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Ann Thorac Surg 2006;81:1291-1296
© 2006 The Society of Thoracic Surgeons

Original article: Cardiovascular

Hemolysis in Mechanical Bileaflet Prostheses: Experience With the Bicarbon Valve

Miguel Josa, MD a , * , Manuel Castellá, MD a , Carles Paré, MD, PhD b , José L. Bedini, MD c , Ramón Cartañá, MD a , Carles A. Mestres, MD, PhD a , José L. Pomar, MD, PhD a , Jaume Mulet, MD, PhD a

a Cardiovascular Service, Hospital Clinic and University of Barcelona, Barcelona, Spain
b Cardiology Service, Hospital Clinic and University of Barcelona, Barcelona, Spain
c Clinical Chemistry Department, Hospital Clinic and University of Barcelona, Barcelona, Spain

Accepted for publication September 21, 2005.

* Address correspondence to Dr Josa, Hospital Clinic and University of Barcelona, Villarroel 170, Barcelona, 08036 Spain (Email: mjosa{at}clinic.ub.es).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
BACKGROUND: Normal functioning mechanical heart valve prostheses are designed to have a certain degree of intrinsic structural regurgitation as a washout mechanism to avoid prosthetic thrombosis. However, intrinsic regurgitation leads to blood cell trauma and hemolysis. Information on hemolysis associated with mechanical bileaflet prostheses is scarce. This study evaluated factors influencing hemolysis in 197 Bicarbon mechanical bileaflet prostheses implanted in 164 patients.

METHODS: Serial office interviews, laboratory studies, and echocardiography evaluations were done in the surviving patients. An assay for measuring lactate dehydrogenase activity was developed, and the presence and severity of subclinical hemolysis was determined using reported criteria and analyzed at 1 and 2 years.

RESULTS: Hospital mortality was 5.5%. Follow-up was 98.1% complete. No patient had clinically significant or severe subclinical hemolysis. Serum lactate dehydrogenase levels were significantly higher when a paravalvular leak was documented (282 ± 85 U/L versus 242 ± 64 U/L; p = 0.0026). Subclinical hemolysis was significantly more frequent after mitral valve (p = 0.001) and double valve replacement (p = 0.001) than after aortic valve replacement, and was unrelated to prosthetic size or to geometric area index, even in those cases with effective orifice area index equal to or less than 0.85 cm2/m2 (p = 0.298).

CONCLUSIONS: Mild subclinical hemolysis is frequently associated with normal functioning Bicarbon heart valves. Subclinical hemolysis was significantly influenced by valve position but not by valve size or effective orifice area index and remained stable through time. The magnitude of hemolysis in Bicarbon prostheses compared favorably with that reported for other bileaflet heart valve prostheses.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Normal function of mechanical prostheses is associated with small volume intrinsic regurgitation intended to provide a washout mechanism of the prosthesis hinges and leaflet coaptation. Absence of this mechanism of hinge washout could lead to prosthesis thrombosis. Transprosthetic blood flow and particularly the regurgitant fraction are associated with high shear stresses, which lead to damage of red blood cells and platelet activation and promote the presence of mild subclinical hemolysis and thrombotic phenomena [1, 2]. The design of mechanical prostheses should provide the best balance between efficient hemodynamic patterns and the potentially harmful effects of intrinsic regurgitation.

Since the clinical introduction of the St. Jude bileaflet prosthesis in 1977, bileaflet prostheses have been widely used in cardiac surgery, and different models are available for surgical use. Although their thrombogenic phenomena are well documented, clinical data on their intrinsic hemolytic behavior are scarce. The Bicarbon heart valve (Sorin Biomedica Cardio, Saluggia, Italy), was introduced in 1990 as a new pyrolytic carbon bileaflet prostheses that differs from other bileaflet prostheses mainly in its hinge design and in that the valve housing is made of a titanium alloy coated with a thin film of turbostratic carbon (Carbofilm) instead of solid pyrolytic carbon [3, 4]. The Bicarbon heart valve has shown excellent hemodynamic performance and low rates of complication, but information about hemolysis associated with this valve is scarce [5–8].

