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J Thorac Cardiovasc Surg 2002;124:146-154
© 2002 The American Association for Thoracic Surgery


Surgery for Acquired Cardiovascular Disease (ACD)

Late hemodynamic and clinical outcomes of aortic valve replacement with the Carpentier-Edwards Perimount pericardial bioprosthesis

Göran Dellgren, MD, Tirone E. David, MD, Ehud Raanani, MD, Susan Armstrong, MSc, Joan Ivanov, MSc, Harry Rakowski, MD

From the Division of Cardiovascular Surgery of Toronto General Hospital and the University of Toronto, Toronto, Ontario, Canada.
The Karolinska Institute and the Swedish Institute provided financial support for Dr Dellgren.

Received for publication Aug 28, 2001. Revisions requested Sept 28, 2001; revisions received Oct 22, 2001. Accepted for publication Nov 1, 2001. Address for reprints: Tirone E. David, MD, Division of Cardiovascular Surgery, Toronto General Hospital, 200 Elizabeth St, EN 13-222, Toronto, Ontario M5N 2C4 Canada (E-mail: tirone.david{at}uhn.on.ca).


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 
Objectives: The aim of this study was to investigate the long-term clinical and hemodynamic outcomes after aortic valve replacement with the Carpentier-Edwards Perimount bioprosthesis (Edwards Lifesciences, Irvine, Calif), which has been used in our institution since 1984.
Methods: From January 1984 to December 1995, the Carpentier-Edwards pericardial bioprosthesis was used for aortic valve replacement in 254 patients (male/female ratio 117:137) with a mean age of 71 years (range 25-87 years). Before the operation, 216 patients (85%) were in New York Heart Association functional class III or IV. The predominant diagnosis was aortic stenosis (n = 219, 86%). Associated surgical procedures included coronary artery bypass grafting in 130 cases (51%), mitral valve replacement in 11 cases (4%), and tricuspid or mitral valve repair in 12 cases (5%). Previous cardiac operations had been performed in 36 cases (14%). Follow-up was 100% complete at a mean of 60 ± 31 months. Univariate estimates of time-related cumulative probabilities were calculated by the Kaplan-Meier method. Multivariable adjustment was performed by Cox proportional hazards regression. Echocardiography was performed in 61% of long-term survivors.
Results: There were 11 early deaths (4%) and 58 late deaths. Actuarial survivals at 5, 10, and 12 years were 80% ± 3%, 50% ± 8%, and 36% ± 9%, respectively. At 12 years the freedom from cardiac death was 73% ± 7%, the freedom from valve-related death was 84% ± 11%, the freedom from valve reoperation was 83% ± 9%, the freedom from primary tissue failure was 86% ± 9%, the freedom from thromboembolism was 67% ± 13%, and the freedom from endocarditis was 98% ± 1%. Echocardiography was performed on long-term survivors (mean follow-up 67 ± 25 months) and showed that transvalvular peak and mean pressure differences measured with Doppler echocardiography were 23.2 ± 9.6 and 12.3 ± 4.8 mm Hg, respectively. Aortic regurgitation was found by Doppler echocardiography to be none or trivial, mild, moderate, and severe in 64%, 30%, 3%, and 1% of patients, respectively. Mean left ventricular mass index was 107.2 ± 35.3 g/m2 (118.9 ± 40.2 g/m2 in men and 98.8 ± 28.8 g/m2 in women) at late follow-up. One third of all patients, regardless of sex (n = 26/64 women and n = 14/45 men), had evidence of left ventricular hypertrophy. However, our analyses indicate that the residual left ventricular hypertrophy was not caused by valve mismatch but was probably multifactorial.
Conclusion: The Carpentier-Edwards Perimount bioprosthesis has provided satisfactory clinical and hemodynamic outcome. However, at long-term follow-up about one third of the patients being investigated still had left ventricular hypertrophy examined by echocardiography.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 
The Carpentier-Edwards Perimount (CEP) bioprosthesis (Edwards Lifesciences, Irvine, Calif) has been in clinical use since 1980 in Canada. We began using it in 1984. The long-term clinical results have previously been reported to be excellent, and this valve is regarded the bioprosthesis of choice by many surgeons.Go Go 1-4 This study reviews our experience with the CEP bioprosthesis and also examines its late hemodynamic performance.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 
Patients
From January 1984 to December 1995 the CEP pericardial bioprosthesis (model 2900; Edwards Lifesciences, Irvine, Calif) was used for aortic valve replacement (AVR) in 254 patients with a mean age of 71 years (range 25-87 years). The clinical profile and the operative data of these patients are summarized in Tables 1 and 2, respectively.


