(Circulation. 1999;100:II-103.)
© 1999 American Heart Association, Inc.
Surgery for Valvular Heart Disease |
From the Department of Academic Surgery, National Heart and Lung Institute, Royal Brompton Hospital, Sydney Street, London, UK.
Correspondence to Prof Sir Magdi Yacoub, Department of Cardiothoracic Surgery, National Heart and Lung Institute, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK. E-mail g.carr-white{at}rbh.nthames.nhs.uk
| Abstract |
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Methods and ResultsA total of 47 patients who had undergone
1
previous aortic valve replacement were randomized to receive either a
pulmonary autograft (24 patients aged 40±11 years) or an
aortic homograft (23 patients aged 37±11 years) for rereplacement of
the aortic valve. One early death occurred in the homograft group, and
1 late (7 months) death occurred in the autograft group. One patient
who received a pulmonary autograft was reoperated on for
inflammatory pulmonary stenosis. One patient in each
group was reopened for bleeding (both within 24 hours). Two patients in
the autograft group had postoperative neurological weakness; they fully
recovered over 2 months. Hospital stay, blood loss, incidence of
perioperative arrhythmia, and markers of
coronary ischemia were similar between the 2 groups. At
6-month follow-up (range, 1 to 12 months), left ventricular
end-diastolic diameter was similar in both groups
(homografts, 5.0±0.9 cm; autografts, 5.2±0.6 cm;
P=NS), and no patient in either group had significant
aortic valve dysfunction.
ConclusionsRereplacement of the aortic valve with a pulmonary autograft is feasible and safe in patients aged 14 to 60, regardless of their preoperative diagnosis or clinical condition.
Key Words: aorta valves autograft surgery
| Introduction |
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| Methods |
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Operative Technique
All operations were performed by the same surgeon (M.Y.).
Cardiopulmonary bypass with moderate hypothermia (30°C) was
used. In both groups, myocardial protection was achieved by either
antegrade crystalloid or cold blood cardioplegia. Patients were cooled
to 28°C under total cardiopulmonary bypass. Myocardial
preservation was achieved using crystalloid cardioplegia at 4°C (St.
Thomas hospital No. 1) infused through the aortic root or directly
into the coronary ostia. The myocardial temperature (measured
by a myocardial temperature probe placed in the ventricular
septum) was reduced to <10°C. Cardioplegia infusions were repeated
every 20 minutes. The left ventricle was vented through the apex in all
cases.
The aortic valve was exposed through a curved aortotomy, commencing anteriorly and extending into the middle of the noncoronary cusp. This allowed excellent exposure of the valve. All patients underwent aortic root replacement with coronary reimplantation. The left ventricular outflow tract was reconstructed with either a homovital or antibiotic sterilized aortic homograft or the pulmonary autograft. In all cases, an interrupted 4-0 proximal suture line was used. For coronary reimplantation, continuous 4-0 sutures were used for the distal aortic suture line. In the autograft group, the right ventricular outflow tract was reconstructed with a large homovital or antibiotic sterilized pulmonary homograft (mean size, 25 mm; range, 23 to 28 mm) conduit inserted by continuous 4-0 sutures, without the inclusion of strips of prosthetic or autologous tissue for support. These suture lines were placed before release of the aortic clamp.
In the presence of endocarditis, aggressive and complete debridement of the infected and necrotic tissue was performed, and no foreign material was used for reconstruction. This subgroup of patients received intravenous antibiotics for 6 weeks after the operation. Even in those patients with endocarditis in whom extensive debridement of the aortic root was necessary, no additional problems with filling tissue defects were encountered with root replacements. In all patients, additional care was necessary in enucleating the pulmonary autograft due to the frequent dense adhesions to the scarred aortic root. When necessary, parts of the adherent aortic root were taken out with the autograft. In all patients, the facing sinus of the autograft (which is thin and not supported by pericardium) was placed in the left coronary sinus position of the new aortic root.
Intraoperative transesophageal echocardiography was used to monitor valve and ventricular function before and after insertion of the graft. Valve function was judged to be good echocardiographically in all patients immediately after release of the aortic clamp. X-clamp and bypass times were significantly longer in the autograft group (132±15 and 194±34 minutes) than the homograft group (98±16 and 136±25 minutes; P<0.001). Trasylol was used routinely in all patients.
