Eur J Cardiothorac Surg 2000;17:763-765
© 2000 Elsevier Science NL
Symptomatic calcific stenosis of a Toronto stentless porcine valve
Patrick D.T. Tansley,
Mary N. Sheppard,
John Pepper
Royal Brompton Hospital, London, UK
Corresponding author. Kirby Lodge, 1 Gullet Lane, Kirby Muxloe, Leicestershire LE9 2BL, UK. Tel.: +44-171-352-8121; fax: +44-171-351-8530
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Abstract
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We describe the calcific structural failure of a Toronto stentless porcine valve (TSPV) which had been used to replace a calcified bicuspid aortic valve in a 46-year-old man. Against expectations, left ventricular hypertrophy persisted and the transvalvular pressure gradient rose to 125 mmHg by 6 years with the patient becoming symptomatic and requiring redo surgery. On removal the TSPV showed atypical calcification of the leaflet hinges and wall. To our knowledge this is the first case reported and it may have implications for long term durability and future surgery using this prosthesis.
Key Words: Stentless valve Calcification
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1. Case report
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A 46-year-old man presented with syncope, dyspnoea and chest pain. He had a systolic murmur and echocardiography identified left ventricular hypertrophy with a calcified bicuspid aortic valve and peak transvalvular pressure gradient of 10 mmHg. Although lost to follow up, he presented with similar complaints five years later in 1993. He smoked 40 cigarettes per day, had a strong family history of ischaemic heart disease and no known history of hypercalcaemia.
On examination, he exhibited signs of aortic stenosis. Cardiac catheterization revealed good left ventricular function with no coronary arterial lesions, a calcified aortic valve with reduced leaflet excursion and a peak transvalvular pressure gradient of 120 mmHg. Echocardiography confirmed aortic stenosis with left ventricular hypertrophy. As the patient wished to avoid anticoagulation, a 27 mm Toronto stentless porcine valve (TSPV) was implanted freehand in April 1993. Interrupted sutures were used for the proximal suture line, a continuous suture distally and mattress sutures to support each of the three commissures. The outflow of this stentless valve is scalloped in all three sinuses.
Post-operative echocardiography showed no aortic regurgitation and his recovery was uneventful.
At 3 month follow-up he was well and reported an exercise tolerance of 2 miles. By April 1994 however, echocardiogram revealed persistent left ventricular hypertrophy and a peak transvalvular pressure gradient of 18 mmHg. By June 1997, despite pharmacological management, echocardiography showed the transvalvular pressure gradient had risen to 36 mmHg. By July 1999, he reported worsening symptoms and echocardiography showed severe calcific TSPV stenosis with very limited valve movement. Left ventricular function was good, but significant left ventricular hypertrophy remained and peak transvalvular pressure gradient had risen to 125 mmHg.
He was admitted for redo aortic valve surgery. Pre-operative cardiac catheterization revealed mild aortic regurgitation and single vessel disease affecting the left anterior descending artery. Echocardiography (August 1999) showed left ventricular hypertrophic progression, a reduction in stroke volume and a peak transvalvular pressure gradient of 85 mmHg. During weekend leave prior to surgery he suffered a myocardial infarct and was transferred back to hospital in left ventricular failure with a raised CK at 309 (25171) and troponin I at 1.5 (00.1). Pre-operative echocardiography (September 1999) revealed further deterioration in left ventricular function along with mild functional mitral regurgitation.
At operation, we found the TSPV to be well seated with no paravalvular dehiscence and calcification confined to the leaflets. The sino-tubular junction was preserved with no outward displacement of the TSPV posts. Due to the Dacron sleeve around the Toronto valve, a dissection plane was easily found and followed. The patient's preference was for a biological stentless valve, although a stented valve could easily have been used. Thus, redo aortic valve replacement was performed with a 23 mm free-standing cryopreserved aortic root homograft. A pedicled left internal thoracic artery graft was simultaneously placed on the left anterior descending artery.
Post operative trans-oesophageal echocardiography demonstrated normal prosthetic and good left ventricular function. Trans-thoracic echocardiography at fourteen days revealed similar findings with no transvalvular pressure gradient and a striking improvement in left ventricular function. At 6 weeks he remained clinically well and echocardiography suggested normal homograft function (Table 1).
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2. Pathology
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The excised TSPV was found to be very heavily calcified in a nodular manner throughout the wall and at the hinge points of attachments of the valve leaflets (see Fig. 1). There was no evidence of infection or paravalvular dehiscence, leaflet calcification, tears or perforations.
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3. Discussion
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Stentless bioprosthetic valves offer the advantages inherent to homografts/autografts but have the added benefits of greater availability and size range. Although technically more difficult to implant and requiring longer ischaemic and cardiopulmonary bypass times, their principal advantage comprises superior haemodynamic function when compared to mechanical valves and stented prostheses. This is thought to be due to elimination of the rigid stent and insertion therefore of a bioprosthesis relatively larger in diameter. In addition, the aorta functions as a physiological stent thus allowing greater flexibility in response to the dynamic changes of the cardiac cycle and leading to reduced mechanical leaflet stress. Resulting transvalvular blood flow is laminar and smoother in nature, contrasting with the turbulence found across the more rigid stented prostheses [1].
However, despite the haemodynamic advantages of stentless porcine valves, the glutaraldehyde-preserved porcine tissue remains subject to intense calcification. Interestingly, stentless bioprostheses in animal studies have been shown as less likely to calcify than stented bioprostheses [2]. Glutaraldehyde fixation denatures tissue by molecular cross-linkage, aiming to preserve tissue and minimize immunological reaction in vivo. Nevertheless, this process has been implicated in tissue calcification itself and therefore must be viewed with caution. Anti-mineralization treatments continue to be developed and aim to protect both the valve leaflets and the aortic wall, a task complicated by their differing histological tissue types. In addition to standard glutaraldehyde fixation, methods to avoid calcification at the cellular level, surfactant usage and tissue engineering of the prosthetic valve matrix are being researched as additional approaches to these difficult problems [1].
The durability of stented bioprosthetic valves is known to be limited by structural degeneration as a result of mechanical stress, tissue calcification, leaflet tears and rupture[3,4]. In contrast, the durability of stentless bioprostheses remains unknown, but it had been reasoned that they would generate less mechanical stresses with expected improved durability [2]. Stentless bioprostheses have only been commonly implanted since the early part of the last decade [5] and are therefore just beginning to approach the length of follow up at which long term durability may be realistically considered. Results of the TSPV pre-approval trial showed no cases of primary tissue failure at six years [5]. Twenty-nine stentless porcine bioprosthetic implants, similar to TSPV's have shown similar durability to stented bioprostheses during an 11 year period [5].
We believe this report to be the first to demonstrate TSPV failure at 6 years due to calcification of the leaflet hinges and bioprosthetic wall rather than the more typical pattern of leaflet calcification seen in stented bioprosthetic valves. This type of structural calcific failure needs to be closely observed in future as a potential cause for long term TSPV failure.
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References
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Huysmans H.A., David T.E., Westaby S. Stentless bioprostheses, 2nd ed Plymouth, UK: Isis Medical Media, 1999.
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Received December 13, 1999;
received in revised form March 14, 2000;
accepted March 21, 2000.