European Journal of Cardio-thoracic Surgery 23 (2003) 560566

www.elsevier.com/locate/ejcts

Homograft replacement of the mitral valve in young recipients:

mid-term resultsq
S. Chauvauda,*, T. Waldmanna, N. dAttellisb, P. Brunevalc, C. Acard, J. Gerotae,
M. Jarrayae, A. Carpentiera
a
Department of Cardiovascular Surgery, Hopital Europeen Georges Pompidou, 20, rue Leblanc, 75015 Paris, France
b
Department of Anesthesiology, Hopital Europeen Georges Pompidou, 20, rue Leblanc, 75015 Paris, France
c
Department of Anatomopathology, Hopital Europeen Georges Pompidou, 20, rue Leblanc, 75015 Paris, France
d
Department of Cardiac Surgery, Hopital Pitie Salpetrie`re, 47/83 Boulevard de lHopital, 75013 Paris, France
e
Human Tissue Bank Hopital Saint Louis, 1 avenue Claude Vellefaux, 75010 Paris, France
Received 24 September 2002; received in revised form 24 December 2002; accepted 29 December 2002

Abstract
Objective: Mitral homograft (MH) can represent an interesting alternative for valve replacement in the young. However, concerns have
been expressed about the durability of valve allografts in children. We report our experience with MH replacement in young patients.
Methods: From 1993 to 1997, 13 young patients aged 3 25 years (mean 15 ^ 6 years) underwent total mitral valve (MV) replacement with
a cryopreserved homograft (CH). All but one had previously undergone one or more cardiac operations. The indications were rheumatic
disease (6), acute and subacute endocarditis (2), congenital heart disease (4), and systemic lupus endocarditis (1). Results: No in hospital
deaths are reported. Discharge echocardiogram showed a well-functioning MH in all but one patient. One patient was lost to follow-up.
Follow-up ranged from 0.7 to 6.6 years (4.1 ^ 2.2). On follow-up two patients were doing well. Two patients died without reoperation and
both had MV stenosis. Seven patients (54%) required reoperation: mean delay 4.17 years (0.7 7). In all cases, thickening, shrinking and
calcification of the allograft were present. None of these seven had contributive histopathologic changes. One patient presenting recurent MV
insufficiency will require a reoperation. Conclusion: MV homograft is a safe and reproducible technique, but does not provide durable results
and should not be used in young patients.
q 2003 Elsevier Science B.V. All rights reserved.
Keywords: Mitral valve homograft; Mitral valve reconstruction

1. Introduction In our current study we review our series from the

beginning of our experience. The aim of this study was to
Homograft valves are largely used in children as a analyze mid-term durability of this valve substitute in young
conduit between the right ventricle and the pulmonary patients.
arteries with various results [1]. Aortic valve homografts are
routinely used in aortic position even in children [2,3]. Due
to the poor results of bioprosthesis and mechanichal
2. Material and methods
prosthesis in the mitral position in young patients, a mitral
homograft (MH) was thought to be an interesting
alternative technique when conservative surgery was not 2.1. Patient population
possible [4].
Between 1993 and 1997, 13 patients less than 25 years
q
Presented at the 16th Annual Meeting of the European Association for old (range 3 25) underwent total mitral valve (MV)
Cardio-thoracic Surgery, Monte Carlo, Monaco, September 22 25, 2002.
* Corresponding author. Tel.: 33-1-56-09-36-26; fax: 33-1-56-09-22- replacement with homograft (Table 1). Indication for
19. surgery was MV insufficiency in all cases with functional
E-mail address: sylvain.chauvaud@egp.ap-hop-paris.fr (S. Chauvaud). class (New York Heart Association, NYHA) III and IV. All
1010-7940/03/$ - see front matter q 2003 Elsevier Science B.V. All rights reserved.
doi:10.1016/S1010-7940(03)00003-4
 S. Chauvaud et al. / European Journal of Cardio-thoracic Surgery 23 (2003) 560566 561