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Table 1. Clinical characteristics
 

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Table 2. Operative data
 
From 1984 to 1989, all patients undergoing valve replacement with the CEP were discharged from the hospital with a regimen of daily warfarin sodium for the first 3 months after the operation, followed by lifelong aspirin therapy. This practice was changed in 1990, after which patients were discharged with a regimen of lifelong aspirin therapy only, with the exception of those in need of warfarin sodium for other indications, such as chronic atrial fibrillation or a concomitant mitral valve procedure.

Operative survivors were followed up by telephone or questionnaire between October 1998 and January 1999. The follow-up was 100% complete. The mean follow-up was 60 ± 31 months (range 1-167 months), and 1214 patient-years of follow-up were available for analysis.

Doppler echocardiography
Transthoracic echocardiography with continuous-wave, pulsed-wave, and color flow Doppler studies were performed with a Hewlett Packard 1000, 1500, 2500, or 5500 Ultrasonoscope (Hewlett-Packard Company, Palo Alto, Calif) equipped with a 2.5-MHz transducer. Sixty-one percent of survivors (n = 109/178) had an echocardiogram performed at our hospital between December 1998 and May 1999. The mean follow-up for these studies was 67 ± 25 months (range 7-172 months). Those patients who did not undergo echocardiography either lived too far away from the hospital or were too old and in too fragile a condition to come without great difficulty.

For further details about measurements and calculations, see the Appendix. Left ventricular hypertrophy (LVH) was defined as a left ventricular mass index (LVMI) higher than 131 g/m2 for men and higher than 100 g/m2 for women.Go 5

Definitions and statistics
This report was based on the guidelines for reporting morbidity and mortality after cardiac valvular operations.Go 6 Survival and time-related event analyses were performed with the Kaplan-Meier method. Multivariable analyses of risk factors for survival and time-related events were done by Cox regression methods previously described. The term actuarial survival was used to describe time-related analysis for that event and not to describe the type of analysis performed. Differences were tested for statistical significance with 1-way analysis of variance. When the F test revealed a significant difference, each pair of means was compared with the Scheffé test.


    Results
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 
Patient survival
There were 11 operative deaths (4%). Eight of the 11 patients (73%) had undergone combined AVR and coronary artery bypass grafting. There were 58 late deaths (23%). Thirty-five of the 58 patients (60%) had undergone combined AVR and coronary artery bypass grafting. Operative mortality and morbidity and late mortality are shown in Table 3. The actuarial survival is shown in Figure 1. Multivariate analysis showed that preoperative New York Heart Association (NYHA) functional class III or IV (odds ratio 1.49, 95% confidence interval 1.02-2.18, P = .04) and the presence of coronary artery disease (odds ratio 2.08, confidence interval 1.26-3.44, P = .004) were independent risk factors for late death.


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Table 3. Operative morbidity and mortality and late mortality
 


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Fig. 1. Actuarial survival. Data points represent mean; error bars represent SEM.

 
Valve-related and cardiac-related deaths
The actuarial freedoms from valve-related death at 5, 10, and 12 years were 98% ± 1%, 96% ± 2%, and 84% ± 11%, respectively. The actuarial freedoms from cardiac death at 5, 10, and 12 years were 87% ± 2%, 73% ± 7%, and 73% ± 7%, respectively.

Complications
Thromboembolism
Thromboembolic events were observed in 17 cases (14 strokes and 3 transient ischemic attacks). The freedoms from thromboembolism at 5, 10, and 12 years were 93% ± 2%, 88% ± 3%, and 67% ± 13%, respectively. The linearized rate for thromboembolic events was 1.4% ± 0.1% events/100 patient-years. At the last follow-up 38 of 178 patients (21%) were taking warfarin sodium and 140 (79%) were taking aspirin daily. Multivariate analysis showed that age (odds ratio 1.11, 95% confidence interval 1.02-1.20, P = .01) was an independent risk factor for thromboembolism.

