Ann Thorac Surg 2008;86:1369-1371. doi:10.1016/j.athoracsur.2008.03.064
© 2008 The Society of Thoracic Surgeons
Case Reports
Early Aortic Bioprosthetic Valve Deterioration in an Octogenarian
Hironori Izutani, MD, PhD*,
Takanori Shibukawa, MD,
Jun Kawamoto, MD,
Shingo Mochiduki, MD,
Dairoku Nishikawa, MD
Division of Cardiovascular Surgery, National Hospital Organization Kure Medical Center, Hiroshima, Japan
Accepted for publication March 27, 2008.
* Address correspondence to Dr Izutani, Division of Cardiovascular Surgery, National Hospital Organization Kure Medical Center, 3-1 Aoyama-cho, Kure, Hiroshima, 737-0023, Japan (Email: h-izutani{at}rgmc.izumisano.osaka.jp).
 |
Abstract
|
|---|
We experienced extremely early aortic bioprosthetic valve deterioration with leaflet calcification and stiffening 2
years after aortic valve replacement in a female octogenarian. We could not identify the possible reason for this devastating complication; however, daily calcium supplement consumption may play a role of acceleration of calcium deposition in the leaflets of implanted bioprosthetic heart valves.
|
Introduction
|
|---|
Long-term durability and stability of the hemodynamic performance of commercially available second generation Carpentier-Edwards stented bovine pericardial aortic bioprostheses (Perimount valve; Edwards Lifesciences, Irvine, CA) is reported based on echocardiographic findings during a 17-year period of follow-up examinations [1]. With a low rate of valve-related events and an especially low rate of structural failure, the Perimount valve (Edwards Lifesciences) is a reliable choice for patients with calcified aortic stenosis by a report of 18 years follow-up study [2]. Prosthetic valve deterioration of the Perimount valve usually occurs late and is age-dependent. Therefore, aortic valve replacement with a bioprosthesis is a reliable surgical management for elderly patients with severe aortic stenosis. We describe bioprosthetic valve deterioration of a Perimount valve with severe congestive heart failure 2 years postoperatively that developed in an octogenarian patient.
An 80-year-old woman who had no history of heart disease was hospitalized for congestive heart failure. She had a history of myelodysplastic disorder, which had been followed regularly with steroids for more than a decade. Her echocardiography showed severe aortic stenosis with a maximum pressure gradient of 100 mm Hg, moderate mitral regurgitation, and moderate tricuspid regurgitation with normal left ventricular function. It was recommended for the patient to undergo elective heart valve surgery. She underwent aortic valve replacement with a 21-mm Perimount valve, mitral annuloplasty with a 26-mm Cosgrove-Edwards annuloplasty ring (Edwards Lifesciences), and tricuspid annuloplasty with modified DeVega technique under standard open heart procedures. The aortic valve was tri-leaflet and degenerative with severe calcification. There were patchy calcified deposits inside the aorta and around the right coronary orifice. There was mild annular calcification. The three leaflets were excised and the aortic bioprosthesis was placed in the supra-annular position with thirteen 2-0 Ethibond Excel interrupted non-everting mattress sutures (Ethicon Inc, Somerville, NJ). Her convalescence was unremarkable. She was discharged home on postoperative day 20. Her primary physician followed her regularly for myelodysplastic disorder, the same as preoperatively. She had dyspnea develop, and she was hospitalized for severe congestive heart failure in 29 postoperative months. Her echocardiography revealed severe aortic stenosis with restricted motion of the prosthetic valve leaflets, with a maximum pressure gradient of 83 mm Hg and an aortic valve area of 0.27 cm2 (Fig 1). Her left ventricular function was poor with an ejection fraction of 25%. Reoperation was considered, but her physical condition deteriorated progressively, despite maximum medical treatment. She expired 26 days after hospitalization and 30 months after her initial aortic valve replacement. An autopsy was performed, and the explanted prosthesis was examined. The three leaflets of the prosthetic valve were stiff with restricted motion and the valve was stenotic (Fig 2). Pathologic examinations showed extensive calcified deposits in the leaflets. There was leaflet calcification without inflammatory cell infiltration (Fig 3). There were no abnormal calcified deposits or calcification of the organs except vascular system, suggesting abnormality of calcium metabolism. The cause of death was congestive heart failure due to severe aortic stenosis of the bioprosthetic valve.
View larger version (78K):
[in this window]
[in a new window]
|
Fig 1. Echocardiographic images of the aortic Perimount valve (Edwards Lifesciences, Irvine, CA) at diastolic phase (A) and systolic phase (B) showed bioprosthetic valve dysfunction with leaflet stiffness and motion restriction (arrows). There was severe aortic stenosis with a maximum flow of 4.6 m/sec (a maximum pressure gradient of 83 mm Hg) and an aortic valve area of 0.27 cm2.
|
|
View larger version (144K):
[in this window]
[in a new window]
|
Fig 2. Autopsy findings of the explanted Perimount valve (Edwards Lifesciences, Irvine, CA) viewing from (A) outflow and (B) inflow. Gross examination revealed that the three leaflets were stiff with restricted motion, and the valve was stenotic.
