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Excellent durability of the Hancock porcine bioprosthesis in the tricuspid position
Excellent durability of the Hancock porcine bioprosthesis in the tricuspid position A sixteen-year follow-up study From February 1975 to August 1981, 23 consecutive patients underwent tricuspid valve replacement, which was either isolated (six patients) or combined with the replacement of other valves (17) by means of a standard, glutaraldehyde-preserved Hancock porcine bioprostheses. Patients' ages ranged from 9 to 53 (mean 36.2) years. The follow-up period ranged from 0.2 to 16.5 years (mean 9.1) and was complete in 100 % of all cases. Structural valve failure of the tricuspid Hancock valve was noticed in two patients, a 9-year-old boy and a 13-year-old girl 3.4 and 16.5 years after implantation, respectively. The actuarial freedom rate from structural valve failure at 10 years was 94 ± 6%. There were six tricuspid prosthesis-related events: structural valve failure in two and valve thrombosis, anticoagulant-related bleeding, prosthetic valve endocarditis, and periprosthetic leak in one each, respectively. The actuarial freedom from these events at 10 years was 78 ± 10%. Five pairs of aortic/ mitral-tricuspid Hancock valves were explanted simultaneously from the same patients after 8.1 to 13.9 (mean 11.4) years postoperatively. A gross examination showed no valve dysfunction in the explants from the tricuspid position, but degenerative changes with valve dysfunction in those from the mitral and aortic position were observed (none of five versus five of seven; p < 0.03). We concluded that the selection of a Hancock bioprosthesis in the tricuspid position is acceptable because of the low incidence of prosthesis-related complications and the excellent durability of more than 10 years. (J THORAC CARDIOVASC SURG 1992;104:1561-6)
Yoshito Kawachi, MD, Ryuji Tominaga, MD, Manabu Hisahara, MD, Atsuhiro Nakashima, MD, Hisataka Yasui, MD, and Kouichi Tokunaga, MD,
Fukuoka, Japan
Rsthetic valve dysfunction as a result of structural deterioration of Hancock porcine bioprostheses (Medtronic, Inc., Minneapolis, Minn.) in either the mitral or aortic position has been noticed as cusp disruption and leafletcalcification, with an incidence of about 25% within 10 years after implantation. However, such complications may be rare in the tricuspid or pulmonary position.l' There is little information available on long-term follow-up studies of tricuspid valve replacement (TVR) with bioprostheses, because the number of such cases is From the Division of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan. Received for publication Jan. 21, 1992 Accepted for publication July I, 1992 Address for reprints: Yoshito Kawachi, MD, Division of Cardiovascular Surgery, Faculty of Medicine, Kyushu University 71, Maidashi 3-1-1, Higashi-ku, Fukuoka 812, Japan
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still small.4-6 In a patient with multiple valve replacement using bioprostheses, we performed a prophylactic replacement of a tricuspid bioprosthesis that had no dysfunction when reoperation of the aortic or mitral bioprosthesis was necessitated for structural valve failure. We made the tricuspid replacement because we thought there was no significant difference in the durability of a bioprosthesis in the tricuspid position and one in the left side of the heart. However, if the valve durability in the tricuspid position is good, it may not be necessary to replace the tricuspid bioprosthesis prophylactically. Thus the aim of this retrospective analysis is to present our 10- to 16-year experience with the Hancock valve in the tricuspid position and to report in particular on its durability. Patients and methods The records of a total of 23 consecutive patients who underwent TVR with the standard, glutaraldehyde-preserved Hancock porcine bioprosthesis at Kyushu University Hospital from
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Fig. 1. Follow-up of 19 patients who underwent tricuspid valve replacement with the Hancock porcine bioprosthesis. Four patients with hospital death were excluded. T, M, A, Tricuspid, mitral, aortic valve replacement; SVF, structural valve failure. PVE, prosthetic valve endocarditis. Asterisk indicates complications related to the Hancock valve in the tricuspid position. February 1975 to August 1981 are the basis for this study. The annular size of the Hancock valve was 33 mm in five patients, 31 mm in 15, 29 mm in two, and 27 mm in one. Some patients who received multiple valve replacement together with TVR were also included. TVR was associated either with a concomitant replacement of the mitral valve in 13 patients (with a Hancock valve in all), or with a concomitant replacement of both the aortic and mitral valves in four patients (with two Hancock valves in three patients and with Bjork-Shiley and Hancock valves in one patient each). An isolated TVR was performed on six occasions in five patients. One of these patients underwent a repeat replacement of the previously implanted Hancock valve with a new Hancock valve (cases 4 and 15) (Fig. 1). The mean age at operation was 36.2 ± 12.6 years (range, 9 to 53). There were three patients under 15 years of age. Ten patients were male and 13 were female. The causes of tricuspid valve disease were annular dilatation with leaflet shrinkage in 13 patients, rheumatic disease in five, infective endocarditis in four, and prosthetic valve dysfunction in one. The predominant valvular lesion was regurgitation in 17 patients and stenosis/insufficiency in six. When valve repair was unsuitable for pathologic changes of the tricuspid valve, TVR was indicated. TVR was performed with the standard cardiopulmonary bypass procedure and moderate systemic hypothermia. Aortic crossclamping using cardioplegia and topical cooling was employed. The Hancock valve was implanted by means of multiple interrupted 2-0 sutures with pledgets in the tricuspid anulus except for a small segment along the His bundle, where sutures were laid at the base of the tricuspid septal leaflet.