Structural valve dysfunction
Structural valve deterioration occurred in 4 patients, and they were reoperated on after 8, 9, 9, and 13 years of follow-up. All 4 patients had cusp tears: 2 had commissural tears and 2 had midcusp tears. In addition, 3 patients had calcification of the cusps. The actuarial freedoms from structural valve dysfunction at 5, 10, and 12 years were 100%, 86% ± 9%, and 86% ± 9%, respectively (Figure 2). The actual freedoms from structural valve dysfunction at the corresponding intervals were 100%, 92% ± 6%, and 92% ± 6%, respectively (Figure 2Go). There were no valve failures in patients older than 65 years.



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Fig. 2. Actuarial (circles) and actual (squares) freedoms from structural valve degeneration (SVD).

 
Bioprosthetic valve endocarditis
Five patients had bioprosthetic valve endocarditis that was diagnosed at 22 days, 4 months, 6 months, 3 years, and 3.5 years after the operation. Two patients were treated with antibiotics and replacement of the bioprosthesis, after which both survived. Three patients were treated with antibiotics alone; 1 survived and 2 died. The patient who survived after treatment with antibiotics alone had only mild aortic regurgitation on echocardiography at follow-up. The actuarial freedoms from bioprosthetic valve endocarditis at 5, 10, and 12 years were 98% ± 1%, 98% ± 1%, and 98% ± 1%, respectively.

Reoperations
Six patients underwent reoperation, and all survived. The indications for reoperation were structural valve deterioration in 4 cases and endocarditis in 2 cases. The actuarial freedoms from reoperation at 5, 10, and 12 years were 99% ± 1%, 83% ± 9%, and 83% ± 9%, respectively.

Other complications
Only 1 patient had a serious anticoagulant-related hemorrhage, even though 21% of the patients were receiving oral anticoagulation. Four patients needed late pacemaker implantation. Eight patients had a late acute myocardial infarction.

Late functional classification
At the latest follow-up 178 patients were alive and had the original CEP bioprosthesis in place. Seventy-two patients (41%) were in NYHA functional class I, 63 (35.5%) were in class II, 41 (23%) were in class III, and 1 (0.5%) was in class IV.

Echocardiography
Echocardiography of long-term survivors (mean 67 ± 25 months) showed that peak and mean gradients for all valve sizes were 23.2 ± 9.6 mm Hg (range 11-66 mm Hg) and 12.3 ± 4.8 mm Hg (range 5-31 mm Hg), respectively. Table 4 shows Doppler-echocardiographic data according to valve sizes at late follow-up. Smaller valves had statistically significantly higher transvalvular peak (P = .02) and mean (P = .003) gradients than did larger valves. Mean aortic valve area for all valves was 1.3 ± 0.3 (range 0.5-2.36 cm2), and area increased significantly with increasing valve size (P = .0001). Also, aortic valve areas were significantly larger in 27-, 25-, and 23-mm valves than in 19- and 21-mm valves (Table 4Go). However, 22 patients (20%) had an aortic valve area smaller than 1 cm2 at late follow-up.


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Table 4. Doppler echocardiographic results of CEP aortic valve bioprosthesis according to valve size at follow-up
 
M-mode Doppler measurements and calculations of left ventricular mass and LVMI are shown in Table 5. In a general linear model there were significant increases in left ventricular end-diastolic dimension (P = .03) and interventricular septum (P = .04) with increasing valve size. However, there was no significant difference in posterior wall measurement (P = .42) with increasing valve size. The only statistically significant difference seen between valve sizes was that left ventricular end-diastolic dimension was increased in patients with 25-mm valves relative to those with 21-mm valves (Table 5Go). Mean left ventricular mass and LVMI were 189.0 ± 70.5 g (range 90-518 g) and 107.2 ± 35.3 g/m2 (range 53-245 g/m2, male 118.9 ± 40.2 g/m2, female 98.8 ± 28.8 g/m2), respectively. Left ventricular mass and LVMI increased statistically significantly with increasing valve size (P = .0001 and P = .01, respectively). Body surface area also increased significantly with increased valve size (P = .0001). One third of all patients, regardless of gender (26/64 of the women and 14/45 of the men), had evidence of LVH. Valve sizes correlated for body surface area (indexed valve size) in patients with LVH were similar to those in patients without LVH (Figure 3). This suggests that valve mismatch was not the reason for LVH seen at long-term follow-up in this subgroup of patients. Indexed valve area stratified according to valve size showed a trend toward higher mean indexed valve sizes for larger valves, which might suggest a relative mismatch for smaller valve sizes (Figure 4). However, LVMI increased with larger valve sizes, again indicating that valve size or valve mismatch was not the final determinant of LVMI or LVH. At follow-up, 69% (n = 75/109) had normal systolic left ventricular function, whereas 25% (n = 28/109) of the patients had mildly impaired left ventricular function, 3% (n = 3/109) had moderately impaired left ventricular function, and 3% (n = 3/109) had severely impaired left ventricular function.