Table 1 The valves were dissected as soon as possible and

Patient characteristicsa cryopreservation was started. In this group, the heart was
Patient Age Etiology Previous Associated procedure not stored in an antibiotic solution. The mean delay between
(years) operation harvesting and cryopreservation was 26 h.
The operative technique performed was that described by
Number Delay Acar et al. [4] without modifications. All patients except one
(years)
(patient 6) had a Carpentier prosthetic ring.
1 19 R 1 4
Homograft characteristics are listed in Table 2. Blood
2 21 R 1 6.6 TVA groups of both recipient and donor are presented in Table 3.
3 13 SBE 1 4.1 Matching of blood groups was not attempted.
4 11 R 1 2.4 TVC Cardiopulmonary bypass was performed at a core
5 25 SBE 1 0.8 TVH temperature of 288C, with cold blood cardioplegia. Average
6 3 CONG 3 0.7
7 25 CONG 0 0 ASD
bypass time was 158 ^ 34 min (120 120) and aortic cross-
8 15 R 1 0.8 AOH clamping 103 ^ 19 min (80 140).
9 12 R 2 0.4
10 18 SLE 2 0.5 2.3. Statistical analysis
11 6 CONG 3 6
12 20 R 1 13 TVA
13 14 CONG 2 9 Continuous or interval-related variables are expressed as
means ^ SD and categoric variables are expressed as
a
R, rheumatic disease; SBE, subacute bacterial endocarditis; CONG, percentage. Events were calculated by the Kaplan Meier
congenital; TVA, tricuspid valve annuloplasty; TVC, tricuspid valve
commissurotomy; TVH, tricuspid valve homograft; AOH, aortic valve
actuarial method.
homograft; ASD, closure of atrial septal defect; SLE, systemic lupus
erythematosus.
3. Results
patients were in sinus rhythm, mean cardiothoracic ratio
was 0.58 ^ 0.08 (range 0.50 0.75). 3.1. Early results
Etiologies were rheumatic disease (6), congenital atrio-
ventricular defect (4) (partial (1), total (1), double No in hospital deaths are reported following MV
discordance (1), isolated congenital MV insufficiency (1)), homograft implantation. A control transesophageal echo-
bacterial endocarditis (2) (one acute, one sterile), and cardiography was performed in the operating room and
systhemic lupus erythematosus (SLE) (1). All patients before hospital discharge (tenth postoperative day). All
except one had at least one attempt of a MV repair. Mean patients except one (patient 13), were free of MV stenosis
delay between the last operation and the replacement with a (Table 4). MV insufficiency was graded from 1 to 4 .
MH was 4.1 ^ 4 years (range 0.4 13.2). One patient had Residual MV insufficiency graded 2 was present in three
two implantations of a MH. The first attempt was not patients, but clinically well tolerated. Cyclosporin (serum
technically satisfactory leading to early reoperation (patient
Table 2
13).
Homograft characteristics
Associated procedures were: tricuspid valve annulo-
plasty (2), tricuspid valve commissurotomy (1), tricuspid Donor age Annulus diameter Duration of storage Antibiotics
valve replacement with a MH (1), aortic valve homograft (years) (mm) (h) (24 h)
(1), and closure of atrial septal defect (1).
1 52 28 19 0
2 27 26 24
2.2. Homograft implantation 3 56 30 40
4 17 32 11 0
In all cases a cryopreserved MV obtained from a tissue 5 41 34 24 0
bank (Banque de Tissus de lAP-HP) was used. Harvesting 6 19 30 24
7 38 34 18 0
of MVs was from two origins. In multiorgan donors, n 6
8 35 34 48
the heart was placed in lactated Ringer solution at 48C. The 9 12 26 17 0
dissection of the valves was performed as soon as possible. 10 45 34 22 0
The valves were stored in RPMI solution for 24 h with 11 49 28 40
antibiotics (vancomycin 500 mg/l, lincomycin 600 mg/l and 12 28 28 19 0
13 14 32 40
gentamycin 320 mg/l). Afterwards, cryopreservation was
started in a medium containing RPMI, human albumin Mean 33 30.5 26
(1.3%) and dimethyl sulfoxide (10%). In living patients SD 15 3.1 10
Max 56 34 40
n 7 scheduled for heart transplant, the heart was
Min 13 26 11
explanted and stored in lactated Ringer solution at 48C.
562 S. Chauvaud et al. / European Journal of Cardio-thoracic Surgery 23 (2003) 560566

