The fate of Hancock II porcine valve recipients 25 years after implant.

OBJECTIVE: The Hancock II (HII) is a second-generation porcine bioprosthesis introduced into clinical use in 1982. This study aimed to evaluate very long-term outcomes for the HII valve in a large patient population. METHODS: Between May 1983 and November 1993, 517 consecutive patients (pts) (309 male, mean age: 64+/-9 years) underwent valve replacement (VR) surgery with HII, with 302 (58.4%) in the aortic VR (AVR) and 215 (41.6%) in the mitral VR (MVR) position, respectively. At implant, 106 pts (20.5%) were <60 years of age (G1), while 411 (79.5%) were > or =60 years of age (G2). The 25-year follow-up was complete for all pts at a median of 12 years (range: 0-25). RESULTS: Long-term death occurred in 208 AVR and in 165 MVR pts. Survival at 15 and 20 years was 39.5% and 23.3% in AVR pts and 39.0% and 15.8% in MVR pts. At 25 years the survival of MVR pts was 13.7% (four pts at risk). Late freedom from re-operation was 85.5% and 79.3% at 15 and 20 years in the AVR pts and 73.3% and 52.8% in the MVR pts, respectively. In the AVR population, 20-year freedom from re-operation was 52.2% in G1 pts and 86.8% in G2 pts (p<0.0001), while in the MVR population it was 41.4% in G1 pts and 61.9% in G2 pts (p=0.201), respectively. CONCLUSIONS: These results confirm the excellent long-term performance of the HII bioprosthesis.

Clinical results of Hancock II versus Hancock Standard at long-term follow-up.

OBJECTIVE: We performed a multi-institutional study to compare the long-term structural valve deterioration of isolated Hancock Standard versus Hancock II bioprostheses. METHODS: From 1983 to 2002, 714 Hancock Standard and 1293 Hancock II bioprostheses were implanted at hospitals of the Venetian territory (Padova, Treviso, and Venice). Follow-up on January 1, 2003, included 14,749 patient-years with a median of 12 years and was 96% complete: 115 Hancock Standard and 53 Hancock II bioprostheses were at risk at 15 years. The 2 series were nonconcomitant, and many covariates differed (Table 1). Survival was analyzed with Cox analysis, and durability was analyzed with Weibull analysis. Balancing analysis with the logistic propensity score model was performed. RESULTS: Perioperative mortality was 6% in Hancock II and 12% in Hancock Standard operations. The overall unadjusted 15-year survival was identical (39.7% +/- 2.3% vs 39.9% +/- 2.4%, respectively), but age-adjusted survival at 15 years was 46% versus 25% (P < .001). Late survival was unrelated to the prosthetic model, whereas it was adversely affected by older age, previous operations, aortic regurgitation, male sex, higher New York Heart Association class, atrial fibrillation, and coronary artery bypass grafting. In Hancock II patients aged 65 years and older, the cumulative hazard of structural valve deterioration at 15 years was 6%, versus 17.5% in Hancock Standard patients. In younger patients, it was 18% and 37%, respectively. Analysis of 541 propensity-balanced patients showed a hazard ratio of the Hancock Standard prosthesis of 2 and a risk reduction of older age of approximately 10% every 10 years. CONCLUSION: After balancing risk factors and calibrating age effects, Hancock II propensity-matched bioprostheses showed similar survival but definitely increased durability.

Fifteen-year results with the Hancock II valve: a multicenter experience.

OBJECTIVES: The purpose of this multi-institutional study was to review the 15-year outcome of patients who received isolated aortic or mitral valve replacement with the Hancock II bioprosthesis. METHODS: From 1983 through 2002, 1274 patients underwent 1293 isolated valve replacements, 809 aortic valve replacements and 484 mitral valve replacements, at hospitals in the Venetian area (Padova, Treviso, and Venice). Mean age was 68 +/- 8 years in patients undergoing aortic valve replacement and 66 +/- 9 years in patients undergoing mitral valve replacement; 52% of patients undergoing aortic valve replacement and 63% of patients undergoing mitral valve replacement were in New York Heart Association class III or greater. Coronary artery disease was present in 32% of patients who had undergone aortic valve replacement and 18% of patients who had undergone mitral valve replacement. Follow-up included 8520 patient-years, with a median of 12 years, and was 97% complete. RESULTS: Overall 15-year survival was 39.7% +/- 2.4%, similar in both the aortic and mitral positions. Multivariable analysis of late survival showed the incremental risk of male sex, higher New York Heart Association class, coronary artery disease, and mitral position. Freedom from embolism was higher in the aortic position (81% +/- 2.9% in aortic vs 72% +/- 4.7% in mitral valve replacements). Freedom from endocarditis was similar in the aortic and mitral position (95% +/- 1.2% vs 94% +/- 1.7%). Freedom from reoperation (82% +/- 3.7% vs 71% +/- 5.0%) and from valve-related morbidity-mortality (52% +/- 3.6% vs 36% +/- 4.4%) was higher in patients who had undergone AVR. Actual freedom from structural valve deterioration for patients 60 years and older who had undergone aortic valve replacement was 96.5% +/- 1.3% versus 88% +/- 3.2% for patients who had undergone mitral valve replacement and 70% +/- 7.5% versus 77.5% +/- 5.3%, respectively, in younger patients. Multivariable Weibull analysis showed structural valve deterioration related to younger age and preoperative valve incompetence and inversely related to coronary artery disease. CONCLUSION: Optimal 15-year durability can be expected in male patients 60 years and older who have undergone aortic valve replacement and in male patients 65 years and older who have undergone mitral valve replacement, extending safely the age limits for the use of this valve.