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Table 5. M-mode echocardiographic results and calculations of CEP aortic valve bioprosthesis according to valve size at follow-up
 


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Fig. 3. Valve size indexed to body surface area (BSA) and LVMI stratified for patients with (squares) and without (circles) LVH.

 


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Fig. 4. Mean valve size indexed to body surface area (BSA) for all aortic valve sizes. Darkest shading, 27 mm; second darkest, 21 mm; median shading, 19 mm; second lightest, 25 mm; lightest, 23 mm.

 
None or trivial, mild, moderate, and severe aortic insufficiencies were found in 65% (n = 71/109), 31% (n = 34/109), 3% (n = 3/109), and 1% (n = 1/109) of the patients, respectively. Mitral regurgitation at follow-up was none or trivial in 28% of the patients (n = 31/109), mild in 49% (n = 53/109), moderate in 19% (n = 21/109), and severe in 4% (n = 4/109). There was no significant difference in mitral regurgitation between patients with and without preoperative coronary artery disease (P = .3). Furthermore, when patients were stratified according to both preoperative aortic insufficiency and mitral regurgitation at follow-up, there was no significant difference in LVMI between groups (Figure 5). However, a trend toward higher LVMI was seen in patients with preoperative aortic insufficiency and more than mild mitral regurgitation at follow-up echocardiography.



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Fig. 5. LVMI stratified for preoperative aortic insufficiency (AI) and mitral regurgitation (MR) on follow-up echocardiogram. Dark bars, Aortic insufficiency value of 1; light bars, aortic insufficiency value of 0.

 

    Discussion
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 
The use of glutaraldehyde-treated bovine pericardial valves for AVR was introduced in 1971 by Ionescu and associates.Go 7 Those valves were at the time superior to porcine valves from a hemodynamic point of viewGo 8 but showed signs of limited durability in fatigue tests, a problem that was later confirmed clinically.Go Go 9,10 The CEP aortic valve was introduced after several design changes, which included improved tissue preservation, a more flexible stent, a modified shape of the cusps, and modified tissue-mounting of the pericardium in the stent. Early clinical and hemodynamic studies showed excellent results.Go Go 11,12 Several studies have shown excellent long-term durability with CEP valves,Go Go 1-4 which seems to be related to a lower risk of primary tissue failure than seen with older porcine and bovine pericardial valves.

In this report of clinical and hemodynamic late outcomes after AVR with the CEP bioprosthesis, we confirm previous studies indicating good results comparable to newer porcine valves.Go Go Go 2,3,13 Banbury and associatesGo 2 and Neville and associatesGo 4 reported similar 5- and 10-year survivals, although in somewhat younger patient populations than in our study, for the CEP bioprosthesis in the aortic position. Table 6 shows survivals and freedoms from structural valve degeneration in earlier reported studies of the CEP pericardial bioprosthesis. Poirier and coworkersGo 3 have reported excellent survival rates in a younger patient population than ours. Survivals for our patient population with the CEP bioprosthesis were lower than in our population with the Hancock II porcine bioprosthesis.Go 13 However, our patients with the CEP bioprosthesis were significantly older than those with the Hancock II porcine bioprosthesis (Table 6Go). We have previously shown that advanced age, male sex, advanced left ventricular dysfunction, coronary artery disease, and advanced NYHA functional class are independent predictors of mortality among patients with AVR.Go 14 Our patient population was in general older and had more coronary artery disease than in other studies.Go Go Go Go 1-4,11,13 Considering the risk factor profile in our study, the survival must be considered satisfactory. As anticipated, the multivariate analysis from our study showed that coronary artery disease and NYHA class III or IV were risk factors for late death and for cardiac non-valve-related death.