Table 3 patient presented massive MV homograft insufficiency and

Blood groups, rhesus and evolution of the homografta was scheduled for valve replacement. Two patients died and
Patient Donor Recipient Evolution had MV stenosis. One of these patients had global cardiac
failure and was not reoperated for geographic reasons. The
1 A B MS Dead other patient died of multiple causes: SLE, renal insuffi-
2 AB B MI ciency and probable recurrent bacterial endocarditis. Seven
3 O O MS R
4 O O DW
patients were reoperated on for MV homograft dysfunction.
5 O2 A MI R Out of seven patients with incompatible patient/homo-
6 A O MI R graft blood groups, six had valve failure (reoperated on or
7 A O MI R not). Out of six patients with compatible patient/homograft
8 O O MS R blood groups, four had valve failure (reoperated on or not)
9 A O DW
10 O A MS Dead
(Table 3). The difference between the two groups was not
11 O A MS R significant.
12 O O ?
13 B A MS R 3.4. Reoperation
a
MS, mitral stenosis; MI, mitral insufficiency; ?, lost to follow-up; R,
reoperated; DW, doing well. Seven patients underwent MV replacement, with a
mechanical bileaflet valve (6) or bioprosthesis (1), without
level 80 ng/ml) and aspirin 50 mg per day were adminis- complication. The smallest diameter of the prosthesis
tered in one patient (patient 11). implanted was 25 mm.
Indications for replacements were massive MV insuffi-
3.2. Follow-up ciency (3) or stenosis (4) (Table 4). Active endocarditis was
present in one patient and degeneration in six patients.
One patient was lost to follow-up. Mean follow-up with Clinical examination of the degenerated homograft
clinical examination and echocardiography was 4 ^ 2.2 during surgery revealed obstructive calcification (3),
years (min 0.7, max 7). Patient follow-up was stopped when chordal rupture (1), valve retraction with an inflammatory
the MV was replaced. aspect (2).
The actuarial freedom from reoperation is 43 ^ 16% at 5
3.3. Clinical evolution years and 30 ^ 16% at 7 years (Fig. 1). The actuarial
freedom from valve failure (association of reoperation and
At the last follow-up, two patients were doing well with dysfunction) was 30 ^ 14% at 5 years and 12 ^ 10% at 7
no sign of homograft dysfunction (patients 4 and 9). One years (Fig. 1b).

Table 4
Echocardiographic results: early and late evaluation correlated with the clinical outcomea

Patient Early examination Follow-up

Mean gradient (mmHg) MVI Delay (years) Mean gradient (mmHg) MVI Outcome

1 6 1 4.76 20 0 Dead
2 0 0 6.6 0 4 To be reoperated
3 7 1 2.4 15 2 Reoperated
4 4 1.5 6.3 5 2 Doing well
5 0 0 5.4 0 4 Reoperated
6 0 1 0.7 14 4 Reoperated
7 2 2 6.3 2 4 Reoperated
8 0 0 1.3 9 0 Reoperated
9 5 2 7 8 2 Doing well
10 4 2 2.3 20 1 Dead
11 4 1 4.4 23 2 Reoperated
12 0 0 Lost to follow-up
13 9 1 2.4 20 1 Reoperated
Mean 13 4.1 13
SD 3.2 2.2 7
Min 0 0.7 0
Max 2 7 23
a
MVI, mitral valve insufficiency.
 S. Chauvaud et al. / European Journal of Cardio-thoracic Surgery 23 (2003) 560566 563

4. Discussion

Following the acceptable clinical experience of aortic

homograft in young patients [5] it was assumed that MV
homograft replacement could be used in children [6].
However, it is known that degeneration of aortic homografts
is related to the young age of the recipient [7] with a
predominance of inflammatory lesions [8]. Clinical mid-
term results of MHs are rare. In Acar et al.s [4] study, mean
follow-up was 14 months with a very low rate of reoperation
and residual MV insufficiency. In contrast, the series of
Kumar et al. [9] is less favorable; the actuarial rate of
normal function was 42 and 10% at 24 and 48 months,
respectively. In the series by Doty and Acar [10], 25% (5/
18) of the MHs was explanted during the first postoperative
year despite the accuracy of the repair confirmed by
intraoperative echocardiography. Patients operated on in
poor clinical condition had good early results, but proved to
evolve toward mid-term failure [11].
When considering the high incidence of failure in our
series we attempted to analyze and understand the causes.

