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The Hancock II porcine bioprosthesis
J
THORAC CARDIOVASC SURG
1989;97:415-20
The Hancock II porcine bioprosthesis A preliminary report From May 1983 to July 1987 a total of 153 Hancock II porcine bioprostheses have been implanted in 130 patients with a mean age of 59 ± 8 years (range 29 to 76 years). Mitral valve replacement was performed in 72 patients, aortic valve replacement in 35, and mitral-aortic valve replacement in 23. Cumulati"e foUow-up of 121 survivorsis 223 patient-years and 100% complete (range 0.4 to 4.5 years). The actuarial survival rate at 4 years is 88% ± 8% for mitral, 86% ± 7.8% for aortic, and 84% ± 8% for mitral-aortic valve replacement. Minor thomboembolism occurred in two patients (0.9% ± 0.6% jpt-yr) with an actuarial freedom from emboli at 4 years of 100% for mitral, 96% ± 3.7% for aortic, and 91 % ± 8.6% for mitral-aortic valve replacement. Anticoagulant-related hemorrhage occurred in 10 patients (4.4% ± 1.4%jpt-yr) with an actuarial freedom at 4 years of 90% ± 4.8% for mitral, 89 % ± 5.8 % for aortic, and 84 % ± 10.6 % for mitral-aortic valve replacement. Failure of the porcine bioprosthesis was observed in three patients with an actuarial freedom at 4 years of 96 % ± 3.6 % for aortic, 91 % ± 8 % for mitral, and 91 % ± 8.6 % for mitral-aortic valvereplacement. Actuarial freedom from all porcine bioprosthesis-related complieations at 4 years is 85.7% ± 6.6 % for aortic, 79 % ± 9 % for mitral, and 70 % ± 13 % for mitral-aortic valve replacement. No instances of primary tissue failure occurred. This preliminary experience justifies a cautious optimism on the performance and durability of the Hancock II porcine bioprosthesis, supporting our current trend to use it in a selected population until data on a longer foUow-up are available.
Uberto Bortolotti, MD, Aldo Milano, MD, Alessandro Mazzucco, MD, Francisco Guerra, MD, Alberto Magni, MD, Francesco Santini, MD, and Vincenzo Gallucci, MD, Padova, Italy
Since primary tissue failure is the factor that most commonly adversely affects the performance of the Hancock porcine bioprosthesis.l" some modifications of manufacturing and tissue processing techniques have been introduced in the standard model of this porcine bioprosthesis with the aim of delaying the onset of this complication and increasing the durability of the valve. These modifications have led to the development of a new porcine bioprosthesis, the Hancock IF (Hancock Extracorporeal Inc., Anaheim, Calif.), which is currently undergoing clinical testing. We report in this paper From the Department of Cardiovascular Surgery, University of Padova Medical School, Padova, Italy. This work was supported in part by Grant No. 87.00719.57 of the National Council of Research, Rome, Italy, Target Project "Biomedical Technology." Received for publication Jan. 26, 1988. Accepted for publication Sept. 2, 1988. Address for reprints: U. Bortolotti, MD, Istituto di Chirurgia Cardiavascolare, Universita di Padova, Via Giustiniani, 2, 35128 Padova, Italy.
our initial experience and preliminary results with this device. Patients and methods From May 1983 to July 1987, 153 Hancock II porcine bioprostheses were implanted in 130 patients, 69 men and 61 women, whose ages ranged from 29 to 76 years (mean 59 ± 8 years). Isolated aortic valve replacement (AVR) was performed in 35 patients, isolated mitral valve replacement (MVR) in 72, and combined mitral-aortic valve replacement (MAVR) in 23. Associated surgical procedures, mainly tricuspid valve annuloplasty and coronary artery bypass grafting, were performed in 24 patients (18.4%). The causes of valve disease and the incidence of previous operations are summarized in Table I. Preoperatively, eight patients were in New York Heart Association (NYHA) class IV, 115 in class III, and seven in class II; 87 were in atrial fibrillation, 42 in sinus rhythm, and one had a permanent pacemaker. Standard surgical techniques were used in all patients as reported elsewhere.v" After the operation all patients were given anticoagulants, which were usually suspended after 3 months; the major indication for indefinite anticoagulation in MVR and MA VR patients was the combination of atrial fibrillation, giant left atrium, and left atrial thrombosis. Definitions of prosthesis-related complications in porcine
415
The Journal of Thoracic and Cardiovascular Surgery
Bortolotti et al.
4I6
Fig. 1. Actuarial survival rates after MVR, AVR, and MA VR with the Hancock II porcine bioprosthesis. Numbers on the horizontal axis indicate the patients at risk; operative deaths are not included.