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Table 6. Survival and structural valve degeneration data for CEP bioprosthesis
 
Our study confirms that the CEP bioprosthesis is associated with a low incidence of structural valve dysfunction comparable to earlier reportsGo Go 1-4 (Table 6Go). In our population, no patient older than 65 years has required reoperation because of structural valve degeneration. Some authors have even indicated that the CEP bioprosthesis may be superior to stented porcine bioprostheses in terms of structural valve dysfunction.Go 2 When the CEP valve is compared with the Hancock II, a second-generation porcine aortic valve, however, the risk of degeneration appears to be similar. In our experience the Hancock II was used in a younger patient population, and the freedom from valve degeneration was similar to that of the CEP valve. The clinical and hemodynamic data of the CEP and Hancock II valves are similar according to our experience.Go 15 Transvalvular gradients and aortic valve areas for the CEP appear to be slightly worse than those of the Hancock II according to retrospective studies. However, neither of these valves has as good hemodynamic data as the Toronto SPV or the Freestyle bioprosthesis.Go Go 16,17 There are a few long-term reports with echocardiography on the CEP. Frater and coworkersGo 11 reported aortic valve areas somewhat similar to those found in our study after a mean follow-up of 67 months.

We found that LVH was still present at long-term follow-up in about a third of the patients. In contrast, as previously reported by our group,Go 16 only 8% of the patients with a Toronto SPV had LVH by echocardiography after a similar mean follow-up of 5 years. However, we have also showed that sex, hypertension, cause of valve disease, and presence of coronary artery disease,Go 16 as well as genetic factors,Go 18 influence both the preoperative degree of LVH and its regression. Thus many confounding factors exists between the previously mentioned studies, which makes it difficult to safely conclude anything regarding the degree of LVH at late follow-up. Maybe the most surprising finding of the late follow-up echocardiography was that 23% of the patients had moderate or severe mitral regurgitation. However, we were not able to show that either mitral regurgitation or preoperative aortic insufficiency was significantly more common among patients with LVH than among those without LVH.


    Limitations of the study
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 
This study was retrospective, and therefore the valve-related complication rates were probably underestimated because follow-up was only obtained once for this population. However, the follow-up was 100% complete and reliable with respect to survival, reoperation, and echocardiographic data. The last, however, must be interpreted with caution, because the analysis was performed retrospectively and only included about 60% of the population who were alive at the time of the study.


    Appendix
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 
Doppler echocardiography
Color flow Doppler echocardiography was used to assess aortic insufficiency in the parasternal long-and short-axis views and in the apical 5- and 3-chamber views. Two-dimensional guided and stand-alone continuous-wave Doppler modes were used to interrogate flow through the aortic valve from multiple positions. Pulsed-wave Doppler was used to assess flow in the left ventricular outflow tract (LVOT).

The peak (VAVmax) and mean (VAVmean) systolic flow velocities (in meters per second) across the aortic valve were recorded with continuous-wave Doppler, and those proximal to the aortic valve in the LVOT (VLVOTmax and VLVOTmean) were recorded with pulsed-wave Doppler. The average of three consecutive cardiac cycles in sinus rhythm or of 10 cardiac cycles in atrial fibrillation was used to calculate transaortic velocities and velocity time integrals (VTIAV and VTILVOT, in centimeters). Peak (PLVOTpeak and PAVpeak) and mean (PAVmean and PLVOTmean) pressure differences (in millimeters of mercury) were calculated according to the modified Bernoulli equationGo 1:
Ppeak = 4 x (VAVmax2 - VLVOTmax2)
Pmean = PAVmean - PLVOTmean
PAVmean - PLVOTmean = 4 x (VAVmean2 - VLVOTmean2)

The LVOT diameter (D, in centimeters) was determined in midsystole from the parasternal long-axis view. The effective orifice area (EOA, in centimeters) was calculated with the continuity equationGo 1:
EOA (cm2) = 3.14 x 2D/4 x VTILVOT/VTIAV

Cardiac output (CO, in liters per minute) was calculated as the product of stroke volume and heart rate (HR, in beats/min)Go 1:
CO = HR x (3.14 x 2D/4 x VTILVOT)/1000

Measurements of interventricular septum (IVS) and posterior wall (PW) thicknesses (in centimeters) and left ventricular end-diastolic dimension (LVEDD, in centimeters) were obtained with 2-dimensional echocardiography in a standard fashion. Left ventricular mass (LVM, in grams) was calculated from IVS and PW thicknesses and the LVEDD according to the American Society of Echocardiography cube methodGo 2:
LVM = 0.8 x 1.04 x [(IVS + PW + LVEDD)3 - (LVEDD)3] + 0.6

The left ventricular mass index was calculated by dividing LVM by body surface area.

