Ann Thorac Surg 2004;78:1821-1823
© 2004 The Society of Thoracic Surgeons
Case report
Regurgitation of the Native Aortic Valve Caused by Thrombus Formation After Heterotopic Heart Transplantation
Omar Mangoush, FRCSa,
Toufan Bahrami, MDa,
Fabio De Robertisa,
Jonathan Swinburn, MRCPa,
Nicholas Banner, FRCPa,
Magdi H. Yacoub, FRCSa,
Asghar Khaghani, FRCSa,*
a Harefield Hospital, Harefield, Middlesex, United Kingdom
Accepted for publication July 17, 2003.
* Address reprint requests to Dr Khaghani, Harefield Hospital, Harefield, Middlesex UB9 6JH, UK
a.khaghani{at}rbh.nthames.nhs.uk
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Abstract
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A 61-year-old man, who had undergone heterotopic heart transplantation, had severe regurgitation through his native aortic valve develop 16 years later, which caused severe heart failure. At operation the regurgitation was found to be due to development of an organized thrombus in the sinuses of Valsalva tethering aortic leaflets. The management of this previously undescribed complication of heterotopic heart transplantation and the implications for other groups of patients (such as those receiving treatment with a left ventricular assist device) are discussed.
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Introduction
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Heart transplantation is a successful treatment for advanced heart failure. Two types of heart transplant have been used: orthotopic and heterotopic [1]. The majority of transplants are performed using the orthotopic technique, but heterotopic transplantation (HHT) can have advantages in certain situations [1]. One hundred thirty of HHT operations have been performed at our center (8.4% of the transplants performed). Complications related to the native heart (such as angina, arrhythmia, and left ventricular thrombus formation) have been reported [2].
Herein we describe a complication of HHT, which has not yet been reported (ie, progressive regurgitation of the native aortic valve due to the development of an organized thrombus in the sinuses of Valsalva).
A 61-year-old man underwent HHT for end-stage ischemic cardiomyopathy in 1986. The operation was performed as previously described [1]. The donor was a 10-year-old child who died of intracranial hemorrhage. There was a 50% discrepancy in weight between the donor and the recipient. Coronary artery bypass grafting and left ventricle (LV) aneurysmectomy were also performed on the native heart. Postoperative recovery was uneventful, and the patient went back to full-time work. He continued to do well until 1992 when he sustained an embolic stroke. He made a satisfactory recovery from the stroke, and he was anticoagulated with warfarin with an international normalized ratio of 2.0 to 3.0 to prevent further embolism.
In 1996, he had angina develop. A coronary angiogram showed all grafts in the native heart to be occluded; however the coronary arteries of the donor heart were angiographically normal. Subsequently, the patient's condition gradually deteriorated with increasing dyspnea and recurrent angina. He sustained two episodes of myocardial infarction of the native heart. In April 2002, the patient had episodes of ventricular tachycardia in the native heart. On one occasion he was found to have ventricular fibrillation, which was successfully cardioverted.
An echocardiogram performed in June, when both hearts were in sinus rhythm, showed very poor native LV function with mild mitral regurgitation and little ejection through the native aortic valve, but no aortic regurgitation. Subsequently, another episode of ventricular fibrillation in the native heart of the patient developed. Again he was successfully cardioverted after anticoagulation with heparin and continued treatment with warfarin. After further investigation, he was listed for re-transplantation and was discharged. One day later he was admitted into the emergency room suffering from severe shortness of breath, and he was found to have pulmonary edema. He was thereafter admitted into the ITU. Transthoracic and transesophageal echocardiograms showed severe native aortic regurgitation, very poor native LV contraction, increased mitral regurgitation, and abnormal echoes in the aortic sinuses (Fig 1) . No vegetations were seen, and blood cultures were subsequently found to be negative. The patient's renal function had deteriorated; therefore he was no longer suitable for further transplantation at this stage.