4.1. Surgical technique

Fig. 1. Actuarial rate of complications (KaplanMeier). (a) Freedom from
reoperation. (b) Freedom from complication combining reoperation and
mitral dysfunction (without reoperation).
3.5. Pathology of explanted valves
Five explanted valves underwent microscopic examin-
ation. The papillary muscles appeared to be fibrotic in all
cases and in one, necrosis was present. Absence of leaflet
tissue endothelium was encountered in all explanted valve.
Massive fibrosis of the stroma was at the origin of a total
disorganization of the leaflet structure. The fibrosa and the
spongiosa were totally replaced by fibrosis in most cases
with hemorrhage in the stroma (Fig. 2a). Intense neovascu-
larization was present in one specimen, (Fig. 2b) on the
leaflet and on the chordae (patient 8). Calcification was
present with ulcerated plaques (Fig. 2c) (patients 11 and 13)
associated with thrombosis (Fig. 2d). The inflammatory
cells when present were non-specific: lymphocytes B and
macrophages (Fig. 3 and Table 5).
In our series we performed a side to side suture of the
papillary muscle [4] and no rupture of papillary muscle
occurred. This complication which can occur irrespective of
the age [12] was prevented. Special attention was given to
the position of the posterior papillary muscle [13] in order to
avoid valve distortion. One of our patients did not receive a
prosthetic ring (patient 6) and had nevertheless good early
result. Unfortunately, reoperation was necessary 0.7 years
later for leaflet retraction, but without annulus dilatation.
Intraoperative control echocardiography demonstrated
one early stenosis and three patients with a mild MV
insufficiency. There was no correlation between excellent
early results and/or mild residual MV insufficiency regard-
ing the evolution toward valve deterioration. In this series, a
technical factor predisposing to valve failure can be
excluded except in the patient presenting residual MV
stenosis after implantation.
4.2. Homograft storage
A large debate regarding the durability of cryopreserved
versus homovital homograft exists. Most results were

Table 5
Pathology of the explanted valves

Patient Endothelium Fibrosis Calcification Neovascularization Inflammatory cells Thrombosis Papillary muscle

6 0 0 Lymphocytes 0 Fibrotic
7 0 Micro 0 0 Fibrotic
8 Fibrosis 0 Necrotic
11 0 Fibrotic
13 0 0 0 Fibrotic
564 S. Chauvaud et al. / European Journal of Cardio-thoracic Surgery 23 (2003) 560566

Fig. 2. Histologic changes of the stroma. Hematoxylin and eosin stain. (a) Hemorrhage associated with fibrosis (original magnification 100). (b)
Subendothelial leaflet calcification (original magnification 100). (c) Inflammatory cells, most of them are macrophages (original magnification 50). (d)
Neovascularization with extensive fibrosis (original magnification 50).

elaborated from the aortic homograft experience. In
cryopreservation without antibiotics, viability of endothelial
cells is decreased but still present 3 weeks after harvesting
[14]. On mid-term examination, explantation of cryopre-
served aortic homografts do not demonstrate cell growth or
metabolic function [15], even when collagen appeared to be
preserved. In explanted aortic homografts from living
donors, the structure of the collagen is perserved early
after explantation [15]. Low dose antibiotics (homovital
aortic homograft) appear to decrease immunologic stimu-
lation (in vitro) [16].
The storage technique used in our series when the MH
was obtained from a multiorgan donor is a combination of
the two described techniques. Due to the conditions during
multiorgan harvesting it appeared appropriate to use low
dose antibiotics for 24 h in order to assure a sterile
homograft. No correlation between the two groups (anti-
biotics and cryopreservation versus cryopreservation alone)
regarding the incidence of homograft valve degeneration
was observed.