Warfarin anticoagulation was initiated after the removal of the chest tube in 19 patients without severe low cardiac output syndrome. Six patients with isolated TVR received warfarin for up to 3 months after implantation and thereafter it was discontinued. In 13 patients who underwent multiple valve replacement, nine were maintained with long-term warfarin therapy. The definition of thromboembolism included pulmonary embolism and valve thrombosis in the tricuspid position, but systemic embolism that occurred in patients with other Hancock valves in the aortic or mitral position was excluded. Anticoagulation-related hemorrhage included all bleeding episodes that either led to fatal results or were severe enough to necessitate blood transfusion or hospitalization. Prosthetic valve endocarditis (PVE) was defined as an episode of septicemia in the absence of a source other than the prosthesis, requiring either prolonged antibiotic therapy or reoperation. Structural valve failure (SVF) was ascertained at the time of either repeat operation, necropsy, or clinical investigation, and was defined by the presence of a characteristic cuspal disruption or leaflet calcification in the absence of PVE. 7 As for prosthesis-related events, only those with Hancock valves in the tricuspid position were considered. The patient follow-up was achieved by maintaining direct contact with patients. The follow-up information was completed over a I-month closing interval ending August 31, 1991. The follow-up was available for all patients, resulting in a 100% rate of completion. The final results were obtained by using a STAX program (a software system custom-designed for life table analysis; Nakayama Shoten, Tokyo, Japan). There was a 173 patient-year follow-up. The mean follow-up period was 9.1 ± 4.7 years (range, 0.2 to 16.5). There were six current
Volume 104 Number 6 December 1992
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Fig. 2. Actuarial survival including hospital deaths (Kaplan-Meier analysis). There was a significant difference between isolated tricuspid valve replacement and multiple valve replacement. An open or closed circle indicates a patient at the time of last contact. survivors, whose follow-up periods ranged from 10.0 to 16.5 years. Patients who had undergone a repeat replacement of the prosthesis in the tricuspid position were considered to be either alive or dead depending upon their status 30 days after reaperation. The standard actuarial statistical technique was used to describe the survival rate and the incidence of prosthesis-related complications.f The actuarial rates were expressed as the percent of the patients' event-free rates. The continuous data are represented as the mean ± the standard deviation. The actuarial probability estimates are expressed as the mean ± the standard error.
Results There were four hospital deaths, indicating a 17.4% hospital mortality. All of these deaths were cases of multiple valvereplacement. The causes were the result of low cardiac output syndrome. Seven patients died in the late postoperative period. All of them had multiple valve replacement. The causes of late death were prosthesis-related in two and cardiac-related in five. There were no noncardiac-related deaths. One of the two prosthesis-related deaths was a tricuspid prosthesis-related event, anticoagulant-related hemorrhage (case No.2). The overall actuarial survival rate including hospital mortality at 10 years was 54 ± II %. There was a significant difference between multiple valve replacement and isolated TVR by a generalized Wilcoxon test (p < 0.05) (Fig. 2). There were no cases of obvious pulmonary embolism. Valve thrombosis was found at necropsy in one patient who died from low output syndrome 3 months after tri-
cuspid/mitral double valve replacement (case No. I). A small thrombosis was noticed in both the tricuspid and mitral Hancock valves on the ventricular side and at the prosthesis suture line in both atria. The leaflet mobility of both Hancock valves was not at all disturbed by the thrombi. The patient received no anticoagulation therapy. Anticoagulation-related bleeding was noticed in one patient who died from cerebral bleeding 4 months after a tricuspid/mitral double-valvereplacement (case No.2). PVE occurred in one patient who underwent an isolated TVR for native valve endocarditis (case No.6). She underwent a repeat replacement in a condition of active endocarditis. The explant appeared stenotic by fusion of the cusps with vegetation, including a bacterial colony. There were no instances of SVF of the tricuspid Hancock valve in 16 adult patients during 8.7 ± 4.4 (range 0.2 to 14.8) years after operation. In a 9-year-old boy receiving isolated TVR, SVF was identified 3.4 years after operation (case No.4). He underwent a second replacement of the Hancock valve because of tricuspid stenosis with hepatomegaly and ascites. The explant appeared immobile as a result of severe calcification of three cusps and fibrous tissue overgrowth with microscopic-sized fibrous thrombus in one cusp.? He received a Hancock valve again at 12 years of age, and it has remained functional with no signs of SVF for 12.9 years (case No. 15). Another Hancock valve with an annular size of 27 mm was implanted in a 13-year-old girl (case No. 19). Sixteen years later, when she was planning to
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The Journal of Thoracic and Cardiovascular Surgery
Kawachi et al.
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Fig. 3. Actuarialcurveof freedom fromreoperation (Kaplan-Meieranalysis). Dashed line indicates thecurvewhen four patients with prophylactic removal are excluded. Open circle indicates a patient at the time of last contact.
have a child because she had no symptoms, the Hancock valve was found to be stenotic by echocardiography. A percutaneous balloon valvotomy was effectively performed on the tricuspid Hancock valve, decreasing the right atrial pressure from 9 to 5 mm Hg, the transvalvular pressure gradient from 11.1 to 7.5 mm Hg, and widening the effective orifice area from 0.67 to 0.9 cm-. The actuarial rate of freedom from SVF at 10 years was 94 ± 6%. Nonstructural valve dysfunction such as minimal periprosthetic leakage was identified at necropsy in one patient, with sudden unexpected death taking place 13.1 years after operation (case No. 16). He had undergone an aortic/mitral/tricuspid triple-valve replacement. A total of six patients underwent a replacement of Hancock valves with no mortality. The mean interval was 9.1 ± 3.3 years (range, 3.4 to 13.9). Reoperation was performed in two patients with an isolated TVR for PVE in one and for SVF in the other (cases No.4 and 6). Another four tricuspid Hancock valves showed no signs of dysfunction. Reoperation was performed as a prophylactic measure at the time of repeat replacement of Hancock valves in the mitral or aortic position as a result of SVF occurring in three patients at 10.1, 11.8, and 13.9 years, respectively, after the initial replacement (cases No. II, 13, and 17). In another patient, a second replacement of Hancock valves was performed for a massive left atrial thrombus after 8.1 years, although the mitral and tricuspid Hancock valves remained functional (case No. 7). The actuarial freedom rate from reoperation at 10 years was 80 ± 10% (Fig. 3).
