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a Department of Cardiothoracic Surgery, Alfred Hospital, Melbourne, Australia
b Department of Cardiology, Alfred Hospital, Melbourne, Australia
Accepted for publication April 25, 2008.
* Address correspondence to Dr Larobina, Department of Cardiothoracic Surgery, Alfred Hospital, 1A View St, Surrey Hills, Melbourne, Victoria, 3127, Australia (Email: marcolarobina{at}hotmail.com).
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Abstract |
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Introduction |
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We report the successful intraoperative mechanical aortic valve replacement in a donor allograft during the orthotopic cardiac transplant procedure for undiagnosed moderate-to-severe aortic stenosis, secondary to a calcified congenitally bicuspid valve. Although inadvertent, the success of this patient highlights that correctable aortic valvular lesions do not preclude the use of offered organs.
Orthotopic cardiac transplantation was undertaken in a 55-year-old man for end-stage cardiac failure due to idiopathic dilated cardiomyopathy. The recipient had a known persistent left superior vena cava diagnosed during attempted percutaneous insertion of an LV lead for cardiac resynchronization therapy. Epicardial lead placement was performed using robotic surgical techniques. No other medical history was noted.
A 34-year-old man was referred as a donor from a very distant regional hospital after the diagnosis of brain death secondary to a head injury that occurred while intoxicated. No medical history was noted. The patient was reported as a fit and active young man, with no clinical evidence of cardiovascular disease. The donor's father had undergone coronary surgery at the age of 55. No vasoactive hemodynamic supports were required in the period prior to organ procurement. Due to limited services in the regional hospital, echocardiography was not performed. The retrieving time from another institution reported no abnormalities in the cardiac allograft. A bilateral sequential lung transplant was performed by this team with the procured lungs. The heart was then couriered 3,000 km unaccompanied to our institution.
Due to anticipated difficulties in preserving the recipient's persistent left superior vena cava and the tenacity of adhesions from the previous robotic surgery, cardiopulmonary bypass was established during transfer of the donor allograft. Recipient cardiectomy was performed with preservation of the left superior vena cava and a cuff of the right atrium containing the coronary sinus ostium, as described by Rabago and colleagues [1] in a bid to reduce donor ischemic time.
After arrival, the donor allograft was inspected prior to implantation at which time marked LV hypertrophy was noted. Inspection of the aortic valve revealed heavy calcification on a congenitally bicuspid valve. The leaflets were thickened and immobile, and it was immediately evident that valve replacement was required. A 25-mm St. Jude medical mechanical prosthesis (St. Jude Medical, St. Paul, MN) was implanted with everted pledgeted 2-0 Ticron interrupted sutures (Tyco Healthcare, Mansfield, MA). The valve was seated satisfactorily with normal prosthetic leaflet function. The remainder of the allograft implant was performed using a standard bi-caval technique and intermittent antegrade cold blood cardioplegia through the aortic root.
Cardiopulmonary bypass was weaned on low-dose adrenaline and noradrenaline infusions, intra-aortic balloon counterpulsation at 1:1 and nitric oxide at 40 ppm. A combination of the 3,000 km procurement distance and technical challenges led to a total ischemic time of 492 minutes. Post-bypass transesophageal echocardiography revealed normal prosthetic valvular function with a peak gradient of 29 mm Hg and a mean gradient of 12 mm Hg. Marked LV hypertrophy was noted with associated global left and right ventricular dysfunction.
The patient was returned to the intensive care unit in stable condition. Ventilatory support was weaned during the ensuing 24 hours. Adrenaline was exchanged for dobutamine, which was continued at a low dose for 5 days postoperatively. The recipient made an uncomplicated recovery and was discharged on day 14 on warfarin, prednisolone, mycophenolate mofetil, and cyclosporin. His management also included irbesartan and metoprolol. Endomyocardial biopsy at day 7 showed no evidence of rejection. Transthoracic echocardiography revealed a well-seated and normally functioning mechanical prosthesis with low normal left ventricular (LV) systolic function and mild LV hypertrophy.
Subsequent transthoracic echocardiograms were performed at 1, 3, 6, and 18 months, documenting significant reduction in LV mass. Immediately postoperative LV mass index was 124.5 g/m2, which had reduced at last review to 95 g/m2 (Table 1).
