TUESDAY AFTERNOON, MAY 5, 1998
1:45 p.m. SIMULTANEOUS
SCIENTIFIC SESSION A CONGENITAL HEART DISEASE
Ballroom A, Hynes Convention
Center
Moderators: Frank L. Hanley, M.D.
Thomas L. Spray, M.D.
19. MULTIPLE VENTRICULAR SEPTAL DEFECTS:
HOW AND WHEN SHOULD WE REPAIR?
Francesco Seddio, M.D.*, Doff B.
McElhinney, M.S.*, V. Mohan Reddy, M.D.*, Wayne Tworetzky, M.D.*, Norman H.
Silverman, M.D.* and Frank L. Hanley, M.D.
San Francisco, California
Discussant: Constantine
Mavroudis, M.D., Chicago, Illinois
Congenital heart lesions with multiple ventricular septal
defects (VSDs) remain a surgical challenge. Difficult exposure of VSDs in the
trabecular component of the septum, especially the apical and anterior
portions, complicates closure of such defects. Traditional approaches often
rely on either ventriculotomy for exposure or palliation with pulmonary artery
banding (PAB). Both of these techniques have potential drawbacks, so it is
important to limit their use to pts in whom they will provide optimal benefit.
However, indications for closure vs palliation and for various approaches to
surgical exposure are not clearly defined. Since 1992, 32 pts with multiple
VSDs have undergone surgery for this condition. Median age was 86 days and all
but 4 pts were infants. Associated lesions were present in 27 pts, including
transposition of the great arteries (9), aortic coarctation (4),
atrioventricular septal defect (3), interrupted arch (2), tetralogy of Fallot
(1), patent ductus arteriosus (3), atrial septal defect (3), and other defects
(3). Prior operations had been performed elsewhere in 8 pts, including PAB in
6. Each pt had ≥ 2 VSDs (median 3). VSDs were perimembranous in 13 pts,
inlet in 6, outlet in 2, anterior muscular in 13, posterior muscular in 10,
apical in 21, and mid-muscular in 15. "Swiss cheese" VSDs were present in 6
pts, 5 of whom had prior PAB. Initially, 25 pts underwent complete repair, all
through right atriotomy except 1 who also required aortotomy. Seven pts were
palliated with PAB (5) or other procedures. No pt received a ventriculotomy. In
the pts who underwent complete repair, a combination of patch and suture
closure was used in 16, patch only in 6, and sutures only in 3. In pts with
muscular VSDs, the left side of the septum was explored through an aortotomy or
a larger VSD when possible, which aids in visualization and closure of defects
in the trabecular septum. There was 1 early death in a pt who had staged repair
of coarctation and multiple VSDs. 3 palliated pts underwent early reoperation
for PAB revision due to failure to thrive (1), PAB revision and then VSD
closure for failure to thrive (1), or PAB removal after spontaneous closure of
the VSDs led to decompensation (1).
Thus, 3 of 7 palliated pts required early reoperation. Pacemakers were placed
for atrioventricular dissociation in 2 pts, but sinus rhythm returned in both.
At median followup of 22 mos (4.49 mos), there was 1 death in a palliated pt
and 1 other palliated pt had a heart transplant for cardiomyopathy. Another
palliated pt had the PAB removed and multiple apical VSDs closed 8 mos later
after outgrowing the band. No pts have hemodynamically significant residual
VSDs or persistent rhythm abnormalities. In our experience, palliation of
multiple VSDs is associated with greater morbidity than primary repair. Almost
all cases of multiple VSDs can be repaired adequately in early infancy without
ventriculotomy, though "swiss cheese" VSDs are still an indication for
palliation.
*By invitation
20. TRANSATRIAL-TRANSPULMONARY TETRALOGY
REPAIR IS EFFECTIVE IN THE PRESENCE OF ANOMALOUS CORONARIES.
Christian P.R. Brizard, M.D.*,
Andrew D. Cochrane, F.R.A.C.S.*and Tom R. Karl, M.D.
Melbourne, Australia
Discussant: John W. Brown,
M.D., Indianapolis, Indiana
Objectives: To analyze the
outcome of transatrial-transpulmonary tetralogy repair in children with an
anomalous coronary crossing the RV outflow tract. Methods: 34/548 (6.2%) of our
tetralogy repairs were associated with surgically relevant coronary artery
anomalies. The median age and weight at repair were 25.8 months (4.4-88) and 10
kg (5-20). All patients had a major branch crossing the right ventricular
outflow tract. Anomalies included LAD from RCA (n = 19), RCA from LCA or LAD (n
= 10), large RCA conus branch (n = 4), and single RCA (n = 1). Diagnosis was
established preoperatively in 24/34 with angiography (n = 23) or echo (n=1).
Transatrial-transpulmonary repair was successfully used in 31 patients, and 24
of whom required a limited transannular patch in the RVOT. Three additional patients
had a RV-PA conduit due to proximity of the coronary branch to the PA annulus,
and inability to relieve the right ventricular outflow obstruction adequately.
Results: There has been no
early or late mortality. Mean RV-PA gradient at last follow-up was 18mm
(SD=10.6), compared to 15mm (SD = 24) for patients with normal coronaries
operated by a similar approach. Actuarial freedom from reoperation at 105
months was 95% (± 4.9%), which was also similar to results of
transatrial-transpulmonary repair in children with TOP and normal coronaries (p
> 1.0).