Tricuspid prosthesis-related events, in which a repeat operation for prophylactic removal of the tricuspid Hancock valve as noted above was not included because the explanted Hancock valve showed no findings of valve failure, occurred in six patients: two with SVF and valve thrombosis, anticoagulant-related hemorrhage, PVE, and periprosthetic leakage in one each, respectively. The actuarial freedom rate from these events at 10 years was 78 ± 10%. A total of 18 Hancock valves (nine tricuspid, seven mitral, and two aortic) were explanted after implantation by reoperation or necropsy (Fig. I). Two tricuspid Hancock valves in cases of SVF and PVE have already been mentioned (cases No.4 and 6). Seven pairs of tricuspid/ mitral Hancock valves were simultaneously removed. Four Hancock valves explanted from the tricuspid and mitral position after 3 and 4 months, respectively, showed no degenerative changes (cases No. I and 2). A gross examination of 12 Hancock valves explanted after 8.1 to 13.9 years (mean, 11.4 ± 2.1) showed the following findings (cases No.7, II, 13, 16, and 17). Five tricuspid Hancock valves showed no signs of dysfunction. The leaflets were functioning adequately without stiffening in four explants. Slight immobility of one cusp, which was induced by mild fibrous tissue overgrowth, was noticed in one explant. There were neither any commissural tears nor cusp perforations. However, the explanted mitral and aortic Hancock valves exhibited cuspal perforation or tears with partial calcification in fivevalves and no significant degeneration in two valves. A comparison of the couples for aortic/mitral and tricuspid Hancock valves
Volume 104 Number 6 December 1992
always showed more severe degenerative changes in either the mitral or aortic Hancock valves than in the tricuspid Hancock valves (five of seven versus none of five; p < 0.03 by chi square test). An echocardiogram was performed on four patients among the six current survivors between postoperative years 9.4 and 16.6 (mean, 12.6 ± 3.1) (cases No. l O, 12, 15, and 19). The findings showed good functioning of the tricuspid Hancock valves either with or without mild stenosis or regurgitation. Discussion The high operative mortality and poor long-term survival rate may probably be attributable to multiple valve replacement including TVR. The major causes of deaths in patients undergoing multiple valve replacements were cardiac-related complications, which were induced by a more compromised preoperative left and right ventricular function and advanced hepatorenal dysfunction. Massive tricuspid regurgitation is considered to be a meaningful predictor of early and late mortality and morbidity after multiple valve surgical procedures.v 10 There were no deaths in the patients who received an isolated TVR. Although it is well known that the incidence ofthromboembolism in patients who have undergone mitral valve replacement with a bioprosthetic valve is low, bioprostheses in the tricuspid position are generally more thromboresistant. I, 2, II In our limited follow-up we did not notice any pulmonary embolism. Perhaps we could not clinically identify any pulmonary thromboembolism such as systemic embolism resulting in neurologic deficits and ischemic events. Infrequent small emboli may not induce major complications in the pulmonary circulation. Valve thrombosis was sometimes noticed in patients with severe low cardiac output.'? Cohen and associates':' reported that thrombosis was frequently observed (in five of six cases) in the ventricular aspects of the tricuspid Hancock valve and in the right ventricle by explants either at necropsy or at reoperation. We had nine tricuspid Hancock valves explanted after 0.2 to 13.9 years, but we found a small thrombosis on the prosthesis and in the right atrium in only one patient who died from low cardiac output. All patients undergoing isolated TVR did not need warfarin therapy beyond 3 months after implantation without embolic episodes. Therefore anticoagulation-related hemorrhage was a rare complication in those patients undergoing TVR with a bioprosthesis. The durability of bioprostheses in the tricuspid position beyond 10 years is still uncertain. Guerra and associates'' reported an acceptable long-term durability and satisfactory performance of Hancock valves after TVR with an actuarial rate of freedom from SVF of 68 ± 13% at 14
Hancock valve in tricuspid position
I 56 5
years. We had two cases with SVF among 19 patients during the 173 patient-year follow-up period. In our experience the SVF freedom rate was 94 ± 6% at 15 years. These findings were later confirmed by a gross inspection of nine explanted valves and by echocardiograms of four current survivors more than 10 years after implantation. We performed a second replacement of a tricuspid Hancock valve with a Hancock valve in a 12-year-old boy who developed calcification of the bioprosthesis that had been implanted when he was 9 years old. We thought a bioprosthesis was more suitable than a mechanical valve in the tricuspid position because the incidence of overall valve-related mortality and morbidity is small.!" The reason why the first Hancock valve calcified whereas the second did not may be related to a PVE-like event and to the difference in pulmonary hypertension. After the first operation, the patient experienced sustained fever and received prolonged high doses of antibiotic therapy based on the PVE protocol. Since he did not demonstrate any positive blood cultures or any new or altered cardiac murmurs, we could not diagnose a PVE. The systolic pulmonary artery pressure of the preoperative study was 80 mm Hg at the first operation and 22 mm Hg at the second operation. In a patient who underwent an isolated TVR at 13 years of age and had been working full time as a library clerk without any symptoms or drugs for 16 years, a stenosis of the Hancock valve was noticed on an echocardiogram and a percutaneous balloon valvotomy was successfully performed. The stenosis might have been caused by tissue overgrowth. Although the valvular orifice area calculated by the Gorlin formula was small, the patient's functional status was good both before and after the balloon valvotomy. We noticed that the Hancock valve in the tricuspid position did not develop SVF for a long time in either adults or children, and several reports': 6, IS, 16 indicated similar findings. However, it is well known that aortic and mitral bioprostheses increase the rate of SVF in a progressive nonlinear fashion more than 7 years after implantation, and accelerate the incidence of SVF in children with a severely calcified leaflet. 1-3, IS, 17 From a comparison of gross inspections of simultaneously implanted and explanted bioprostheses in the tricuspid and aortic/mitral position, degenerative changes were found to be more extensive in the aortic/mitral than in the tricuspid bioprostheses.sP Similar findings were confirmed in our experience as well. Degenerative changes and dysfunction of bioprosthetic valves in the tricuspid position progress very slowly based on the speed of leaflet calcification, fibrous tissue overgrowth, and cusp fraying.