Table I. Causes of valvular disease and incidence of previous operations No. Cause Rheumatic Degenerative Endocarditis Congenital Unknown Failing prosthesis Total Previous operations Mitral valve repair Coarctectomy MVR AVR MAVR Total
69 31 2
1 1
-.1Q
%
53 24 1.6 0.7 0.7 20
Table II. Summary offollow-up data Current survivors Mean follow-up (yr) Minimum follow-up (yr) Maximum follow-up (yr) Cumulative follow-up (pt-yr)
MVR
AVR
MAVR
Total
64
30
17
111
2.1 ± 1.2 1.5 ± 0.8 1.5 ± 0.9 1.8 ± 1.0
0.6
0.4
0.4
0.6
4.5
3.3
4.2
4.5
141
50
32
223
130 15 I 17
5 _5 43
11.5 0.8 13.1 3.8
.....il. 33
valve recipients have been reported previously.v' Such complications were considered as porcine bioprosthesis failure when death or reoperation resulted and as overall porcine bioprosthesis-related complications regardless of the patient outcome. Patient survival and freedom from porcine bioprosthesisrelated complications are expressed in actuarial fashion excluding operative deaths and as linearized rates as percent per patient-year (%/pt-yr).
Results Hospital mortality and follow-up. There were nine operative deaths (7%), two after AVR (5.7%), five after MVR (7%), and two after MAVR (8.7%). A total of 121 patients discharged were observed from 0.4 to 4.5
years (mean 1.8 ± 1.0 years); cumulative duration of follow-up, ending in December 1987 and being 100% complete, is 223 patient-years (Table II). There were nine late deaths with a linearized incidence of 4.0% ± l.3%/pt-yr; three patients died after AVR, three after MVR, and three after MAVR. The causes of late death were heart failure in five patients; lo~ output syndrome at reoperation for paravalvular leak in one patient who had had MVR; cerebral anticoagulant-related hemorrhage in one patient after AVR, malignancy in one patient after MA VR, and unknown in one patient. The actuarial survival rates at 4 years are 88% ± 8% for MVR,86% ± 7.8% for AVR, and 84% ± 8 for MAVR patients (Fig. 1). Of the III current survivors, 10 are in NYHA class III, 74 in class II, and 27 in class I. Almost 50% of them are in atrial fibrillation, 40% are receiving long-term anticoagulant therapy, and 10% are receiving antiplatelet drugs. Porcine bioprosthesis-related complications. Porcine bioprosthesis-related complications occurred in 15
Volume 97 Number 3
Hancock II porcine bioprosthesis
March 1989
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o
..
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~
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-
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o AVR
96±3.7
o
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91±8.6
w
W
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LL
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27
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Table
m. Summary of postoperative complications MVR
Late deaths Embolic episodes Hemorrhage Endocarditis Paravalvular leak Primary tissue failure Porcine bioprosthesis-related complications
AVR
Total
MAVR
No.
%/pt-yr
No.
%/pt-yr
No.
%/pt-yr
3
2.1 ± 1.2
5 1 1
3.5 ± 1.5 0.7 ± 0.7 0.7 ± 0.7
3 1 3
6.0 ± 3.4 2.0 ± 2.0 6.0 ± 3.4
3 1 2
9.3 ± 5.4 3.1 ± 3.1 6.2 ± 4.4
10
3.1 ± 3.1
I 2
7
4.9 ± 1.8
12.5 ± 6.2
15
4
patients (6.7% ± 1.7%jpt-yr) and are summarized in Table III. Minor thromboembolic episodes occurred in two patients (0.9% ± 0.6%jpt-yr), 8 months after AVR and 16 months after MAVR, respectively; neither was receiving anticoagulants and both recovered without sequelae. Actuarial freedom from embolism at 4 years is 100% for MVR, 96% ± 3.7% for AVR, and 91% ± 8.6% for MAVR patients (Fig. 2). Anticoagulantrelated hemorrhage occurred in 10 patients (after MVR in five, after AVR in three, and after MAVR in two), after a mean interval of 10 ± 8 months, and was fatal in one patient. The linearized incidence of this complication is 4.4% ± 1.4%jpt-yr in the entire series and 12% ± 4.0%jpt-yr in patients receiving anticoagulants; actuarial freedom from anticoagulant-related hemorrhage at 4 years is 90% ± 4.8% for MVR, 89% ± 5.8% for AVR, and 84% ± 10.6% for MAVR (Fig. 3). Paravalvular leak occurred in two patients (0.9% ± 0.6%jpt-yr); one died of low output syndrome at reoperation 3 years, 4 months after MVR and another
8.0 ± 5.6
4
No. 9 2
%/pt-yr 4.0 0.9 4.4 0.4 0.9
± ± ± ± ±
1.3 0.6 1.4 0.4 0.6
6.7 ± 1.7
underwent successful mitral prosthetic replacement 1 year, 4 months after MAYR. Endocarditis was observed in one patient 2 months after MVR (0.4 ± O.4%jpt-yr), and the infection has apparently been cured by antibiotic therapy. Porcine bioprosthesis failure was observed in three patients: fatal anticoagulant-related hemorrhage in one and reoperation because of paravalvular leak in two. Actuarial freedom from porcine bioprosthesis failure at 4 years is 96% ± 3.6% for AVR, 91% ± 8% for MVR, and 91% ± 8.6% for MAVR patients (Fig. 4). Actuarial freedom from overall porcine bioprosthesis-related complications at 4 years is 85.7% ± 6.6% for AVR, 79% ± 9% for MVR, and 70% ± 13% for MAVR patients (Fig. 5). No instances of primary tissue failure have been observed during the follow-up period.
