J Thorac Cardiovasc Surg 2004;127:1851-1852
© 2004 The American Association for Thoracic Surgery
Reply to the Editor
Hideki Teshima, MD,
Nobuhiko Hayashida, MD,
Shigeaki Aoyagi, MD
Department of Surgery, Kurume University, 67 Asahi-machi, Kurume, Japan
Reply to the Editor:
We read with interest the letter by Dr Baciewicz regarding his experience of two young female patients with prosthetic valve dysfunction as a result of pannus formation. In our study, we showed histologic and immunohistochemical findings of pannus tissue that caused prosthetic valve dysfunction after aortic valve replacement. We believe that our study provides information useful to elucidate the mechanisms of pannus formation in patients receiving prosthetic valves. We also think, however, that our findings are not sufficient to reach conclusion regarding the complete pathogenetic mechanisms of this disorder, and further prospective studies including more patients and control specimens are required.
The sizes of the prosthesis explanted in this study were 21 mm in 6 patients (all female), 23 mm in 2 (1 male and 1 female), 25 mm in 1 (male), and 27 mm in 1 (male). The ratio of effective orifice area (according to the manufacturer's report) to body surface area, as an index of patient-prosthesis mismatch, in our patients with pannus receiving 21-mm prostheses was 1.0 ± 0.1 cm2. The ratio was slightly lower than that in patients with normally functioning 21-mm aortic prostheses (1.2 ± 0.2 cm2).1 Because remaining significant transvalvular gradient after valve replacement may induce shear stress at the periannular tissue, patient-prosthesis mismatch per se can be a cause of excessive intimal growth. Another important issue in patients with small aortic annuli is mechanical contact between the ventricular septum and the pivot guard of the prosthesis. It is conceivable that the pivot guard protrudes to the left ventricular side, which is unique to the design of St Jude Medical valves,2 and thus is readily in contact with the hypertrophied ventricular septum. Recently, we carefully examined patients with prosthetic valve dysfunction in the aortic position with multidetector row computed tomography.3 In that study, these pathognomic conditions and pannus formation located mainly on the pivot guard of the septal side were confirmed. Therefore the possibility exists that patients with small aortic annuli are predisposed toward pannus formation regardless of the absence of patient-prosthesis mismatch, especially when the patient has a small left ventricular outflow tract.
During the period of this study, 615 patients underwent aortic valve replacement with St Jude Medical valves, and 265 of those were female (43%). Therefore, as indicated by Dr Baciewicz, the female proportion of patients who had prosthetic valve dysfunction develop tended to be higher than that of patients with normal prosthetic valve function. A major reason for this appears to be simply that female patients had smaller aortic annulus diameters. The mean age of our 7 female patients who developed pannus formation was 62.6 ± 6.7 years, which did not differ from our 265 female patients with normally functioning aortic valve prostheses. Although the number of patients is small and our results do not have statistical power, patient age per se may not be an important factor in pannus formation.
In our study, 4 of 11 patients with prosthetic valve dysfunction had a short-term history of warfarin withdrawal during treatments for noncardiac disease (abdominal operations and dental treatment). The remaining 7 patients received adequate anticoagulation therapy with warfarin throughout the postoperative period. The observations during reoperations and histologic examinations of periannular tissue did not demonstrate thrombus in all patients. These findings, however, do not negate the presence of perivalvular thrombus at an earlier period of prosthetic valve dysfunction. Because pannus can develop as a result of prosthetic valve thrombosis, inadequate anticoagulation also is considered to be a risk factor for this disorder.
The cause of prosthetic valve dysfunction related to pannus may be multifactorial, and definitive mechanisms for this disorder have not yet been conclusively shown. On the basis of our findings that excessive expression of transforming growth factor ß was observed in the pannus, however, chronic inflammatory reaction in the periannular lesions—perhaps as a result of surgical trauma, reaction to the foreign materials, mechanical contact, inadequate anticoagulation, and shear stress at the annulus—may be associated with pannus formation.
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References
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- Aoyagi S, Nishimi Y, Kawano H, Tayama E, Fukunaga S, Hayashida N, et al. Obstruction of St. Jude Medical valves in the aortic position: significance of a combination of cineradiography and echocardiography. J Thorac Cardiovasc Surg. 2000;120:142–147[Abstract/Free Full Text]
- Aoyagi S, Nishimi Y, Tayama E, Fukunaga S, Hayashida N, Akashi H, et al. Obstruction of St. Jude Medical valves in the aortic position: a consideration for pathogenic mechanism of prosthetic valve obstruction. J Cardiovasc Surg. 2002;10:339–344
- Teshima H, Hayashida N, Enomoto N, Aoyagi S, Okuda K, Uchida M. Diagnosis of prosthetic valve dysfunction by multidetector-row computed tomography. Ann Thorac Surg. 2003;75:1631–1633[Abstract/Free Full Text]
Related Article
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Obstruction of St Jude Medical valves in the aortic position
- Frank A. Baciewicz, Jr
J. Thorac. Cardiovasc. Surg. 2004 127: 1851.
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