|
|
View larger version (107K):
[in this window]
[in a new window]
|
Fig 3. Microscopic examination of the explanted Perimount valve (Edwards Lifesciences, Irvine, CA) leaflet showed calcification deposits (intrinsic calcification) into the leaflet without inflammatory reaction. (Hematoxylin and eosin; x100).
|
|
|
Comment
|
|---|
The second-generation Carpentier-Edwards bioprosthesis (ie, the supra-annular Perimount valve) has long-term stability of the hemodynamic performance with a low rate of valve dysfunction [3]. Bioprosthetic valve deterioration may result from infection, calcification, thickening perforation, degeneration, suture abrasion, instrument trauma, and leaflet detachment from the valve strut. The Perimount valves rarely fail from design-related causes. They fail at almost equal rates from calcific and non-calcific degeneration, both of which occur late and are age-dependent [4]. The latest data from Edwards Lifesciences showed the actuarial freedom from explant due to structural valve deterioration as 81.5% at 20 years from implantation with the Perimount valves in the patients who were 65 years and older. There were a few reports of early calcification of prosthetic valves. Prosthetic valve deterioration requiring reoperation due to calcification of the valve leaflets occurred as early as 45 months after mitral Perimount valve implantation [5].
The principal underlying pathologic process of bioprosthetic valve deterioration is leaflet calcification [6]. Leaflet calcification is initiated primarily within residual cells that have been devitalized by glutaraldehyde pretreatment. The mechanism involves reaction of calcium-containing extracellular fluid with membrane-associated phosphorus to yield calcium phosphate mineral deposits. Calcification causes prosthetic valve deterioration with valve stenosis owing to leaflet stiffening. Calcific deposits are usually localized intrinsic to leaflet tissue, but sometimes extrinsic to the leaflet. Calcification is markedly accelerated in younger patients. Older patients have a lower rate of bioprosthetic valve deterioration. Although the relationship is well established, the mechanisms accounting for the effect of age are uncertain [7].
Recent studies have suggested that pathologic calcification is regulated by inductive and inhibitory factors, similar to the physiologic mineralization of bone [8]. Calcification can result when calcium in the circulatory system is attracted to phospholipids and glutaraldehyde residuals in the bioprosthetic tissue [7]. Although the pathophysiology is obscure, presumably rapid bioprosthetic valve degeneration and vascular calcification are frequently seen in dialysis patients. The risk factors for vascular calcification in dialysis patients include calcium or vitamin D supplementation. If bioprosthetic valve calcification occurs in the similar mechanism as vascular calcification in dialysis patients, there is a speculation that high systemic calcium level can lead to early bioprosthetic valve calcification. There is a potential relationship between the consumption of daily calcium supplements and early leaflet calcification. Reduced kidney function may further increase the deposition of calcium in valve leaflets.
In our current case, there was no definitive risk factor for prosthetic valve calcification, such as chronic renal failure or calcium metabolic disorder. Although the blood calcium level was normal at her last hospitalization, she had had daily calcium supplements for osteoporosis. Although the reason for early prosthetic valve deterioration in the current case is still unknown, such calcium supplements may increase the risk of calcium deposition in the leaflets of the implanted bioprosthetic valve.
|
References
|
|---|
- Banbury MK, Cosgrove 3rd DM, Thomas JD, et al. Hemodynamic stability during 17 years of the Carpentier-Edwards aortic pericardial bioprosthesis Ann Thorac Surg 2002;73:1460-1465.[Abstract/Free Full Text]
- Aupart MR, Mirza A, Meurisse YA, Sirinelli AL, Neville PH, Marchand MA. Perimount pericardial bioprosthesis for aortic calcified stenosis: 18-year experience with 1133 patients J Heart Valve Dis 2006;15:768-775.[Medline]
- Dellgren G, David TE, Raanani E, Armstrong S, Ivanov J, Rakowski H. Late hemodynamic and clinical outcomes of aortic valve replacement with the Carpentier-Edwards Perimount pericardial bioprosthesis J Thorac Cardiovasc Surg 2002;124:146-154.[Abstract/Free Full Text]
- Roselli EE, Smedira NG, Blackstone EH. Failure modes of the Carpentier-Edwards pericardial bioprosthesis in the aortic position J Heart Valve Dis 2006;15:421-427.[Medline]
- Polo ML, Legarra JJ, Vilar M, et al. Early calcification of a Carpentier-Edwards Perimount mitral valve in an elderly woman J Thorac Cardiovasc Surg 2002;124:1043-1044.[Free Full Text]
- Butany J, Nair V, Leong SW, Soor GS, Feindel C. Carpentier-Edwards Perimount valves—morphological findings in surgical explants J Card Surg 2007;22:7-12.[Medline]
- Schoen FJ, Levy RJ. Calcification of tissue heart valve substitutes: progress toward understanding and prevention Ann Thorac Surg 2005;79:1072-1080.[Abstract/Free Full Text]
- Speer MY, Giachelli CM. Regulation of vascular calcification Cardiovasc Pathol 2004;13:63-70.[Medline]
Top
Abstract
Introduction