The purpose of this prospective study was to evaluate the degree of hemolysis associated with the Bicarbon prosthesis and the effect of different clinical factors that may influence hemolysis presence and severity in normal functioning bileaflet prostheses.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Patient Population
From May 1994 to January 1998 164 patients, 95 males, had 197 Bicarbon prostheses implanted. Mean age was 58.2 ± 10.0 years (range, 28 to 82 years). Fifty-three patients were in New York Heart Association functional class I or II, 102 were in class III or IV, and in 9 patients functional class was not recorded. Rheumatic heart disease and calcific degeneration of the aortic valve were the most common etiologic diagnoses (Table 1). Aortic valve replacement (AVR) was done in 74 patients (45.1%), mitral valve replacement (MVR) in 58 patients (35.3%), and aortic and mitral valve replacement (DVR) in 31 patients (18.9%). Triple valve replacement was done in only 1 patient. Coronary artery bypass grafting and tricuspid annuloplasty were the most frequently concomitant procedures (Table 2).


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  		Table 1. Etiologic Diagnosis of Valvular Disease in Operated On Patients
 

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  		Table 2. Concomitant Surgical Procedures
 
Anticoagulation was initiated in most cases on the second postoperative day with oral warfarin maintaining an international normalized ratio of 3 in AVR cases, and 3.5 to 4 in MVR and multiple valve replacement cases. Intravenous sodium heparin was used when oral warfarin could not temporarily be administered, maintaining an activated thromboplastin time around 40 seconds. All patients in whom a coronary artery bypass graft procedure was done were treated with lipid-reducing drugs.

Study Protocol
All patients had office interviews and examinations, laboratory testing, and echocardiographic studies done preoperatively and serially postoperatively with an end point follow-up at 1 and 3 years. Morbidity and mortality events were recorded and reported following the guidelines of The Society of Thoracic Surgeons and the American Association for Thoracic Surgery [9].

The clinical follow-up was extended up to 4.3 years, with a mean and cumulative values of 2.03 ± 0.96 years and 335 years, respectively. Nine patients (5.5%) died during hospitalization or during the first 30 days postoperatively. Three patients were lost to follow-up after 1 year (follow-up rate was 98.2% complete). Seven patients (4.5%) died late, but only one death was attributable to cardiac origin. None of the deaths were valve related. Three of them occurred before the end of the first year of follow-up and were excluded from the assessments of hemolysis. In 16 patients laboratory data were incomplete at 1 year. These patients were also excluded from hemolysis evaluation. A total of 128 patients (78% of the initial group: 62 AVR, 44 MVR, and 22 DVR) were examined at 1 year. Comparison of hemolysis degree in 85 patients with matched data at 1 and 2 years was performed.

Serum levels of lactate dehydrogenase (LDH) are considered the main variable to establish the presence of hemolysis and its degree. Hemolysis was evaluated following the criteria established by both Skoularigis and colleagues [10] and Horstkotte [11]. According to Skoularigis and coworkers [10], hemolysis is present if serum LDH, as major criteria, is above normal and two other minor criteria are present. Horstkotte's criteria [11] establish hemolysis severity based on the serum levels of LDH and haptoglobin (Table 3). Normal LDH values are different when measured by Horstkotte [11] (<220 U/L) than by Skoularigis and associates [10] (<450 U/L). This difference is attributable to measuring LDH at two different ends of a reversible enzymatic reaction: formation of lactate from pyruvate (L) or pyruvate from lactate (P), and it is usually converted using a 0.483 factor. However, indiscriminate use of a standard conversion factor is not advisable because assay conditions of analyzers and reagents are different. An assay was conducted in our center measuring LDH activity by both methods using serum samples of 100 healthy individuals, and the conversion formula (P = 0.464 L + 15) was applied when needed to analyze data by both criteria or to establish reliable comparisons with published data [12].