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Comment |
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Heterotopic cardiac transplants [2], valvular and coronary intervention on donor allografts have been well described to enable the use of smaller organs with longer ischemic times, and organs with valvular and coronary disease that may have been functioning suboptimally prior to procurement. Mitral and tricuspid valve repairs [3] and coronary artery bypass grafting [4] have been used to reduce post-transplant tricuspid regurgitation, reduce known pre-procurement mitral regurgitation, and bypass known coronary artery disease.
Although mitral valve disease is a relative contraindication for cardiac allograft donation, aortic stenosis with significant LV hypertrophy has been considered an absolute contraindication. Valve replacement surgery is well described in patients during the early years post-transplant, presumably for progression of valvular disease present, but not hemodynamically significant at the time of transplantation [5]. However, the reported replacement of the aortic valve during the orthotopic cardiac transplant procedure is very rare. Aortic valve repair for moderate central aortic regurgitation has been reported during orthotopic transplant from a donor with normal LV function.
Aortic valve replacement during orthotopic heart transplant has been reported for new onset aortic regurgitation diagnosed at the conclusion of the implant [6]. The bicuspid valve was functioning normally at the time of procurement, and torsion of the aortic root was the postulated mechanism of the aortic regurgitation. In contrast to our patient, the donor heart in each of these 2 patients had not been exposed to the pathophysiology of chronic stenotic aortic valvular disease with its consequent LV remodeling.
The long-term survival of marginal organs is compromised. Allografts with evidence of obstructive coronary disease have a reduced long-term survival compared with nondiseased allografts and more commonly required revascularization [7].
The presence of LV hypertrophy has been shown to adversely affect both the short-term and longer-term survival of cardiac transplant recipients. Echocardiographic findings of LV hypertrophy have been correlated with high rates of primary allograft failure resulting in death, a requirement for mechanical circulatory support and re-transplantation [8].
Hypertrophic changes in the left ventricle are associated with suboptimal myocardial preservation and subsequent subendocardial ischemia [8]. Furthermore, cardiac ischemia and ischemia–reperfusion injury exacerbates the restrictive physiology seen in hypertrophic hearts. Ischemia–reperfusion injury leads to myocardial interstitial edema, cellular dysfunction, areas of necrosis that physiologically manifest as the restrictive pre-load dependent heart commonly seen post-cardiopulmonary bypass, and exacerbated by the longer periods of ischemia experienced during transplantation.
In the nontransplant cardiotomy, these inflammatory changes regress in time. In aortic stenotic hearts, adequate relief of any aortic outflow tract obstruction and control of systemic hypertension leads to near complete regression of LV mass. However, in the transplanted heart, LV hypertrophy often develops denovo postoperatively [9], related in part to cyclosporine, hypertension, and the altered neurohormonal state seen in transplant recipients. There is some evidence this can be ameliorated with medical therapy [10].
Despite appropriate medical management, donor LV hypertrophy, particularly with a history of hypertension has been show to decrease 1-year survival by 15% to 35% [11]. However, the prognostic influence of LV hypertrophy related to corrected aortic valve disease in the post- transplant setting, and whether it portends a similar prognosis to other causes of LV hypertrophy is unknown. The reduction in LV mass seen in the reported case suggests that some improvement will be seen in time, likely related to the correction of the LV outflow tract obstruction.
This case presentation indicates the feasibility of valve replacement during organ implant, with subsequent regression of LV hypertrophy during the early follow-up period. The patient's early post-transplant course was not marred by significant hemodynamic problems, and cardiac allograft function has remained preserved, with normal left and right ventricular systolic function and normal mechanical aortic valve function seen at 18-months post-transplant.
In conclusion, traditional selection criteria for cardiac allografts have strictly excluded those organs with known aortic valvular disease or significant LV hypertrophy. This report documents the transplantation of an organ requiring simultaneous mechanical aortic valve replacement for aortic stenosis. A successful short-term outcome with preserved allograft function, a well-seated mechanical prosthesis, and regression in LV mass without any major morbidity suggests that strict exclusion of organs because of known aortic valvular disease may not be justified in all cases. In patients in whom a marginal allograft is being considered, an offered heart with aortic valve disease that would require concomitant valve replacement does not preclude successful transplantation.
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