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These findings could be explained by the greater closing pressure on the bioprosthesis and the pressure difference across the closed bioprosthesis in the mitral position compared with the tricuspid position. The degree of pulmonary hypertension may therefore be an important predictor of durability of the bioprosthesis in the tricuspid position. In our patients the systolic pulmonary artery pressure before the initial operation was 50 ± 25 mm Hg (range, 22 to 112), but this pressure was expected to decrease after surgery. We had four cases of prophylactic replacement of a tricuspid Hancock valve that had no dysfunction during the 8- to 14-year period after implantation. Previously we developed the following principle. In a patient with multiple valve replacement with bioprostheses, if one bioprosthesis revealed SVF, other existing bioprostheses should also be replaced at the time of first reoperation, because another reoperation would likely soon be necessitated for SVF of the reserved bioprosthesis and might result in a higher mortality and morbidity. From this retrospective study we determined that the Hancock valve in the tricuspid position was much more durable than that in the left side of the heart, and the prophylactic replacement of a bioprosthesis in the tricuspid position may therefore not be recommended. In conclusion, it can be said as a result of our study that a patient with a Hancock valve in the tricuspid position needs no long-term warfarin anticoagulation therapy, and that this valve produces a low incidence of valve-related complications and has good long-term durability not only in adults but also in children. These findings encourage us to use bioprostheses in the tricuspid position. However, we shall continue to conduct a careful follow-up, while keeping in mind that a repeat operation may be required in the future for SVF in those patients. REFERENCES 1. Foster AH, Greenberg GJ, Underhill OJ, McIntosh CL, Clark RE. Intrinsic failure of Hancock mitral bioprostheses: 10- to IS-year experience. Ann Thorac Surg 1987;44: 568-77. 2. Jamieson WRE, Allen P, Miyagishima RT, et al. The Carpentier-Edwards standard porcine bioprosthesis:a firstgeneration tissue valve with excellent long-term clinical performance. J THORAC CARDIOVASC SURG 1990;99:54361. 3. Kawachi Y, Tanaka J, Tominaga R, Kinoshita K, Tokunaga K. More than ten years' follow-up of the Hancock porcine bioprosthesis in Japan. J THORAC CARDIOVASC SURG 1992;I04:5-13. 4. Fleming WH, Sarafian LB, Moulton AL, Robinson LA,
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15. 16.
17.
Kugler JD. Valve replacement in the right side of the heart in children: long-term follow-up. Ann Thorac Surg 1989;48:404-8. McGrath LB, Gonzalez-Lavin L, Bailey BM, Grunkemeier GL, Fernadez J, Laub GW. Tricuspid valve operations in 530 patients. Twenty-five-year assessment of early and late phase events. J THORAC CARDIOVASC SURG 1990;99: 124-33. Guerra F, Bortolotti U, Thiene G, et al. Long-term performance of the Hancock porcine bioprosthesis in the tricuspid position. A review of forty-five patients with fourteenyear follow-up. J THORAC CARDIOVASC SURG 1990;99: 838-45. Edmunds LH Jr, Clark RE, Cohn LH, Miller C, Weisel RD. Guidelines for reporting morbidity and mortality after cardiac valvular operations. Ann Thorac Surg 1988;46: 257-9. Grunkemeier GL, Thomas DR, Starr A. Statistical considerations in the analysis and reporting of time-related events. Application to analysis of prosthetic valve-related thromboembolism and pacemaker failure. Am J Cardiol 1977;39:257-8. Kado H, Tanaka J, Yasui H, Tokunaga K. Late calcification of a Hancock tricuspid xenograft in a child. J Jpn Assoc Thorac Surg 1981;29:131-6. Teoh KH, Christakis GT, Weisel RD, et al. The determinants of mortality and morbidity after multiple-valve operations. Ann Thorac Surg 1987;43:353-8. Wellens F, VanDale P, Deuvaert FE, Leclerc JL, Primo G. The role of porcine heterografts in a l4-year experience with tricuspid valvereplacement. In: Cohn LH, Gallucci V, eds. Cardiac bioprostheses. New York: Yorke Medical Books, 1982:502-15. Spray TL, Roberts We. Structural changes in porcine xenografts used as substitute cardiac valves.Gross and histologic observations in 51 glutaraldehyde-preserved Hancock valves in 41 patients. Am J Cardiol 1977;40:319-30. Cohen SR, Silver MA, McIntosh CL, Roberts we. Comparison oflate (62 to 140 months) degenerative changes in simultaneously implanted and explanted porcine (Hancock) bioprostheses in the tricuspid and mitral valve positions in six patients. Am J Cardiol 1984;53: 1599-602. Kawachi Y, Masuda M, Tominaga R, Tokunaga K. Comparative study between St. Jude Medical and bioprosthetic valvesin the right side of the heart. Jpn Circ J 1991 ;55:55362. Dunn JM. Porcine valve durability in children. Ann Thorae Surg 1981;32:357-68. Pasque M, Williams WG, Coles JG, Trusler GA, Freedom RM. Tricuspid valve replacement in children. Ann Thorac Surg 1987;44:164-8. Williams DB, Danielson GK, McGoon DC, Puga FJ, Mair DO, Edwards WD. Porcine heterograft valve replacement in children. J THORAC CARDIOVASC SURG 1982;84:446-50.