Discussion The standard Hancock valve has been the bioprosthesis of choice at our department over the past 15
The Journal of Thoracic and Cardiovascular Surgery
4 1 8 Bortolotti et al.
__
.100~~
0:: 0::
o ~
LU
:I:
90±4.8 89±5.8
~:::::::""~-o---=:::::*===*.a
•
MVR
o AVR
o
MAVR
80
u.
o
84±10.6
LU
~
u.
60
•
60
44
2 7
0
2 8
1 4
6
0
1 8
10
3
1
2
\ 1 3
3
4
YEARS POSTOP Fig. 3. Actuarial probability of being free from anticoagulant-related hemorrhage.
-60
i~
•
• MVR o AVR o MAVR
..........
6 0
44
2 8
1 2
2 7
1 4
6
3
1 8
11
1
.2
4
3
.
4
YEARS POSTOP Fig. 4. Actuarial freedom from valve failure. PR. Porcine bioprosthesis.
years. 4, 6, 8 During this period the results of our clinical and pathologic experience," 6, 8-10 together with that of others.!-" 5.10-14 have contributed to clarify the major complications and disadvantages related to the use of this device. Among them are those related to (1) a disproportion between the high prosthetic profile and the left ventricular cavity": 16; (2) a permanent deformation ("creeping") of the polypropylene flexible frame with inward bending of the stent posts'<"; (3) a suboptimal hemodynamic performance in the small sizes because of a prominent muscular shelf on the right coronary CUSpI9; (4) a limited durability resulting from tissue calcification, which is progressive in most cases"
and accelerated in children and adolescents." in patients with chronic renal failure," and possibly during pregnancy," and whose onset is favored by poor tissue preservation. IO, 22 Because of these observations, in the Hancock II porcine bioprosthesis the stent is of lower profile and made of new material (Delrin) with better fatigue and tensile properties, tissue selection has been improved, low-pressure fixation has been introduced, and a calcium-retarding agent (water soluble C-12 alkyl sulfate, T6) has been added to tissue processing.' Since the Hancock II porcine bioprosthesis has been made available for clinical use only recently, the experi-
Volume 97 Number 3 March 1989
Hancock II porcine bioprosthesis 419
~
•
100
MVR
o AVR
1-(1)
:5z wO
o
MAVR
0:: -
I~
79±9
~U
u..:::J
00..
w~
wO o::U u, '(§:.
•
60
4 3
2 6
o
28
1 3
6
018
1 0
3
1
2
70±13 11 3
3
4
YEARS POSTOP Fig. 5. Actuarial probability of being free from overall prosthesis-related complications. PR, Porcine bioprostheSIS.
ence with this device is obviously limited. Our results indicate that at short-term follow-up this device has a negligible thrombogenicity although almost 40% of the patients are receiving long-term anticoagulant therapy. These results may explain the high incidence of anticoagulant-related hemorrhage and again make anticoagulation in tissue valve recipients questionable. No instances of primary tissue failure were observed and only two patients required reoperation for paravalvular leak. It must be considered, however, that the Hancock II porcine bioprosthesis was never used in children or in patients with clear-cut risk factors for calcification and that the mean age of patients in this series is higher than that of patients receiving a standard Hancock porcine bioprosthesis at our institution.' Although a longer follow-up will be needed to verify the impact of the new manufacturing techniques on both durability and overall performance of this device, the results of this preliminary experience substantiate so far a cautious optimism. Our current trend is to employ any tissue valve in a patient population selected mainly on the basis of age (>55 years) and on peculiar situations." The use of the Hancock II porcine bioprosthesis might be expanded particularly when the role of the anticalcification treatment on valve durability will be better assessed.
2.
3.
4.
5.
6.
7.
8.
We express our gratitude to Gian Carlo Pengo for his skilled technical assistance.