Ten-year experience with cryopreserved aortic allografts in the surgical treatment of aortic valve pathologies.

BACKGROUND: The aim of this study was to evaluate the performance of cryopreserved aortic allografts (CAA) in the treatment of adult aortic valve pathologies. METHODS: Between May 1992 and October 2002, 122 CAA were implanted in 119 adult patients with pathologies of the aortic valve. The mean age of the patients was 38.03 +/- 13.6 years (range 17-78 years). Thirty had had previous cardiac surgery. The principal indication was endocarditis (n = 45). In 66 patients one or more associated pathologies were present including: an abscess of the left ventricular outflow tract (n = 32), an aneurysm of the ascending aorta (n = 22), mitral incompetence (n = 10), and coronary artery disease (n = 3). The indications for surgery were elective in 77 cases and urgent in 45. The CAA was implanted as a total root replacement in 46 patients and as a free-hand in 76. In 66 patients an associated procedure such as a left ventricular outflow tract reconstruction (in 27 cases) was performed. RESULTS: The in-hospital mortality was 5.73% (7/122). In one patient the CAA was replaced before discharge with another CAA because of a mediastinitis with endocarditis by Candida albicans. At the follow-up of the 114 patients discharged from the hospital (mean 50.11 months, range 1-126 months), 6 patients died and 6 were reoperated. The actuarial 10-year survival, reoperation-free, endocarditis-free, structural degeneration-free rates were respectively 83.88, 81.70, 86.30, and 92.80%. CONCLUSIONS: From our experience we conclude that CAA are good substitutes for aortic valve replacement and even in desperate situations exhibit an acceptable long-term performance.

Hancock II bioprosthesis: a glance at the microscope in mid-long-term explants.

BACKGROUND AND OBJECTIVES: The Hancock II bioprosthesis is a second-generation porcine valve xenograft treated with the detergent sodium dodecyl sulphate (T6) to retard calcification. The aim of this investigation was to study the gross and microscopic features in Hancock II explants to assess the structural changes occurring with time. METHODS: Among 1382 Hancock II bioprostheses (701 isolated aortic, 421 isolated mitral, 130 double) implanted from 1983 to 1997 in 1252 patients, 22 (16 mitral, 6 aortic) were removed at reoperation until 1999 and were available for pathological investigation: infective endocarditis occurred in 5 and structural deterioration in 8, whereas in the remaining 9 xenografts reoperation was performed for nonstructural valve deterioration (paravalvular leak in 4 and prophylactic replacement in 5). Morphological investigation consisted of gross examination and x-ray, histologic, immunohistochemistry, electron microscopic, and atomic absorption spectroscopic examination. RESULTS: The cause of structural valve deterioration was dystrophic calcification in 4 cases (1 aortic, 3 mitral; range of time graft was in place, 101 to 144 months), non-calcium-related tears in 3 cases (all mitral, range 121 to 163 months), and commissural dehiscence in 1 (aortic, range 156 months). Five of the nonstructural valve deterioration explants (range 42 to 122 months) showed only pinpoint mineralization at the commissures. Mean calcium content in nonstructural deterioration explants was 14.70 +/- 22.33 versus 99.11 +/- 81.52 mg/g in explants with structural valve deterioration. Electron microscopic examination showed early nuclei of mineralization mostly consisting of calcospherulae upon cell debris. Local or diffuse lipid insudation was observed in all but 2 explants and consisted of cholesterol clefts, lipid droplets, and lipid-laden macrophages featuring foam cells. The lipid insudation was the most plausible cause of tearing in 2 explants. CONCLUSIONS: These pathologic findings support the clinical results of a delayed occurrence of structural failure of Hancock II bioprostheses and a mitigation of mineralization by the anti-calcification treatment. However, other factors such as lipid insudation may come into play in the long term.

[Acute dysfunction of Liotta mitral bioprosthesis 8 years after implantation]. / Disfunzione acuta di una bioprotesi liotta in sede mitralica a otto anni dall'impianto.

The low-profile porcine bioprosthesis Liotta was introduced in clinical practice in order to reduce the potential complications related to excessive protrusion of the stent into the left ventricle after mitral valve replacement. Otherwise the particular design of this device seems to determine an excessive stress at the commissural level. We describe a case of acute dysfunction of the Liotta bioprosthesis secondary to commissural tear associated with minimal calcifications that required a reoperation in emergency.