Yoshito Kawachi, MD, Ryuji Tominaga, MD, Manabu Hisahara, MD, Atsuhiro Nakashima, MD, Hisataka Yasui, MD, and Kouichi Tokunaga, MD,
Fukuoka, Japan
Rsthetic valve dysfunction as a result of structural deterioration of Hancock porcine bioprostheses (Medtronic, Inc., Minneapolis, Minn.) in either the mitral or aortic position has been noticed as cusp disruption and leafletcalcification, with an incidence of about 25% within 10 years after implantation. However, such complications may be rare in the tricuspid or pulmonary position.l' There is little information available on long-term follow-up studies of tricuspid valve replacement (TVR) with bioprostheses, because the number of such cases is From the Division of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan. Received for publication Jan. 21, 1992 Accepted for publication July I, 1992 Address for reprints: Yoshito Kawachi, MD, Division of Cardiovascular Surgery, Faculty of Medicine, Kyushu University 71, Maidashi 3-1-1, Higashi-ku, Fukuoka 812, Japan
12/1/40780
still small.4-6 In a patient with multiple valve replacement using bioprostheses, we performed a prophylactic replacement of a tricuspid bioprosthesis that had no dysfunction when reoperation of the aortic or mitral bioprosthesis was necessitated for structural valve failure. We made the tricuspid replacement because we thought there was no significant difference in the durability of a bioprosthesis in the tricuspid position and one in the left side of the heart. However, if the valve durability in the tricuspid position is good, it may not be necessary to replace the tricuspid bioprosthesis prophylactically. Thus the aim of this retrospective analysis is to present our 10- to 16-year experience with the Hancock valve in the tricuspid position and to report in particular on its durability. Patients and methods The records of a total of 23 consecutive patients who underwent TVR with the standard, glutaraldehyde-preserved Hancock porcine bioprosthesis at Kyushu University Hospital from
I 56 I
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The Journal of Thoracic and Cardiovascular Surgery
Kawachi et al.
No Age Procedure
1 2
41 30
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years after operation
Fig. 1. Follow-up of 19 patients who underwent tricuspid valve replacement with the Hancock porcine bioprosthesis. Four patients with hospital death were excluded. T, M, A, Tricuspid, mitral, aortic valve replacement; SVF, structural valve failure. PVE, prosthetic valve endocarditis. Asterisk indicates complications related to the Hancock valve in the tricuspid position. February 1975 to August 1981 are the basis for this study. The annular size of the Hancock valve was 33 mm in five patients, 31 mm in 15, 29 mm in two, and 27 mm in one. Some patients who received multiple valve replacement together with TVR were also included. TVR was associated either with a concomitant replacement of the mitral valve in 13 patients (with a Hancock valve in all), or with a concomitant replacement of both the aortic and mitral valves in four patients (with two Hancock valves in three patients and with Bjork-Shiley and Hancock valves in one patient each). An isolated TVR was performed on six occasions in five patients. One of these patients underwent a repeat replacement of the previously implanted Hancock valve with a new Hancock valve (cases 4 and 15) (Fig. 1). The mean age at operation was 36.2 ± 12.6 years (range, 9 to 53). There were three patients under 15 years of age. Ten patients were male and 13 were female. The causes of tricuspid valve disease were annular dilatation with leaflet shrinkage in 13 patients, rheumatic disease in five, infective endocarditis in four, and prosthetic valve dysfunction in one. The predominant valvular lesion was regurgitation in 17 patients and stenosis/insufficiency in six. When valve repair was unsuitable for pathologic changes of the tricuspid valve, TVR was indicated. TVR was performed with the standard cardiopulmonary bypass procedure and moderate systemic hypothermia. Aortic crossclamping using cardioplegia and topical cooling was employed. The Hancock valve was implanted by means of multiple interrupted 2-0 sutures with pledgets in the tricuspid anulus except for a small segment along the His bundle, where sutures were laid at the base of the tricuspid septal leaflet.