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  		Table 3. Criteria for Hemolysis
 
Transthoracic echocardiographic studies were performed by observers who were blind to the hematologic findings from each patient, using commercially available phased-array Doppler echocardiographic systems. Color-Doppler flow imaging was used to characterize intrinsic and perivalvular regurgitation. The presence of a slight trace of regurgitation was defined as mild prosthesis regurgitation even if considered secondary to normal prosthesis washout. The maximal instantaneous pressure gradient across the aortic valve was calculated using a modified Bernoulli equation [13]. Mean gradients were calculated by integrating the Doppler velocity signals. The effective orifice area (EOA) was calculated with the continuity equation [14]. The EOA index was calculated by normalizing the valve EOA with the patient's body surface area.

Statistical Analysis
Survival and adverse events incidence were statistically evaluated, at this point in time, by means of the Kaplan-Meier method. Comparison between continuous variables was performed using Student's t test (for paired or independent samples) or analysis of variance statistical methods. Lactate dehydrogenase values at 1 and 2 years have been compared adopting a linear regression statistical model.

Clinical correlations were established at 1 year for presence and degree of hemolysis versus prosthesis position, size, geometric orifice area, and EOA index. Degree of hemolysis was also compared for the group of patients with mild prosthesis regurgitation versus the group with no echocardiographic evidence of regurgitant flows. Statistical analysis was conducted using SPSS 10.0 statistical software package (Chicago, IL). Statistical p values equal or less than 0.05 were considered significant.

All patients were informed on all the clinical evaluations being done and signed a consent form for the operation. As routine standard procedures were done no institutional review board was required.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
No cases of structural valve failure were documented during follow-up. Four patients had documented thromboembolic episodes, with permanent neurologic deficits in 3 of them (1 AVR, 1 MVR, and 2 DVR; overall freedom from embolic events was 95.3% ± 2.85%). Three of these patients had previous history of thromboembolism, and 2 had documented suboptimal anticoagulation at the time the event occurred. Six patients experienced bleeding events, but none required blood transfusion and all of them recovered uneventfully (overall freedom from bleeding events was 95.8% ± 1.7%). Four patients experienced bacterial endocarditis (overall freedom from endocarditis was 93.5% ± 4.5%), and there was only one instance of valve thrombosis (overall freedom from valve thrombosis was 99.3% ± 0.7%). During follow-up 1 patient experienced iron deficiency anemia secondary to malignant renal disease. Five patients were reoperated on; 3 of them had bacterial endocarditis, 1 had acute valve thrombosis, and 1 patient had paravalvular leak repair (overall freedom from reoperation was 95.4% ± 2.3%).

At 1 year 27 (21.0%) of the 128 evaluated patients had evidence of subclinical hemolysis according to the criteria of Skoularigis and associates [10]: 8.1% (5 of 62) of the AVR patients, 25.0% (11 of 44) of MVR, and 50.0% (11 of 22) of DVR. According to Horstkotte's criteria [11], subclinical hemolysis was found in 62.5% (80 of 128) of patients. The subclinical hemolysis was mild in 59.4% (76 of 128) of patients, and it was more frequent after MVR (79.5%, 35 of 44) and DVR (68.2%, 15 of 22) than after AVR (41.9%, 26 of 62). Moderate hemolysis was only detected in 4 patients, and all of them underwent DVR.

Detectable or trivial prosthetic intrinsic regurgitant leaks by echocardiography were observed in 102 of 128 patients. Paravalvular leaks were mild in 25 patients (13 AVR, 5 MVR, and 7 DVR) and moderate in 1 DVR. Serum LDH was significantly higher when a regurgitant paravalvular leak of any size was detected (282 ± 85 U/L versus 248 ± 64 U/L; p = 0.026). Because some intrinsic prosthetic leaks could have been identified as mild paravalvular leaks by echocardiography, the echocardiograms of the patients with mild paravalvular leaks were reevaluated and relabeled as having intrinsic paravalvular leak. However, to clarify the issue we compared the severity of hemolysis between patients having no detectable leaks and those having leaks labeled as trace or mild. There was no significant difference in LDH levels between patients with mild paravalvular leaks and those without leaks (249 ± 57 U/L versus 219 ± 42 U/L; p = 0.095)

No difference was found in age in AVR patients with and without subclinical hemolysis (58 ± 14 versus 59 ± 16 years; p = 0.4782), indicating that age did not influence serum LDH levels in these patients. Lactate dehydrogenase levels were similar in AVR patients and in those with AVR and coronary artery bypass grafts ({chi}2 = 0.4542), suggesting that LDH was not influenced by the presence of coronary artery disease or lipid-reducing therapy.