9.
REFERENCES I. Oyer PE, Miller DC, Stinson EB, Reitz BA, MorenoCabral RJ, Shumway NE. Clinical durability of the
10.
Hancock porcine bioprosthesis. J THORAC CARDIOVASC SURG 1980;80:824-33. Borkon AM, McIntosh CL, Von Rueden TJ, Morrow AG. Mitral valve replacement with the Hancock bioprosthesis: five to ten year follow-up. Ann Thorac Surg 1981; 32:127-37. Cohn LH, Mudge GH, Pratter F, Collins JJ Jr. Five to eight year follow-up of patients undergoing porcine heart valve replacement. N Engl J Med 1981;304:258-62. Gallucci V, Bortolotti U, Milano A, et al. The Hancock porcine valve 15 years later: an analysis of 575 patients. In: Bodnar E, Yacoub M, eds. Biologic and bioprosthetic valves. New York: Yorke Medical Books, 1986:91-7. Gallo I, Ruiz B, Duran CG. Isolated mitral valve replacement with the Hancock porcine bioprosthesis in rheumatic heart disease: analysis of 213 operative survivors followed up 4.5 to 8.5 years. Am J Cardiol 1984; 53:178-81. Bortolotti U, Milano A, Mazzucco A, et al. Results of reoperation for primary tissue failure of porcine bioprostheses. J THORAC CARDIOVASC SURG 1985;90:564-9. Wright JTM, Eberhardt CE, Gibbs ML, Saul T, Gilpin CB. Hancock II: an improved bioprosthesis. In: Cohn LH, Gallucci V, eds. Cardiac bioprostheses, New York: Yorke Medical Books, 1982:424-44. Gallucci V, Bortolotti U, Milano A, Valfre C, Mazzucco A, Thiene G. Isolated mitral valve replacement with the Hancock bioprosthesis: a 13-year appraisal. Ann Thorac Surg 1984;38:571-8. Milano A, Bortolotti U, Talenti E, et al. Calcific degeneration as the main cause of porcine bioprosthetic failure. Am J Cardiol 1984;53:1066-70. Valente M, Bortolotti U, Thiene G: Ultrastructural substrates of dystrophic calcification in porcine bioprosthetic valve failure. Am J Pathol 1985;119:12-21.
The Journal of
420
Thoracic and Cardiovascular Surgery
Bortolotti et at.
II. Spray TL, Roberts We. Structural changes in porcine xenografts used as substitute cardiac valves: gross and histological observations in 51 glutaraldehyde-preserved Hancock valves in 41 patients. Am J Cardiol 1977; 40:319-30. 12. Ferrans VJ, Boyce SW, Billingham ME, Jones M, Ishihara T, Roberts We. Calcific deposits in porcine bioprostheses: structure and pathogenesis. Am J Cardiol 1980;46:721-34. 13. Schoen FJ, Collins JJ, Cohn LH. Long-term failure rate and morphologic correlations in porcine bioprosthetic cardiac valves. Am J Cardiol 1983;51:957-64. 14. Gallo I, Ruiz B, Nistal F, Duran CMG. Degeneration in porcine bioprosthetic cardiac valves: incidence of primary tissue failures among 938 bioprostheses at risk. Am J Cardiol 1984;53:1061-5. 15. Bortolotti U, Thiene G, Casarotto D, Mazzucco A, Gallucci V. Left ventricular rupture followingmitral valve replacement with a Hancock bioprosthesis. Chest 1980; 46:721-34. 16. Thiene G, Bortolotti U, Casarotto D, Valfre C, Gallucci V. Prosthesis-left ventricle disproportion in mitral valve replacement with the Hancock bioprosthesis: pathologic observations. In: Sebening F, Klovekorn WP, Meisner H, Struck E, eds. Bioprosthetic cardiac valves. Irnmenstadt/
17.
18.
19.
20.
21.
22.
Algau, Federal Republic of Germany: Eberl GmbH, 1979:357-65. Schoen FJ, Schumann LJ, Cohn LH. Quantitative anatomic analysis of "stent creep" of explanted Hancock standard porcine bioprostheses used for cardiac valve replacement. Am J Cardiol 1985;56:110-4. Valente M, Bortolotti U, Thiene G, et al. Post bending of the polypropylene flexible stent in mitral Hancock bioprostheses. Eur J Cardiothorac Surg 1987;1:134-8. Jones EL, Craver JM, Morris DC, et al. Hemodynamic and clinical evaluation of the Hancock xenograft bioprosthesis for aortic valve replacement (with emphasis on the management of the small aortic root). J THORAC CARDlOVASC SURG 1978;75:300-8. Sanders SP, Levy RJ, Freed MD, Norwood WI, Castaneda AR. Use of Hancock porcine xenografts in children and adolescents. Am J Cardiol 1980;46:429-38. Bortolotti U, Milano A, Mazzucco A, et al. Pregnancy in patients with a porcine valve bioprosthesis. Am J Cardiol 1982;50:I 051-4. Riddle JM, Magilligan DJ, Stein PD. Surface morphology of degenerated porcine bioprosthetic valves four to seven years following implantation. J THORAC CARDIOVASC SURG 1981;81:279-87.