Aortic insufficiency was assessed with color flow Doppler and CW and PW Doppler in any view.Go 3 The ejection fraction was determined according to the Simpson rule and left ventricular function was classified by ejection fraction as grade 1 (>60%), grade 2 (40%-60%), grade 3 (20%-40%), or grade 4 (<20%).Go 1


    Acknowledgments
 
We are grateful to Drs C.M. Feindel, R.D. Weisel, H.E. Scully, C.M. Peniston, B.S. Goldman, R.J. Baird, and L.L. Mickelborough for allowing us to use their patients' data for this study.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 

  1. Pellerin M, Mihaileanu S, Couëtil JP, Relland JY, Deloche A, Fabiani JN, et al. Carpentier-Edwards pericardial bioprosthesis in aortic position: long-term follow-up 1980 to 1994. Ann Thorac Surg. 1995;60(2 Suppl):S292-5.
  2. Banbury MK, Cosgrove DM, Lyric BW, Smedira NG, Sabik JF, Saunders CR. Long-term results of the Carpentier-Edwards pericardial aortic valve: a 12-year follow-up. Ann Thorac Surg. 1998;66:S73-6.
  3. Poirier NC, Pelletier CL, Pellerin M, Carrier M. 15-year experience with the Carpentier-Edwards pericardial bioprosthesis. Ann Thorac Surg. 1998;66(6 Suppl):S57-61.
  4. Neville PH, Aupart MR, Diemont FF, Sirinelli AL, Lemoine EM, Marchand MA. Carpentier-Edwards pericardial bioprosthesis in aortic or mitral position: a 12-year experience. Ann Thorac Surg. 1998;66(6 Suppl):S143-7.
  5. Levy D, Savage DD, Garrison RJ, Andersson KM, Kannel WB, Castelli WP. Echocardiographic criteria for left ventricular hypertrophy: the Framingham heart study. Am J Cardiol. 1987;59:956-60.[Medline]
  6. Edmunds LH, Clark RE, Cohn LH, Grunkemeier GL, Miller DC, Weisel RD. Guidelines for reporting morbidity and mortality after cardiac valvular operations. Eur J Cardiothorac Surg. 1996;10:812-6.[Abstract]
  7. Ionescu MI, Tandon AP, Mary DA, Abid A. Heart valve replacement with the Ionescu-Shiley pericardial xenograft. J Thorac Cardiovasc Surg. 1977;73:31-42.[Abstract]
  8. Becket RM, Strom J, Frischman W, Oka Y, Lin YT, Yellin EL, et al. Hemodynamic performance of the Ionescu-Shiley valve prosthesis. J Thorac Cardiovasc Surg. 1980;80:613-20.[Abstract]
  9. Gabbay S, Bortolotti V, Wasserman F, Factor S, Strom J, Frater RW. Fatigue-induced failure of the Ionescu-Shiley pericardial xenograft in the mitral position: in vivo and in vitro correlation and a proposed classification. J Thorac Cardiovasc Surg. 1984;87:836-44.[Abstract]
  10. Walley VM, Keon WJ. Patterns of failure in Ionescu-Shiley bovine pericardial bioprosthetic valves. J Thorac Cardiovasc Surg. 1987;93:925-33.[Abstract]
  11. Frater RW, Salomon NW, Rainer WG, Cosgrove DM, Wickman E. The Carpentier-Edwards pericardial aortic valve: intermediate results. Ann Thorac Surg. 1992;53:764-71.[Abstract]
  12. Cosgrove DM, Lytle BW, Williams GW. Hemodynamic performance of the Carpentier-Edwards pericardial valve in the aortic position in vivo. Circulation. 1985;72 Suppl 2:II146-52.
  13. David TE, Armstrong S, Sun Z. The Hancock II bioprosthesis at 12 years. Ann Thorac Surg. 1998;66(6 Suppl):S95-8.
  14. Fremes SE, Goldman BS, Ivanov J, Weisel RD, David TE, Salerno T. Valvular surgery in the elderly. Circulation. 1989;80 Suppl 1:I77-90.
  15. David TE, Armstrong S, Sun Z. Clinical and hemodynamic assessment of the Hancock II bioprosthesis. Ann Thorac Surg. 1992;54:661-8.[Abstract]
  16. Dellgren G, David TE, Raanani E, Bos J, Ivanov J, Rakowski H. The Toronto SPV: hemodynamic data at 1 and 5 years' postimplantation. Semin Thorac Cardiovasc Surg. 1999;11(4 Suppl 1):107-13.[Medline]
  17. Doty DB, Cafferty A, Cartier P, Huysmans HA, Kon ND, Krause AH, et al. Aortic valve replacement with Medtronic Freestyle bioprosthesis: 5-year results. Semin Thorac Cardiovasc Surg. 1999;11(4 Suppl 1):35-41.[Medline]
  18. Dellgren G, Eriksson MJ, Blange I, Brodin LA, Radegran K, Sylven C. Angiotensin-converting enzyme gene polymorphism influences degree of left ventricular hypertrophy and its regression in patients undergoing operation for aortic stenosis. Am J Cardiol. 1999;84:909-13.[Medline]