Follow-Up
Early mortality was defined as any death within 30 days or
during initial hospitalization. Postoperative valve-related morbidity
and mortality were evaluated and reported according to standard
definitions.13 All patients had a clinical examination,
chest x-ray, ECG, and color flow Doppler echocardiogram before
discharge, at 6 months, and at yearly intervals after that. Doppler
velocities were calculated at the level of the right and left
ventricular outflow tracts and at the level of the aortic
valve orifice, and mean and peak gradients were derived by the modified
Bernoulli equation. Aortic valve insufficiency was graded according to
the method described by Perry et al.14
Regurgitation not severe enough to be measured by these
criteria was considered trivial. Fractional shortening (FS) was
calculated as FS=[(EDD-ESD)/EDD]x100, where EDD is the
end-diastolic dimension and ESD is the end-systolic
dimension.
Statistical Analysis
Statistical analysis was performed with a commercially
available software package (SPSS Inc). Comparison of demographic and
preoperative data between groups was performed with the use of an
unpaired t test. Comparison of data over time was done with
the use of a 1-way ANOVA. P<0.05 was significant.
| Results |
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Reoperation
One patient in the autograft group needed reoperation 18
months postoperatively for pulmonary stenosis. During
the operation, the pulmonary homograft was compressed by
granulation tissue, and subsequent histological and
microbiological examination showed only an inflammatory response, with
no evidence of endocarditis or an underlying cause.
Morbidity
Postoperative complications included re-exploration for
bleeding in 2 patients (1 in each group) and hemiparesis, which
completely resolved over 2 to 3 months, in 2 patients in the autograft
group. No statistically significant differences were identified between
the 2 groups with regard to total blood loss or hospital stay. No
patient in either group had electrocardiographic or biochemical
(creatinine kinase MB) evidence of significant
postoperative myocardial ischemia or infarction. Transient
atrial arrhythmia, which had resolved by discharge, was
present in 5 patients in each group. One patient in each group
developed complete heart block, necessitating implantation of a
permanent pacemaker. Postoperatively, all patients were either in New
York Heart Association class I or II, with no significant difference
between the 2 valve groups (P=0.63, unpaired t
test). No evidence of postoperative endocarditis was seen in either
group.
Hemodynamic Follow-Up
Postoperative echocardiographic evaluation of left
ventricular diameters and aortic and pulmonary
valve function were carried out at regular intervals (Table 2
). Left ventricular
diastolic diameter was reduced in both groups over the
first postoperative year when compared with the preoperative value
(homografts by 22%, autografts by 11%; P=NS by 1-way
ANOVA).
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| Discussion |
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Our study population was a subset of an ongoing randomized, controlled trial, and it was not part of a separate randomization process; however, we think that the patient groups are similar enough to allow simple comparisons regarding the short-term safety of using a pulmonary autograft. Two potential early disadvantages of using a pulmonary autograft, particularly in patients who have undergone previous cardiac surgery, are the increased complexity of the surgery and the increased risk of coronary artery injury. It is, therefore, reassuring to note that in our group of patients, no differences existed between the groups with regard to blood loss, hospital stay, inotrope use, or postoperative myocardial ischemia. Given the patient numbers involved and the diversity of ventricular function in patients who have undergone previous aortic valve replacement, precise comparisons of ventricular function are impossible. However, in both groups, left ventricular function seems to be preserved, with improvement in end-diastolic diameters over the first postoperative year. In addition, all patients postoperatively are either in New York Heart Association class I or II.
One patient developed inflammatory pulmonary stenosis, but the cause of this was unclear. The lack of cusp involvement or valve destruction suggests that an immunologically mediated mechanism or occult infection was not the cause; the histologic examination demonstrated an extrinsic perivalvular inflammatory infiltrate and suggests a chronic perivalvular inflammatory process, the cause of which is not known.
This study shows that although pulmonary autograft implantation is a technically more complex operation in patients having a second or subsequent aortic valve replacement, it carries a low risk of death and complications. The mortality and complication rates were comparable to those for the implantation of either homografts or other substitutes, both in this study and others.7 15 17 18 Further follow-up is needed to determine if the potential long-term advantages of pulmonary autografts are realized. Long-term monitoring of pulmonary valve and right ventricular function and neurological events will continue to be important in those who have undergone pulmonary autograft operations.
| Acknowledgments |
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| References |
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