THORAC CARDIOVASC SURG
1989;97:415-20
The Hancock II porcine bioprosthesis A preliminary report From May 1983 to July 1987 a total of 153 Hancock II porcine bioprostheses have been implanted in 130 patients with a mean age of 59 ± 8 years (range 29 to 76 years). Mitral valve replacement was performed in 72 patients, aortic valve replacement in 35, and mitral-aortic valve replacement in 23. Cumulati"e foUow-up of 121 survivorsis 223 patient-years and 100% complete (range 0.4 to 4.5 years). The actuarial survival rate at 4 years is 88% ± 8% for mitral, 86% ± 7.8% for aortic, and 84% ± 8% for mitral-aortic valve replacement. Minor thomboembolism occurred in two patients (0.9% ± 0.6% jpt-yr) with an actuarial freedom from emboli at 4 years of 100% for mitral, 96% ± 3.7% for aortic, and 91 % ± 8.6% for mitral-aortic valve replacement. Anticoagulant-related hemorrhage occurred in 10 patients (4.4% ± 1.4%jpt-yr) with an actuarial freedom at 4 years of 90% ± 4.8% for mitral, 89 % ± 5.8 % for aortic, and 84 % ± 10.6 % for mitral-aortic valve replacement. Failure of the porcine bioprosthesis was observed in three patients with an actuarial freedom at 4 years of 96 % ± 3.6 % for aortic, 91 % ± 8 % for mitral, and 91 % ± 8.6 % for mitral-aortic valvereplacement. Actuarial freedom from all porcine bioprosthesis-related complieations at 4 years is 85.7% ± 6.6 % for aortic, 79 % ± 9 % for mitral, and 70 % ± 13 % for mitral-aortic valve replacement. No instances of primary tissue failure occurred. This preliminary experience justifies a cautious optimism on the performance and durability of the Hancock II porcine bioprosthesis, supporting our current trend to use it in a selected population until data on a longer foUow-up are available.
Uberto Bortolotti, MD, Aldo Milano, MD, Alessandro Mazzucco, MD, Francisco Guerra, MD, Alberto Magni, MD, Francesco Santini, MD, and Vincenzo Gallucci, MD, Padova, Italy
Since primary tissue failure is the factor that most commonly adversely affects the performance of the Hancock porcine bioprosthesis.l" some modifications of manufacturing and tissue processing techniques have been introduced in the standard model of this porcine bioprosthesis with the aim of delaying the onset of this complication and increasing the durability of the valve. These modifications have led to the development of a new porcine bioprosthesis, the Hancock IF (Hancock Extracorporeal Inc., Anaheim, Calif.), which is currently undergoing clinical testing. We report in this paper From the Department of Cardiovascular Surgery, University of Padova Medical School, Padova, Italy. This work was supported in part by Grant No. 87.00719.57 of the National Council of Research, Rome, Italy, Target Project "Biomedical Technology." Received for publication Jan. 26, 1988. Accepted for publication Sept. 2, 1988. Address for reprints: U. Bortolotti, MD, Istituto di Chirurgia Cardiavascolare, Universita di Padova, Via Giustiniani, 2, 35128 Padova, Italy.
our initial experience and preliminary results with this device. Patients and methods From May 1983 to July 1987, 153 Hancock II porcine bioprostheses were implanted in 130 patients, 69 men and 61 women, whose ages ranged from 29 to 76 years (mean 59 ± 8 years). Isolated aortic valve replacement (AVR) was performed in 35 patients, isolated mitral valve replacement (MVR) in 72, and combined mitral-aortic valve replacement (MAVR) in 23. Associated surgical procedures, mainly tricuspid valve annuloplasty and coronary artery bypass grafting, were performed in 24 patients (18.4%). The causes of valve disease and the incidence of previous operations are summarized in Table I. Preoperatively, eight patients were in New York Heart Association (NYHA) class IV, 115 in class III, and seven in class II; 87 were in atrial fibrillation, 42 in sinus rhythm, and one had a permanent pacemaker. Standard surgical techniques were used in all patients as reported elsewhere.v" After the operation all patients were given anticoagulants, which were usually suspended after 3 months; the major indication for indefinite anticoagulation in MVR and MA VR patients was the combination of atrial fibrillation, giant left atrium, and left atrial thrombosis. Definitions of prosthesis-related complications in porcine
415
The Journal of Thoracic and Cardiovascular Surgery
Bortolotti et al.