    References 
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Limitations of the study
 Appendix
 References
 References 
 
  1. Feigenbaum H. Hemodynamic information derived from echocardiography. In: Feigenbaum H, editor. Echocardiography. 5th ed. Philadelphia: Lea & Febiger; 1994. p. 138-40, 181-215.
  2. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986:57:450-8.
  3. Perry GJ, Helmcke F, Nanda NC, Byard C, Soto B. Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Coll Cardiol. 1987;9:952-9.[Abstract]



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Ann. Thorac. Surg.Home page
H. Izutani, T. Shibukawa, J. Kawamoto, S. Mochiduki, and D. Nishikawa
Early aortic bioprosthetic valve deterioration in an octogenarian.
Ann. Thorac. Surg., October 1, 2008; 86(4): 1369 - 1371.
[Abstract] [Full Text] [PDF]


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Ann. Thorac. Surg.Home page
T. Eitz, S. Schenk, D. Fritzsche, A. Bairaktaris, O. Wagner, H. Koertke, and R. Koerfer
International Normalized Ratio Self-Management Lowers the Risk of Thromboembolic Events After Prosthetic Heart Valve Replacement
Ann. Thorac. Surg., March 1, 2008; 85(3): 949 - 955.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
T. E. David, C. M. Feindel, J. Bos, J. Ivanov, and S. Armstrong
Aortic valve replacement with Toronto SPV bioprosthesis: Optimal patient survival but suboptimal valve durability
J. Thorac. Cardiovasc. Surg., January 1, 2008; 135(1): 19 - 24.
[Abstract] [Full Text] [PDF]


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Card Surg AdultHome page
N. D. Desai and G. T. Christakis
Bioprosthetic Aortic Valve Replacement: Stented Pericardial and Porcine Valves
Card. Surg. Adult, January 1, 2008; 3(2008): 857 - 894.
[Full Text]


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Ann. Thorac. Surg.Home page
E. Hickey, S. M. Langley, O. Allemby-Smith, S. A. Livesey, and J. L. Monro
Subcoronary Allograft Aortic Valve Replacement: Parametric Risk-Hazard Outcome Analysis to a Minimum of 20 Years
Ann. Thorac. Surg., November 1, 2007; 84(5): 1564 - 1570.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
F. Bakhtiary, O. Dzemali, U. Steinseiffer, C. Schmitz, B. Glasmacher, A. Moritz, and P. Kleine
Opening and closing kinematics of fresh and calcified aortic valve prostheses: An in vitro study
J. Thorac. Cardiovasc. Surg., September 1, 2007; 134(3): 657 - 662.
[Abstract] [Full Text] [PDF]


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Eur. J. Cardiothorac. Surg.Home page
J. Nowell, E. Wilton, H. Markus, and M. Jahangiri
Antithrombotic therapy following bioprosthetic aortic valve replacement
Eur. J. Cardiothorac. Surg., April 1, 2007; 31(4): 578 - 585.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
F. Bakhtiary, M. Schiemann, O. Dzemali, S. Dogan, V. Schachinger, H. Ackermann, A. Moritz, and P. Kleine
Impact of Patient-Prosthesis Mismatch and Aortic Valve Design on Coronary Flow Reserve After Aortic Valve Replacement
J. Am. Coll. Cardiol., February 20, 2007; 49(7): 790 - 796.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
C. Valfre, G. Rizzoli, C. Zussa, P. Ius, E. Polesel, S. Mirone, T. Bottio, and G. Gerosa
Clinical results of Hancock II versus Hancock Standard at long-term follow-up.
J. Thorac. Cardiovasc. Surg., September 1, 2006; 132(3): 595 - 601.e2.
[Abstract] [Full Text] [PDF]