Warfarin anticoagulation was initiated after the removal of the chest tube in 19 patients without severe low cardiac output syndrome. Six patients with isolated TVR received warfarin for up to 3 months after implantation and thereafter it was discontinued. In 13 patients who underwent multiple valve replacement, nine were maintained with long-term warfarin therapy. The definition of thromboembolism included pulmonary embolism and valve thrombosis in the tricuspid position, but systemic embolism that occurred in patients with other Hancock valves in the aortic or mitral position was excluded. Anticoagulation-related hemorrhage included all bleeding episodes that either led to fatal results or were severe enough to necessitate blood transfusion or hospitalization. Prosthetic valve endocarditis (PVE) was defined as an episode of septicemia in the absence of a source other than the prosthesis, requiring either prolonged antibiotic therapy or reoperation. Structural valve failure (SVF) was ascertained at the time of either repeat operation, necropsy, or clinical investigation, and was defined by the presence of a characteristic cuspal disruption or leaflet calcification in the absence of PVE. 7 As for prosthesis-related events, only those with Hancock valves in the tricuspid position were considered. The patient follow-up was achieved by maintaining direct contact with patients. The follow-up information was completed over a I-month closing interval ending August 31, 1991. The follow-up was available for all patients, resulting in a 100% rate of completion. The final results were obtained by using a STAX program (a software system custom-designed for life table analysis; Nakayama Shoten, Tokyo, Japan). There was a 173 patient-year follow-up. The mean follow-up period was 9.1 ± 4.7 years (range, 0.2 to 16.5). There were six current
Volume 104 Number 6 December 1992
Hancock valve in tricuspid position
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Fig. 2. Actuarial survival including hospital deaths (Kaplan-Meier analysis). There was a significant difference between isolated tricuspid valve replacement and multiple valve replacement. An open or closed circle indicates a patient at the time of last contact. survivors, whose follow-up periods ranged from 10.0 to 16.5 years. Patients who had undergone a repeat replacement of the prosthesis in the tricuspid position were considered to be either alive or dead depending upon their status 30 days after reaperation. The standard actuarial statistical technique was used to describe the survival rate and the incidence of prosthesis-related complications.f The actuarial rates were expressed as the percent of the patients' event-free rates. The continuous data are represented as the mean ± the standard deviation. The actuarial probability estimates are expressed as the mean ± the standard error.
Results There were four hospital deaths, indicating a 17.4% hospital mortality. All of these deaths were cases of multiple valvereplacement. The causes were the result of low cardiac output syndrome. Seven patients died in the late postoperative period. All of them had multiple valve replacement. The causes of late death were prosthesis-related in two and cardiac-related in five. There were no noncardiac-related deaths. One of the two prosthesis-related deaths was a tricuspid prosthesis-related event, anticoagulant-related hemorrhage (case No.2). The overall actuarial survival rate including hospital mortality at 10 years was 54 ± II %. There was a significant difference between multiple valve replacement and isolated TVR by a generalized Wilcoxon test (p < 0.05) (Fig. 2). There were no cases of obvious pulmonary embolism. Valve thrombosis was found at necropsy in one patient who died from low output syndrome 3 months after tri-
cuspid/mitral double valve replacement (case No. I). A small thrombosis was noticed in both the tricuspid and mitral Hancock valves on the ventricular side and at the prosthesis suture line in both atria. The leaflet mobility of both Hancock valves was not at all disturbed by the thrombi. The patient received no anticoagulation therapy. Anticoagulation-related bleeding was noticed in one patient who died from cerebral bleeding 4 months after a tricuspid/mitral double-valvereplacement (case No.2). PVE occurred in one patient who underwent an isolated TVR for native valve endocarditis (case No.6). She underwent a repeat replacement in a condition of active endocarditis. The explant appeared stenotic by fusion of the cusps with vegetation, including a bacterial colony. There were no instances of SVF of the tricuspid Hancock valve in 16 adult patients during 8.7 ± 4.4 (range 0.2 to 14.8) years after operation. In a 9-year-old boy receiving isolated TVR, SVF was identified 3.4 years after operation (case No.4). He underwent a second replacement of the Hancock valve because of tricuspid stenosis with hepatomegaly and ascites. The explant appeared immobile as a result of severe calcification of three cusps and fibrous tissue overgrowth with microscopic-sized fibrous thrombus in one cusp.? He received a Hancock valve again at 12 years of age, and it has remained functional with no signs of SVF for 12.9 years (case No. 15). Another Hancock valve with an annular size of 27 mm was implanted in a 13-year-old girl (case No. 19). Sixteen years later, when she was planning to
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Fig. 3. Actuarialcurveof freedom fromreoperation (Kaplan-Meieranalysis). Dashed line indicates thecurvewhen four patients with prophylactic removal are excluded. Open circle indicates a patient at the time of last contact.
have a child because she had no symptoms, the Hancock valve was found to be stenotic by echocardiography. A percutaneous balloon valvotomy was effectively performed on the tricuspid Hancock valve, decreasing the right atrial pressure from 9 to 5 mm Hg, the transvalvular pressure gradient from 11.1 to 7.5 mm Hg, and widening the effective orifice area from 0.67 to 0.9 cm-. The actuarial rate of freedom from SVF at 10 years was 94 ± 6%. Nonstructural valve dysfunction such as minimal periprosthetic leakage was identified at necropsy in one patient, with sudden unexpected death taking place 13.1 years after operation (case No. 16). He had undergone an aortic/mitral/tricuspid triple-valve replacement. A total of six patients underwent a replacement of Hancock valves with no mortality. The mean interval was 9.1 ± 3.3 years (range, 3.4 to 13.9). Reoperation was performed in two patients with an isolated TVR for PVE in one and for SVF in the other (cases No.4 and 6). Another four tricuspid Hancock valves showed no signs of dysfunction. Reoperation was performed as a prophylactic measure at the time of repeat replacement of Hancock valves in the mitral or aortic position as a result of SVF occurring in three patients at 10.1, 11.8, and 13.9 years, respectively, after the initial replacement (cases No. II, 13, and 17). In another patient, a second replacement of Hancock valves was performed for a massive left atrial thrombus after 8.1 years, although the mitral and tricuspid Hancock valves remained functional (case No. 7). The actuarial freedom rate from reoperation at 10 years was 80 ± 10% (Fig. 3).