4I6
Fig. 1. Actuarial survival rates after MVR, AVR, and MA VR with the Hancock II porcine bioprosthesis. Numbers on the horizontal axis indicate the patients at risk; operative deaths are not included.
Table I. Causes of valvular disease and incidence of previous operations No. Cause Rheumatic Degenerative Endocarditis Congenital Unknown Failing prosthesis Total Previous operations Mitral valve repair Coarctectomy MVR AVR MAVR Total
69 31 2
1 1
-.1Q
%
53 24 1.6 0.7 0.7 20
Table II. Summary offollow-up data Current survivors Mean follow-up (yr) Minimum follow-up (yr) Maximum follow-up (yr) Cumulative follow-up (pt-yr)
MVR
AVR
MAVR
Total
64
30
17
111
2.1 ± 1.2 1.5 ± 0.8 1.5 ± 0.9 1.8 ± 1.0
0.6
0.4
0.4
0.6
4.5
3.3
4.2
4.5
141
50
32
223
130 15 I 17
5 _5 43
11.5 0.8 13.1 3.8
.....il. 33
valve recipients have been reported previously.v' Such complications were considered as porcine bioprosthesis failure when death or reoperation resulted and as overall porcine bioprosthesis-related complications regardless of the patient outcome. Patient survival and freedom from porcine bioprosthesisrelated complications are expressed in actuarial fashion excluding operative deaths and as linearized rates as percent per patient-year (%/pt-yr).
Results Hospital mortality and follow-up. There were nine operative deaths (7%), two after AVR (5.7%), five after MVR (7%), and two after MAVR (8.7%). A total of 121 patients discharged were observed from 0.4 to 4.5
years (mean 1.8 ± 1.0 years); cumulative duration of follow-up, ending in December 1987 and being 100% complete, is 223 patient-years (Table II). There were nine late deaths with a linearized incidence of 4.0% ± l.3%/pt-yr; three patients died after AVR, three after MVR, and three after MAVR. The causes of late death were heart failure in five patients; lo~ output syndrome at reoperation for paravalvular leak in one patient who had had MVR; cerebral anticoagulant-related hemorrhage in one patient after AVR, malignancy in one patient after MA VR, and unknown in one patient. The actuarial survival rates at 4 years are 88% ± 8% for MVR,86% ± 7.8% for AVR, and 84% ± 8 for MAVR patients (Fig. 1). Of the III current survivors, 10 are in NYHA class III, 74 in class II, and 27 in class I. Almost 50% of them are in atrial fibrillation, 40% are receiving long-term anticoagulant therapy, and 10% are receiving antiplatelet drugs. Porcine bioprosthesis-related complications. Porcine bioprosthesis-related complications occurred in 15
Volume 97 Number 3
Hancock II porcine bioprosthesis
March 1989
::::::i 100"~=--""""'' ' ----'' ---'' ' '--'' ' ~"'~~::J----o-----o-----!;:1
o
..
co
~
LL
o
~
100
I
-
80
•
4 17
MVR
o AVR
96±3.7
o
MAVR
91±8.6
w
W
0:::
LL
60
I
•
60
44
28
o
27
13
6
3
18
11
4
1
o
1
2
11
3
4
YEARS POSTOP Fig. 2. Actuarial freedom from thromboembolic episodes.
Table
m. Summary of postoperative complications MVR
Late deaths Embolic episodes Hemorrhage Endocarditis Paravalvular leak Primary tissue failure Porcine bioprosthesis-related complications
AVR
Total
MAVR
No.
%/pt-yr
No.
%/pt-yr
No.