Serum LDH levels were significantly higher after MVR than after AVR and were highest after DVR (Fig 1). In contrast, serum LDH levels were not influenced by prosthetic size (Fig 2).


Figure 1
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  		Fig 1. Mean serum lactate dehydrogenase (LDH) levels at 1 year after surgery. (AVR = aortic valve replacement; DVR = double valve replacement; MVR = mitral valve replacement.)

 

Figure 2
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  		Fig 2. Mean serum lactate dehydrogenase (LDH) levels at 1 year after surgery grouped by size in each valve position. There was no significant difference in serum lactate dehydrogenase levels related to different valve sizes or large-size groups versus small-size groups. For sizes 25 and 27 serum lactate dehydrogenase levels were higher for the mitral prostheses, but the difference was not significant. (AVR = aortic valve replacement; MVR = mitral valve replacement.)

 
Serum LDH levels had a poor correlation with the geometric orifice area reported by the manufacturer (r = 0.16 for aortic prostheses; r = 0.12 for mitral prostheses). The influence of the EOA was further analyzed by studying the effect of prosthesis size mismatch in patients with normal functioning aortic prostheses, comparing the group of patients with an EOA index less than 0.85 cm2/m2 (n = 22) with those with an EOA index greater than or equal to 0.85 cm2/m2 (n = 20). Mean (14.3 ± 5.5 mm Hg versus 9.5 ± 3.1 mm Hg; p < 0.001) and peak (24.2 ± 8.7 mm Hg versus 14.7 ± 4.8 mm Hg; p < 0.001) prosthetic gradients at 1-year follow-up were significantly higher in the patients with an EOA index less than 0.85 cm2/m2. However, serum LDH levels were similar in both groups (211 ± 39 U/L versus 224 ± 41 U/L; p < 0.298).

The evolution of hemolysis with time was evaluated by comparing the 1- and 2-year follow-up data of 85 patients (66.4% of the total) who had complete laboratory studies obtained at both points in time. Lactate dehydrogenase levels were similar at the different follow-up times with good correlation between the values matched for each patient (r = 0.70; Fig 3).


Figure 3
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  		Fig 3. Degree of correlation between serum lactate dehydrogenase (LDH) matched for each patient at 1 and 2 years. Implant site: {circ} = AVR; {blacktriangleup} = MVR; {blacktriangledown} = DVR. (AVR = aortic valve replacement; DVR = double valve replacement; MVR = mitral valve replacement.)

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
Since the clinical introduction of the St. Jude valve in 1977 and the publication of the excellent results of performance of bileaflet valves [15, 16], these prostheses have become the mechanical heart valve substitute of choice for many surgeons. However, design of this new generation of valve prostheses has not eliminated the problem of flow separation and stagnation and high degree of turbulent shear stresses associated with potential damage to blood elements, particularly to red blood cells and platelet activation [17].

Prosthesis regurgitation, particularly regurgitation after valve closure, has been associated with high-velocity jets and severe turbulent stresses, which create damage to blood elements. Red blood cell destruction and platelet damage and activation lead to hemolysis and thrombotic phenomena [17, 18]. Regurgitant stresses are more severe in the mitral position than in the aortic position. Forward turbulent flow and cavitation phenomena have also been associated with hemolysis [19]. Our data show a greater degree of blood damage in the presence of a mitral valve, with serum LDH levels significantly higher in patients with MVR or DVR than in those with AVR. In contrast, neither valve size nor the indexed EOA influenced hemolysis. This was true even in those patients in whom a prosthesis-to-body surface area mismatch was present. These findings are consistent with those of other investigators and are similar to results with other bileaflet and disc prostheses [10, 20].