4.3. Immunology
Fig. 3. Histologic changes of the endothelium. Thrombosis adherant to the
leaflet tissue and absence of endothelium cells, the stroma is highly fibrotic. Very little is known with respect to the antigenicity of the
Hematoxylin and eosin stain (original magnification 50). MV. Aortic homografts in primates appear to have a
 S. Chauvaud et al. / European Journal of Cardio-thoracic Surgery 23 (2003) 560566
decreased antigenicity [17]. One of the main differences
between the aortic valve and the MV is the presence of
muscle tissue in the subvalvular apparatus of the MV.
Muscular tissue results in greater immunologic stimulation
and production of antibodies from the recipient [8].
Conditioning of papillary muscles with glutaraldehyde [9]
was presumed to decrease immunologic stimulation and the
risk of necrosis. However, the rate of papillary muscle
dysfunction was not reduced by glutaraldehyde as reported
by Kumar et al. [9] and this technique is no longer used.
One of our patients (patient 11) received cyclosporin
following homograft insertion. However, immunodepres-
sion did not prevent early failure (0.7 years) and this patient
was reoperated. Attempts at immunodepression with
azothioprine have been used in children undergoing
cryopreserved aortic allograft [18]. Allo-immune human
leukocyte antigens (HLA) antibody response in such cases
was not reduced and the influence on graft dysfunction was
not significant. A high incidence of infection was underlined
by Hawkins et al. as an important drawback to this protocol
[19].
Experimental studies such as cyclosporine in the rat [20]
or g interferon [21] in vitro have been demonstrated to
decrease T-cell response to valve allograft. However,
immunodepression cannot be extensively used in children.
Blood group mismatch appears to have no effect on the
outcome of the homograft as previously published by
Schutz et al. [22] and confirmed in our series. Production of
antibodies to HLA has not been proven to be a risk of
homograft degeneration [23].
In conclusion, due to the early occurrence of degener-
ation, MV homograft replacement should not be used in
young patients.
References
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failure of cryopreserved homograft pulmonary valves in children:
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[2] Jones TK, Lupinetti FM. Comparison of Ross procedures and aortic
valve allografts in children. Ann Thorac Surg 1998;66:S170 3.
[3] Luciani GB, Casali G, Santini F, Mazucco A. Aortic root replacement
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Appendix A. Conference discussion
Dr V. DiSesa (Philadelphia, Pennsylvania, USA): Do you have a
similar experience with aortic homografts in young patients? And do you
believe that an immune reaction is a significant component of your
observations?
Dr Chauvaud: We have not an extensive experience of aortic valve
replacement in children and young patients.
Reviewing all the literature on this subject, there is a lot of confusion
about the causes of degeneration. Most probably its from immunologic
origin, but its not totally clear which kind of process is involved.
Dr C. Yankah (Berlin, Germany): I congratulate you for this very
interesting study and results with the critical comments. I do also agree with
your conclusion, entirely, that this type of valve replacement is not suitable
566 S. Chauvaud et al. / European Journal of Cardio-thoracic Surgery 23 (2003) 560566
for children or young patients. My question is more technical. How did you
size the valves for the replacement?
Dr Chauvaud: We followed strictly the Acars guidelines regarding to
the size of the annulus of the recipient compared to the size of a homograft
and also the length of the anterior leaflet. We adapted the length of the
chordae to the distance between the tip of a papillary muscle to the
annulus,during the implantation of the homograft.
Dr A. Moritz (Frankfurt, Germany): May I ask you, the difference
between the durability of the aortic homograft is not as catastrophic as this
mitral homograft, fortunately. But the durability of the pulmonary side
seems to be somewhat better than the aortic, so it may very well be that the
mechanical stress plays a role. Do you have any experience, or do you
know, there are only a few cases I think reported about the tricuspid
homograft, is there an improved durability compared to the mitral?
Dr Chauvaud: In our experience, and in what is published on the
tricuspid replacement with mitral homograft on the tricuspid valve, patients
are adults. And we know that a gradient of 5 10 mm could be well
tolerated on the right side. At the present time, I have no data, about early
degeneration of mitral homograft on the right side compared to what I
presented on the left side.
Dr Acar: I just wish to make a comment in addition to Dr Chauvauds
presentation. Regarding the durability of the mitral homograft, presently we
are reviewing the whole series of patients. We have a series of over 90
cases, including two-thirds of complete homograft and one-third of partial
homograft. Definitely, as Sylvain just mentioned, its the durability that
doesnt seem to meet the expectation, and we do not feel that we can
recommend today using a mitral homograft in a young patient. This could
have been a good alternative to bioprosthetic valve since there is no idea of
substitute in this age group. But meanwhile, waiting for the complete results
of our series, which has now a 10-year follow-up, we feel that it is not a
good alternative in this age group.
Dr C. Mestres (Barcelona, Spain): You just mentioned that there is
degeneration in both the chordae tendineae. But at which level, tip of the
papillary muscle, halfway the chordae in the subleaflet area, or whatever?
And you say that 20 h before cryopreservation, that means how was warm
ischemic time and cold ischemic time on the average?
Dr Chauvaud: Regarding the final aspect of a chordae tendineae, there
is an absence of endothelium and the collagen is totally disorganized, the
inflammatory response on the chordae is very weak. Inflammation is much
more important on the leaflet tissue itself. The ischemic time was 25 h
between harvesting and cryopreservation. Is that the answer you expected?
Dr Mestres: I was asking how long was the warm ischemic time and the
cold ischemic time?
Dr Chauvaud: The warm ischemic time is very short. As soon as the
heart is arrested, it is placed in cold saline, which is not cryopreservation.
And later it is prepared for cryopreservation.