%/pt-yr
3
2.1 ± 1.2
5 1 1
3.5 ± 1.5 0.7 ± 0.7 0.7 ± 0.7
3 1 3
6.0 ± 3.4 2.0 ± 2.0 6.0 ± 3.4
3 1 2
9.3 ± 5.4 3.1 ± 3.1 6.2 ± 4.4
10
3.1 ± 3.1
I 2
7
4.9 ± 1.8
12.5 ± 6.2
15
4
patients (6.7% ± 1.7%jpt-yr) and are summarized in Table III. Minor thromboembolic episodes occurred in two patients (0.9% ± 0.6%jpt-yr), 8 months after AVR and 16 months after MAVR, respectively; neither was receiving anticoagulants and both recovered without sequelae. Actuarial freedom from embolism at 4 years is 100% for MVR, 96% ± 3.7% for AVR, and 91% ± 8.6% for MAVR patients (Fig. 2). Anticoagulantrelated hemorrhage occurred in 10 patients (after MVR in five, after AVR in three, and after MAVR in two), after a mean interval of 10 ± 8 months, and was fatal in one patient. The linearized incidence of this complication is 4.4% ± 1.4%jpt-yr in the entire series and 12% ± 4.0%jpt-yr in patients receiving anticoagulants; actuarial freedom from anticoagulant-related hemorrhage at 4 years is 90% ± 4.8% for MVR, 89% ± 5.8% for AVR, and 84% ± 10.6% for MAVR (Fig. 3). Paravalvular leak occurred in two patients (0.9% ± 0.6%jpt-yr); one died of low output syndrome at reoperation 3 years, 4 months after MVR and another
8.0 ± 5.6
4
No. 9 2
%/pt-yr 4.0 0.9 4.4 0.4 0.9
± ± ± ± ±
1.3 0.6 1.4 0.4 0.6
6.7 ± 1.7
underwent successful mitral prosthetic replacement 1 year, 4 months after MAYR. Endocarditis was observed in one patient 2 months after MVR (0.4 ± O.4%jpt-yr), and the infection has apparently been cured by antibiotic therapy. Porcine bioprosthesis failure was observed in three patients: fatal anticoagulant-related hemorrhage in one and reoperation because of paravalvular leak in two. Actuarial freedom from porcine bioprosthesis failure at 4 years is 96% ± 3.6% for AVR, 91% ± 8% for MVR, and 91% ± 8.6% for MAVR patients (Fig. 4). Actuarial freedom from overall porcine bioprosthesis-related complications at 4 years is 85.7% ± 6.6% for AVR, 79% ± 9% for MVR, and 70% ± 13% for MAVR patients (Fig. 5). No instances of primary tissue failure have been observed during the follow-up period.
Discussion The standard Hancock valve has been the bioprosthesis of choice at our department over the past 15
The Journal of Thoracic and Cardiovascular Surgery
4 1 8 Bortolotti et al.
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years. 4, 6, 8 During this period the results of our clinical and pathologic experience," 6, 8-10 together with that of others.!-" 5.10-14 have contributed to clarify the major complications and disadvantages related to the use of this device. Among them are those related to (1) a disproportion between the high prosthetic profile and the left ventricular cavity": 16; (2) a permanent deformation ("creeping") of the polypropylene flexible frame with inward bending of the stent posts'<"; (3) a suboptimal hemodynamic performance in the small sizes because of a prominent muscular shelf on the right coronary CUSpI9; (4) a limited durability resulting from tissue calcification, which is progressive in most cases"
and accelerated in children and adolescents." in patients with chronic renal failure," and possibly during pregnancy," and whose onset is favored by poor tissue preservation. IO, 22 Because of these observations, in the Hancock II porcine bioprosthesis the stent is of lower profile and made of new material (Delrin) with better fatigue and tensile properties, tissue selection has been improved, low-pressure fixation has been introduced, and a calcium-retarding agent (water soluble C-12 alkyl sulfate, T6) has been added to tissue processing.' Since the Hancock II porcine bioprosthesis has been made available for clinical use only recently, the experi-
Volume 97 Number 3 March 1989
Hancock II porcine bioprosthesis 419
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ence with this device is obviously limited. Our results indicate that at short-term follow-up this device has a negligible thrombogenicity although almost 40% of the patients are receiving long-term anticoagulant therapy. These results may explain the high incidence of anticoagulant-related hemorrhage and again make anticoagulation in tissue valve recipients questionable. No instances of primary tissue failure were observed and only two patients required reoperation for paravalvular leak. It must be considered, however, that the Hancock II porcine bioprosthesis was never used in children or in patients with clear-cut risk factors for calcification and that the mean age of patients in this series is higher than that of patients receiving a standard Hancock porcine bioprosthesis at our institution.' Although a longer follow-up will be needed to verify the impact of the new manufacturing techniques on both durability and overall performance of this device, the results of this preliminary experience substantiate so far a cautious optimism. Our current trend is to employ any tissue valve in a patient population selected mainly on the basis of age (>55 years) and on peculiar situations." The use of the Hancock II porcine bioprosthesis might be expanded particularly when the role of the anticalcification treatment on valve durability will be better assessed.
2.
3.
4.
5.
6.
7.
8.
We express our gratitude to Gian Carlo Pengo for his skilled technical assistance.
9.
REFERENCES I. Oyer PE, Miller DC, Stinson EB, Reitz BA, MorenoCabral RJ, Shumway NE. Clinical durability of the
10.