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CirculationHome page
A. Ali, J. C. Halstead, F. Cafferty, L. Sharples, F. Rose, R. Coulden, E. Lee, J. Dunning, V. Argano, and S. Tsui
Are Stentless Valves Superior to Modern Stented Valves?: A Prospective Randomized Trial
Circulation, July 4, 2006; 114(1_suppl): I-535 - I-540.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
O. Lund and M. Bland
Risk-corrected impact of mechanical versus bioprosthetic valves on long-term mortality after aortic valve replacement
J. Thorac. Cardiovasc. Surg., July 1, 2006; 132(1): 20 - 26.
[Abstract] [Full Text] [PDF]


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Asian Cardiovasc. Thorac. Ann.Home page
W. E. Jamieson, E. Germann, M. R Aupart, P. H Neville, M. A Marchand, and G. J Fradet
15-Year Comparison of Supra-Annular Porcine and PERIMOUNT Aortic Bioprostheses
Asian Cardiovasc Thorac Ann, June 1, 2006; 14(3): 200 - 205.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
J. B. Chambers, H. M. Rimington, F. Hodson, R. Rajani, and C. I. Blauth
The subcoronary Toronto stentless versus supra-annular Perimount stented replacement aortic valve: Early clinical and hemodynamic results of a randomized comparison in 160 patients
J. Thorac. Cardiovasc. Surg., April 1, 2006; 131(4): 878 - 882.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
F. Bakhtiary, M. Schiemann, O. Dzemali, T. Wittlinger, M. Doss, H. Ackermann, A. Moritz, and P. Kleine
Stentless bioprostheses improve postoperative coronary flow more than stented prostheses after valve replacement for aortic stenosis
J. Thorac. Cardiovasc. Surg., April 1, 2006; 131(4): 883 - 888.
[Abstract] [Full Text] [PDF]


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Ann. Thorac. Surg.Home page
Y. Sakamoto, K. Hashimoto, H. Okuyama, H. Takakura, S. Ishii, S. Taguchi, and H. Kagawa
Prevalence and Avoidance of Patient-Prosthesis Mismatch in Aortic Valve Replacement in Small Adults
Ann. Thorac. Surg., April 1, 2006; 81(4): 1305 - 1309.
[Abstract] [Full Text] [PDF]


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Ann. Thorac. Surg.Home page
M. R. Moon, M. K. Pasque, N. A. Munfakh, S. J. Melby, J. S. Lawton, N. Moazami, J. E. Codd, T. D. Crabtree, H. B. Barner, and R. J. Damiano Jr
Prosthesis-Patient Mismatch After Aortic Valve Replacement: Impact of Age and Body Size on Late Survival
Ann. Thorac. Surg., February 1, 2006; 81(2): 481 - 489.
[Abstract] [Full Text] [PDF]


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Ann. Thorac. Surg.Home page
C. W. Akins, A. D. Hilgenberg, G. J. Vlahakes, J. C. Madsen, T. E. MacGillivray, G. M. LaMuraglia, and R. P. Cambria
Late Results of Combined Carotid and Coronary Surgery Using Actual Versus Actuarial Methodology
Ann. Thorac. Surg., December 1, 2005; 80(6): 2091 - 2097.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
P. Totaro, N. Degno, A. Zaidi, A. Youhana, and V. Argano
Carpentier-Edwards PERIMOUNT Magna bioprosthesis: A stented valve with stentless performance?
J. Thorac. Cardiovasc. Surg., December 1, 2005; 130(6): 1668 - 1674.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
W.R. E. Jamieson, L. H. Burr, R. T. Miyagishima, E. Germann, J. S. MacNab, E. Stanford, F. Chan, M. T. Janusz, and H. Ling
Carpentier-Edwards supra-annular aortic porcine bioprosthesis: Clinical performance over 20 years
J. Thorac. Cardiovasc. Surg., October 1, 2005; 130(4): 994 - 1000.
[Abstract] [Full Text] [PDF]


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Ann. Thorac. Surg.