Because aortic regurgitation of the native heart remained, which had severely affected the hemodynamics of the patient, a decision was made to replace or close the regurgitant aortic valve. At surgery an organized thrombus was found to be filling the seat of the coronary sinuses between the wall of the aorta and the valve cusps causing restriction of leaflet movement. The thrombus was removed and the aortic leaflets were then found to be able to coapt normally. On weaning from cardiopulmonary bypass, the aortic valve was competent, but the right ventricle of the native heart started to distend and fail. Therefore, a connection was fashioned between the donor and native pulmonary arteries using a size 28-Dacron tube graft to add assistance from the donor right ventricle to the native right ventricle. The patient was then weaned from cardiopulmonary bypass and an intraaortic balloon pump was inserted. However, 1 hour later the donor's right ventricle also started to fail; therefore a right ventricular assist device (Abiomed BVS 500 [Abiomed, Inc]) was inserted. The inflow and outflow cannulas of the right ventricular assist device were connected through the Dacron tube, with the inflow cannula directed toward the donor pulmonary artery and the outflow cannula directed toward the native pulmonary artery; the tube was tied off between the two cannulas.
The patient was then transferred to the intensive care unit and was managed with the support of high doses of inotropic agents. His condition gradually deteriorated, and he died from multiorgan failure. A postmortem examination was not carried out because the family did not give consent.
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Comment
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With HHTs there are complications related to the native heart including angina, arrhythmia, and thrombus formation in the native LV. Medical treatment including anticoagulation are usually effective, but in the case of progressive severe heart failure, re-transplantation may have to be considered in selected patients [3].
In the HHT recipient, the donor LV propels blood from the pulmonary circulation to the systemic circulation. Although the native LV can function in parallel with the donor, frequently the native aortic valve does not open normally because of the aortic pressure generated by the donor LV [4]. This may contribute to chronic changes in the structure of the valve; there is often a degree of regurgitation through the native aortic valve, which can be continuous throughout the cardiac cycle. In the present case, the development of an organized thrombus in the sinuses of Valsalva tethered the aortic leaflets and made the valve incompetent, which produced severe regurgitation. As the valve became incompetent, the workload of the donor LV increased and it started to fail, which caused increased left atrial pressure and pulmonary edema, as well as a fall in cardiac output to the systemic circulation.
Stasis and blocked grafts decreased the flow around the aortic root and in the ascending aorta that probably played a major role in the formation of the thrombus, which developed despite adequate anticoagulation. The ventricular fibrillation episodes in the native heart would have prevented even occasional opening of the aortic valve, which may have precipitated this complication. This underscores the need for prompt treatment of ventricular tachycardia and ventricular fibrillation in the native heart of HHT recipients, despite the fact that such arrhythmias are often relatively well tolerated hemodynamically, because of the function of the donor heart. Once severe native aortic regurgitation has developed, the best probable therapeutic option is re-transplantation (ie, replacing the native heart with an orthotopic transplant while leaving the original heterotopic transplant in situ). However this approach can only be used while the patient's general condition remains suitable for transplantation.
In conclusion, this case demonstrated a new mechanism for acquired aortic valve regurgitation after HHT. We speculate that tethering of the aortic valve leaflets with thrombus may also explain some cases of aortic regurgitation in other situations in which the aortic valve rarely opens (eg, during long-term support with a left ventricular assist device).
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References
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- Banner NR, Khaghani A, Fitzgerald M, Mitchell AG, Radley-Smith R, Yacoub MH. The expanding role of cardiac transplantation. Unger F. Assisted circulation, III. Berlin Heidelberg: Springer-Verlag; 1989. p. 448–467
- Tagusari O, Kormos RL, Kawai A, et al. Native heart complications after heterotopic heart transplantation: insight into the potential risk of left ventricular assist device. J Heart Lung Transpl. 1999;18:1111–1119[Medline]
- Novitzky D, Cooper DK, Lanza RP, Barnard CN. Further cardiac transplant procedures in patients with heterotopic heart transplants. Ann Thorac Surg. 1985;39:149–154[Abstract]
- Akasaka T, Lythall D, Cheng A, et al. Continuous aortic regurgitation in severely dysfunctional native hearts after heterotopic cardiac transplantation. Am J Cardiol. 1989;63:1483–1488[Medline]
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Abstract
Introduction