Hancock porcine bioprosthesis. J THORAC CARDIOVASC SURG 1980;80:824-33. Borkon AM, McIntosh CL, Von Rueden TJ, Morrow AG. Mitral valve replacement with the Hancock bioprosthesis: five to ten year follow-up. Ann Thorac Surg 1981; 32:127-37. Cohn LH, Mudge GH, Pratter F, Collins JJ Jr. Five to eight year follow-up of patients undergoing porcine heart valve replacement. N Engl J Med 1981;304:258-62. Gallucci V, Bortolotti U, Milano A, et al. The Hancock porcine valve 15 years later: an analysis of 575 patients. In: Bodnar E, Yacoub M, eds. Biologic and bioprosthetic valves. New York: Yorke Medical Books, 1986:91-7. Gallo I, Ruiz B, Duran CG. Isolated mitral valve replacement with the Hancock porcine bioprosthesis in rheumatic heart disease: analysis of 213 operative survivors followed up 4.5 to 8.5 years. Am J Cardiol 1984; 53:178-81. Bortolotti U, Milano A, Mazzucco A, et al. Results of reoperation for primary tissue failure of porcine bioprostheses. J THORAC CARDIOVASC SURG 1985;90:564-9. Wright JTM, Eberhardt CE, Gibbs ML, Saul T, Gilpin CB. Hancock II: an improved bioprosthesis. In: Cohn LH, Gallucci V, eds. Cardiac bioprostheses, New York: Yorke Medical Books, 1982:424-44. Gallucci V, Bortolotti U, Milano A, Valfre C, Mazzucco A, Thiene G. Isolated mitral valve replacement with the Hancock bioprosthesis: a 13-year appraisal. Ann Thorac Surg 1984;38:571-8. Milano A, Bortolotti U, Talenti E, et al. Calcific degeneration as the main cause of porcine bioprosthetic failure. Am J Cardiol 1984;53:1066-70. Valente M, Bortolotti U, Thiene G: Ultrastructural substrates of dystrophic calcification in porcine bioprosthetic valve failure. Am J Pathol 1985;119:12-21.
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II. Spray TL, Roberts We. Structural changes in porcine xenografts used as substitute cardiac valves: gross and histological observations in 51 glutaraldehyde-preserved Hancock valves in 41 patients. Am J Cardiol 1977; 40:319-30. 12. Ferrans VJ, Boyce SW, Billingham ME, Jones M, Ishihara T, Roberts We. Calcific deposits in porcine bioprostheses: structure and pathogenesis. Am J Cardiol 1980;46:721-34. 13. Schoen FJ, Collins JJ, Cohn LH. Long-term failure rate and morphologic correlations in porcine bioprosthetic cardiac valves. Am J Cardiol 1983;51:957-64. 14. Gallo I, Ruiz B, Nistal F, Duran CMG. Degeneration in porcine bioprosthetic cardiac valves: incidence of primary tissue failures among 938 bioprostheses at risk. Am J Cardiol 1984;53:1061-5. 15. Bortolotti U, Thiene G, Casarotto D, Mazzucco A, Gallucci V. Left ventricular rupture followingmitral valve replacement with a Hancock bioprosthesis. Chest 1980; 46:721-34. 16. Thiene G, Bortolotti U, Casarotto D, Valfre C, Gallucci V. Prosthesis-left ventricle disproportion in mitral valve replacement with the Hancock bioprosthesis: pathologic observations. In: Sebening F, Klovekorn WP, Meisner H, Struck E, eds. Bioprosthetic cardiac valves. Irnmenstadt/
17.
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Algau, Federal Republic of Germany: Eberl GmbH, 1979:357-65. Schoen FJ, Schumann LJ, Cohn LH. Quantitative anatomic analysis of "stent creep" of explanted Hancock standard porcine bioprostheses used for cardiac valve replacement. Am J Cardiol 1985;56:110-4. Valente M, Bortolotti U, Thiene G, et al. Post bending of the polypropylene flexible stent in mitral Hancock bioprostheses. Eur J Cardiothorac Surg 1987;1:134-8. Jones EL, Craver JM, Morris DC, et al. Hemodynamic and clinical evaluation of the Hancock xenograft bioprosthesis for aortic valve replacement (with emphasis on the management of the small aortic root). J THORAC CARDlOVASC SURG 1978;75:300-8. Sanders SP, Levy RJ, Freed MD, Norwood WI, Castaneda AR. Use of Hancock porcine xenografts in children and adolescents. Am J Cardiol 1980;46:429-38. Bortolotti U, Milano A, Mazzucco A, et al. Pregnancy in patients with a porcine valve bioprosthesis. Am J Cardiol 1982;50:I 051-4. Riddle JM, Magilligan DJ, Stein PD. Surface morphology of degenerated porcine bioprosthetic valves four to seven years following implantation. J THORAC CARDIOVASC SURG 1981;81:279-87.