Tricuspid prosthesis-related events, in which a repeat operation for prophylactic removal of the tricuspid Hancock valve as noted above was not included because the explanted Hancock valve showed no findings of valve failure, occurred in six patients: two with SVF and valve thrombosis, anticoagulant-related hemorrhage, PVE, and periprosthetic leakage in one each, respectively. The actuarial freedom rate from these events at 10 years was 78 ± 10%. A total of 18 Hancock valves (nine tricuspid, seven mitral, and two aortic) were explanted after implantation by reoperation or necropsy (Fig. I). Two tricuspid Hancock valves in cases of SVF and PVE have already been mentioned (cases No.4 and 6). Seven pairs of tricuspid/ mitral Hancock valves were simultaneously removed. Four Hancock valves explanted from the tricuspid and mitral position after 3 and 4 months, respectively, showed no degenerative changes (cases No. I and 2). A gross examination of 12 Hancock valves explanted after 8.1 to 13.9 years (mean, 11.4 ± 2.1) showed the following findings (cases No.7, II, 13, 16, and 17). Five tricuspid Hancock valves showed no signs of dysfunction. The leaflets were functioning adequately without stiffening in four explants. Slight immobility of one cusp, which was induced by mild fibrous tissue overgrowth, was noticed in one explant. There were neither any commissural tears nor cusp perforations. However, the explanted mitral and aortic Hancock valves exhibited cuspal perforation or tears with partial calcification in fivevalves and no significant degeneration in two valves. A comparison of the couples for aortic/mitral and tricuspid Hancock valves
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always showed more severe degenerative changes in either the mitral or aortic Hancock valves than in the tricuspid Hancock valves (five of seven versus none of five; p < 0.03 by chi square test). An echocardiogram was performed on four patients among the six current survivors between postoperative years 9.4 and 16.6 (mean, 12.6 ± 3.1) (cases No. l O, 12, 15, and 19). The findings showed good functioning of the tricuspid Hancock valves either with or without mild stenosis or regurgitation. Discussion The high operative mortality and poor long-term survival rate may probably be attributable to multiple valve replacement including TVR. The major causes of deaths in patients undergoing multiple valve replacements were cardiac-related complications, which were induced by a more compromised preoperative left and right ventricular function and advanced hepatorenal dysfunction. Massive tricuspid regurgitation is considered to be a meaningful predictor of early and late mortality and morbidity after multiple valve surgical procedures.v 10 There were no deaths in the patients who received an isolated TVR. Although it is well known that the incidence ofthromboembolism in patients who have undergone mitral valve replacement with a bioprosthetic valve is low, bioprostheses in the tricuspid position are generally more thromboresistant. I, 2, II In our limited follow-up we did not notice any pulmonary embolism. Perhaps we could not clinically identify any pulmonary thromboembolism such as systemic embolism resulting in neurologic deficits and ischemic events. Infrequent small emboli may not induce major complications in the pulmonary circulation. Valve thrombosis was sometimes noticed in patients with severe low cardiac output.'? Cohen and associates':' reported that thrombosis was frequently observed (in five of six cases) in the ventricular aspects of the tricuspid Hancock valve and in the right ventricle by explants either at necropsy or at reoperation. We had nine tricuspid Hancock valves explanted after 0.2 to 13.9 years, but we found a small thrombosis on the prosthesis and in the right atrium in only one patient who died from low cardiac output. All patients undergoing isolated TVR did not need warfarin therapy beyond 3 months after implantation without embolic episodes. Therefore anticoagulation-related hemorrhage was a rare complication in those patients undergoing TVR with a bioprosthesis. The durability of bioprostheses in the tricuspid position beyond 10 years is still uncertain. Guerra and associates'' reported an acceptable long-term durability and satisfactory performance of Hancock valves after TVR with an actuarial rate of freedom from SVF of 68 ± 13% at 14
Hancock valve in tricuspid position
I 56 5
years. We had two cases with SVF among 19 patients during the 173 patient-year follow-up period. In our experience the SVF freedom rate was 94 ± 6% at 15 years. These findings were later confirmed by a gross inspection of nine explanted valves and by echocardiograms of four current survivors more than 10 years after implantation. We performed a second replacement of a tricuspid Hancock valve with a Hancock valve in a 12-year-old boy who developed calcification of the bioprosthesis that had been implanted when he was 9 years old. We thought a bioprosthesis was more suitable than a mechanical valve in the tricuspid position because the incidence of overall valve-related mortality and morbidity is small.!" The reason why the first Hancock valve calcified whereas the second did not may be related to a PVE-like event and to the difference in pulmonary hypertension. After the first operation, the patient experienced sustained fever and received prolonged high doses of antibiotic therapy based on the PVE protocol. Since he did not demonstrate any positive blood cultures or any new or altered cardiac murmurs, we could not diagnose a PVE. The systolic pulmonary artery pressure of the preoperative study was 80 mm Hg at the first operation and 22 mm Hg at the second operation. In a patient who underwent an isolated TVR at 13 years of age and had been working full time as a library clerk without any symptoms or drugs for 16 years, a stenosis of the Hancock valve was noticed on an echocardiogram and a percutaneous balloon valvotomy was successfully performed. The stenosis might have been caused by tissue overgrowth. Although the valvular orifice area calculated by the Gorlin formula was small, the patient's functional status was good both before and after the balloon valvotomy. We noticed that the Hancock valve in the tricuspid position did not develop SVF for a long time in either adults or children, and several reports': 6, IS, 16 indicated similar findings. However, it is well known that aortic and mitral bioprostheses increase the rate of SVF in a progressive nonlinear fashion more than 7 years after implantation, and accelerate the incidence of SVF in children with a severely calcified leaflet. 1-3, IS, 17 From a comparison of gross inspections of simultaneously implanted and explanted bioprostheses in the tricuspid and aortic/mitral position, degenerative changes were found to be more extensive in the aortic/mitral than in the tricuspid bioprostheses.sP Similar findings were confirmed in our experience as well. Degenerative changes and dysfunction of bioprosthetic valves in the tricuspid position progress very slowly based on the speed of leaflet calcification, fibrous tissue overgrowth, and cusp fraying.