Although some cases of severe clinical hemolysis have been reported with normal functioning St. Jude valves (St. Jude Medical Inc, Minneapolis, MN) in the absence of paravalvular leaks [21, 22], clinically significant hemolysis is almost always associated with the presence of detectable paravalvular leaks [11]. In our study no cases of clinically significant hemolysis were detected even in presence of paravalvular leaks. Flow patterns and identification of regurgitant valve leaks can be readily done with transesophageal echocardiography. However, differentiation of trivial intrinsic valve leaks from mild paravalvular leaks may be difficult with regular transthoracic echocardiography [6, 23]. Our data indicate that the degree of subclinical hemolysis in patients with normal functioning valves was similar to those in whom a mild paravalvular leak was detected, suggesting that some intrinsic trivial leaks related to regular hinge washout could have been labeled as mild paravalvular regurgitation by echocardiography.

Subclinical hemolysis is rarely severe and seems to be more frequent in patients with bileaflet valves than in those with tilting disc valves [10, 11, 24]. Our study shows that although subclinical hemolysis is frequently associated with normal functioning Bicarbon prostheses, its incidence and severity compares favorably with reports of hemolysis in other bileaflet prostheses [10, 11]. In fact, Bicarbon valve-associated hemolysis is of a similar magnitude as that reported for disc valves [10], indicating a low degree of prosthesis-related red blood cell trauma. This is consistent with the in vitro studies performed by Steegers and colleagues [2], in which blood damage index and hemolysis associated with the Bicarbon prosthesis was lower than that observed with other bileaflet prostheses.

Modern designs of mechanical valves are associated with improved performance and lower incidence of complications than older ones. However, aside from major complications, prosthetic blood flow dynamics may have deleterious effects not evident clinically. Blood flow through mechanical valves damages red blood cells and activates platelets. It can be postulated that subclinical hemolysis is also an indicator of the degree of latent platelet damage and activation and potential for valve thrombotic phenomena, and should be given a strong consideration in the evaluation of the performance of any heart valve prosthesis. Only 1 patient in this study experienced acute valve thrombosis and 3 more had thromboembolic phenomena. These patients had suboptimal anticoagulation levels at the time the episodes were detected and had many risk factors for these complications. We can speculate that the infrequent thrombotic and thromboembolic phenomena observed could be related to the low degree of blood element damage associated with the Bicarbon valve prosthesis.

The clinical performance of the Bicarbon prosthesis does not show increased rates of thrombotic phenomena [5]. We do not have information about the structural integrity of the prostheses or their carbon coating in the patients in our series. However the rate of hemolysis associated with the Bicarbon prosthesis has been low in our patients, and acute valve thrombosis developed in only 1 patient. Furthermore, valve-related subclinical hemolysis at the end of the first year remained the same in the second year of follow-up, suggesting stability with time. This good valve performance does not support the postulate of accelerated damage to blood elements secondary to carbon coating wear.

A limitation of this study is that it does not compare hemolysis between different prostheses. Previous studies suggested a lower incidence of hemolysis of Bicarbon mechanical valves when compared with other prosthetic valves [25]. We elected to focus on only one model to avoid small number subgrouping and eliminate difficult variable comparisons between designs of different models.

In summary, mild subclinical hemolysis occurred frequently in association with normal functioning Bicarbon heart valves. However, the magnitude of hemolysis compared favorably with hemolysis reported in association with other bileaflet prostheses and was similar to that of disc mechanical prostheses. Hemolysis was influenced by valve position but not by valve size or valve EOA index and remained stable with time.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Ellis JT, Wick TM, Yoganathan AP. Prosthesis-induced hemolysismechanisms and quantification of shear stress. J Heart Valve Dis 1998;7:376-386.[Medline]
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  21. Okita Y, Shigehito M, Kusuhara K, et al. Intractable hemolysis caused by perivalvular leakage following mitral valve replacement with the St. Jude Medical prosthesis Ann Thorac Surg 1988;46:89-92.[Abstract]
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