrombectomy was performed, pulsatile flow was never reestablished, and the patient died. Autopsy findings identified multifocal thrombi within the left coronary artery, left iliac artery, and the SMA, with associated regional bowel infarction. There were pathologic signs of multifocal hepatic and renal infarction. No thrombus or fibrin deposits were identified within the VAD.
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Although ECMO could certainly have improved the hypoxemia and low cardiac output, we thought that because there was no intrinsic pulmonary disease and the primary problem was ventricular failure, VAD support would provide effective improvement in cardiac output and subsequent Glenn flow. More importantly, we believed that Berlin Heart VAD support would be more appropriate than ECMO because of the anticipated prolonged wait period before transplantation and risks of coagulopathy and bleeding with ECMO [3].
Our patient experienced significant improvements in cyanosis and oxygen saturation with the VAD. These improvements likely occurred because of the summation of two competing physiologic effects (Fig 1B). First, the VAD support improved systemic ventricular unloading, Glenn shunt flow, and cardiac output, resulting in better oxygenation. Second, enhanced inferior vena caval flow and subsequent atrial mixing could have lead to oxygen desaturation. The Berlin Heart VAD performed well in our patient with the balance favoring improved oxygen saturations, from 60% to 85%. Although mechanical support has been described in Fontan circulation, we report the effect of pulsatile mechanical circulatory support in a patient with Glenn physiology.
Thromboembolism was paramount in our patient, raising concerns about anticoagulation and optimal monitoring. We followed standard guidelines for the Berlin Heart VAD [3] by initiating a heparin infusion to keep the aPTT within 60 to 80 seconds and daily aspirin (2 mg/kg). Because of fibrin deposition within the device, we increased our heparin dosage to target therapeutic antifactor Xa levels (0.50 to 1.00 IU/mL), which eliminated any further visible fibrin (Fig 2). Alternative anticoagulation strategies included additional antiplatelet agents, such as clopidogrel and dipyridamole; however, there was little evidence to support their use. It was also possible that the thrombus propagated from the previously existing thrombi in the jugular vein or rudimentary left ventricle; however, these thrombi were chronic in nature, making embolism less likely. In our experience, we would advocate titrating heparin therapy according to an anti-Xa protocol, rather than aPTT measurements, and using antiplatelet agents such as clopidogrel or dipyridamole in addition to aspirin.
In conclusion, the Berlin Heart VAD performed well in improving cardiac output and oxygenation in our patient with a failing single ventricle; however, thromboembolic complications were paramount despite following guidelines for anticoagulation strategy and monitoring. A multidisciplinary team approach, focusing on an aggressive anticoagulation strategy, should be considered for any congenital cardiac patient requiring mechanical circulatory support.
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This article has been cited by other articles:
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  M. G. Cardarelli, M. Salim, J. Love, S. Simone, J. Tumulty, D. Conway, and B. Griffith Berlin heart as a bridge to recovery for a failing fontan. Ann. Thorac. Surg., March 1, 2009; 87(3): 943 - 946. [Abstract] [Full Text] [PDF]
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 F. B. Pearce, J. K. Kirklin, W. L. Holman, C. S. Barrett, R. L. Romp, and Y. R. Lau Successful cardiac transplant after Berlin Heart bridge in a single ventricle heart: use of aortopulmonary shunt as a supplementary source of pulmonary blood flow. J. Thorac. Cardiovasc. Surg., January 1, 2009; 137(1): e40 - e42. [Full Text] [PDF]
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