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These findings could be explained by the greater closing pressure on the bioprosthesis and the pressure difference across the closed bioprosthesis in the mitral position compared with the tricuspid position. The degree of pulmonary hypertension may therefore be an important predictor of durability of the bioprosthesis in the tricuspid position. In our patients the systolic pulmonary artery pressure before the initial operation was 50 ± 25 mm Hg (range, 22 to 112), but this pressure was expected to decrease after surgery. We had four cases of prophylactic replacement of a tricuspid Hancock valve that had no dysfunction during the 8- to 14-year period after implantation. Previously we developed the following principle. In a patient with multiple valve replacement with bioprostheses, if one bioprosthesis revealed SVF, other existing bioprostheses should also be replaced at the time of first reoperation, because another reoperation would likely soon be necessitated for SVF of the reserved bioprosthesis and might result in a higher mortality and morbidity. From this retrospective study we determined that the Hancock valve in the tricuspid position was much more durable than that in the left side of the heart, and the prophylactic replacement of a bioprosthesis in the tricuspid position may therefore not be recommended. In conclusion, it can be said as a result of our study that a patient with a Hancock valve in the tricuspid position needs no long-term warfarin anticoagulation therapy, and that this valve produces a low incidence of valve-related complications and has good long-term durability not only in adults but also in children. These findings encourage us to use bioprostheses in the tricuspid position. However, we shall continue to conduct a careful follow-up, while keeping in mind that a repeat operation may be required in the future for SVF in those patients. REFERENCES 1. Foster AH, Greenberg GJ, Underhill OJ, McIntosh CL, Clark RE. Intrinsic failure of Hancock mitral bioprostheses: 10- to IS-year experience. Ann Thorac Surg 1987;44: 568-77. 2. Jamieson WRE, Allen P, Miyagishima RT, et al. The Carpentier-Edwards standard porcine bioprosthesis:a firstgeneration tissue valve with excellent long-term clinical performance. J THORAC CARDIOVASC SURG 1990;99:54361. 3. Kawachi Y, Tanaka J, Tominaga R, Kinoshita K, Tokunaga K. More than ten years' follow-up of the Hancock porcine bioprosthesis in Japan. J THORAC CARDIOVASC SURG 1992;I04:5-13. 4. Fleming WH, Sarafian LB, Moulton AL, Robinson LA,
5.
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Kugler JD. Valve replacement in the right side of the heart in children: long-term follow-up. Ann Thorac Surg 1989;48:404-8. McGrath LB, Gonzalez-Lavin L, Bailey BM, Grunkemeier GL, Fernadez J, Laub GW. Tricuspid valve operations in 530 patients. Twenty-five-year assessment of early and late phase events. J THORAC CARDIOVASC SURG 1990;99: 124-33. Guerra F, Bortolotti U, Thiene G, et al. Long-term performance of the Hancock porcine bioprosthesis in the tricuspid position. A review of forty-five patients with fourteenyear follow-up. J THORAC CARDIOVASC SURG 1990;99: 838-45. Edmunds LH Jr, Clark RE, Cohn LH, Miller C, Weisel RD. Guidelines for reporting morbidity and mortality after cardiac valvular operations. Ann Thorac Surg 1988;46: 257-9. Grunkemeier GL, Thomas DR, Starr A. Statistical considerations in the analysis and reporting of time-related events. Application to analysis of prosthetic valve-related thromboembolism and pacemaker failure. Am J Cardiol 1977;39:257-8. Kado H, Tanaka J, Yasui H, Tokunaga K. Late calcification of a Hancock tricuspid xenograft in a child. J Jpn Assoc Thorac Surg 1981;29:131-6. Teoh KH, Christakis GT, Weisel RD, et al. The determinants of mortality and morbidity after multiple-valve operations. Ann Thorac Surg 1987;43:353-8. Wellens F, VanDale P, Deuvaert FE, Leclerc JL, Primo G. The role of porcine heterografts in a l4-year experience with tricuspid valvereplacement. In: Cohn LH, Gallucci V, eds. Cardiac bioprostheses. New York: Yorke Medical Books, 1982:502-15. Spray TL, Roberts We. Structural changes in porcine xenografts used as substitute cardiac valves.Gross and histologic observations in 51 glutaraldehyde-preserved Hancock valves in 41 patients. Am J Cardiol 1977;40:319-30. Cohen SR, Silver MA, McIntosh CL, Roberts we. Comparison oflate (62 to 140 months) degenerative changes in simultaneously implanted and explanted porcine (Hancock) bioprostheses in the tricuspid and mitral valve positions in six patients. Am J Cardiol 1984;53: 1599-602. Kawachi Y, Masuda M, Tominaga R, Tokunaga K. Comparative study between St. Jude Medical and bioprosthetic valvesin the right side of the heart. Jpn Circ J 1991 ;55:55362. Dunn JM. Porcine valve durability in children. Ann Thorae Surg 1981;32:357-68. Pasque M, Williams WG, Coles JG, Trusler GA, Freedom RM. Tricuspid valve replacement in children. Ann Thorac Surg 1987;44:164-8. Williams DB, Danielson GK, McGoon DC, Puga FJ, Mair DO, Edwards WD. Porcine heterograft valve replacement in children. J THORAC CARDIOVASC SURG 1982;84:446-50.