Conclusions: Surgically
important coronary anomalies in TOP can be dealt with using the
transatrial-transpulmonary approach in most cases, without major alterations in
technique. Outcome is similar to that for other TOP patients. Thus, the
presence of anomalous coronary has not imparted incremental risk following this
surgical strategy.
*By invitation
21. SINGLE STAGE REPAIR OF AORTIC ARCH
OBSTRUCTION AND ASSOCIATED INTRACARDIAC DEFECTS USING PULMONARY HOMOGRAFT PATCH
AORTOPLASTY.
Christo I. Tchervenkov, M.D.*,
Stephen A. Tahta, M.D.*, Marie J. Beland* and Luc C. Jutras*
Montreal, Quebec, Canada
Sponsored by: Ray C.-J. Chiu, M.D., Ph.D. Montreal,
Quebec, Canada
Discussant: Claude Planche,
M.D., Paris, France
Intracardiac malformations associated with coarctation and
aortic arch hypoplasia have traditionally been repaired in two stages, with a
high mortality. Recently, improved survival has been reported with a
single-stage approach predominantly using an extended end-to-end anastomosis to
repair the aortic arch. Herein, we review our experience with a single-stage
biventricular repair of intracardiac defects associated with aortic arch
hypoplasia using a pulmonary homograft patch aortoplasty. Between October 1988
and October 1997, 39 of 40 consecutive patients underwent a single-stage
biventricular repair for aortic arch obstruction and associated intracardiac
defects. The median age at operation was 17 days and the mean weight was 3.71 ±
1.09 kg. Nineteen patients had either d-transposition of the great arteries or
the Taussig-Bing anomaly. Sixteen patients had multiple left-sided obstructive
lesions (2 critical aortic stenosis, 3 subaortic stenosis and VSD, 11 class III
hypoplastic left heart syndrome as defined by Kirklin). One patient had an
associated complete atrioventricular septal defect. Four patients had only an
associated ventricular septal defect. By median sternotomy, the hypoplastic
aortic arch was enlarged with a pulmonary homograft patch in 36 patients. In 4
patients, an extended end-to-end anastomosis was performed.
There were 2 early deaths (5%) and 21 late deaths (5%).
One late death was non-cardiac related. The median followup time was 25 months
(range 1 month to 8 years). The recoarctation rate was 11% but excluding those
patients with associated left-sided obstructive lesions, this decreases to 0%.
No aneurysm formation in the aorta has occurred. The actuarial survival rate at
8 years is 89 ± 10%.
One-stage biventricular repair of aortic arch obstruction
and associated intracardiac defects can achieve excellent survival. We
recommend the pulmonary homograft patch aortoplasty of the hypoplastic arch
because it achieves complete relief of anatomical afterload with a tension-free
anastomosis and low incidence of recoarctation.
2:45 p.m. INTERMISSION - VISIT EXHIBITS
*By invitation
3:15 p.m. SIMULTANEOUS SCIENTIFIC SESSION A
CONGENITAL HEART DISEASE
Ballroom A, Hynes Convention
Center
Moderators: Frank L. Hanley, M.D.
Thomas L. Spray, M.D.
22. PRIMARY REPAIR IS SUPERIOR TO
INITIAL PALLIATION IN CHILDREN WITH ATRIOVENTRICULAR SEPTAL DEFECT AND
TETRALOGY OF FALLOT.
Hani K. Najm, M.D.*, Glen S. Van
Arsdell, M.D.*, Stefan Watzka*, Lisa Hornberger, M.D.*, John G. Coles, M.D.*
and William G. Williams, M.D.
Toronto, Ontario, Canada
Discussant: Hillel Laks, M.D.,
Los Angeles, California
Children presenting with atrioventricular septal defect in
conjunction with tetralogy of Fallot (AVSD/TOF) represent an uncommon complex
lesion. To explore the best management algorithm we undertook a review of this
institution's experience. From March 1981 to August 1997, 38 children were
referred to our division with the diagnosis of AVSD/TOF. Down's syndrome was
present in 32 (84%). Twenty one children were initially palliated with a
systemic to pulmonary artery shunt. Two (9.5%) died prior to repair. Complete
repair has been performed on 31 children. Of these 14 underwent initial
palliation with systemic to pulmonary artery shunt (mean age at shunt 20 ± 24
months). During complete repair the endocardial cushion defect was repaired
with two patches in 29 children. Relief of the right ventricular outflow
obstruction was by a transannular patch in 22 (70%), 12 (54%) of those had a
monocusp inserted, and 4 required an infundibular patch. Operative mortality
occurred in 2 (6.4%) children, one was previously palliated. Reoperations were
performed in 11 children, 7 (58%) were for pulmonary arterioplasty. The
incidence of reoperation was higher in the palliated versus the non palliated
groups (64% vs. 12%, P= 0.007). The palliated group were repaired at an older
age (78 ± 52 vs. 36 +19 months, P= 0.005), had longer ventilatory support (8 ±
11 rs. 4 ± 3 days, P= 0.05), longer inotropic support (8 ± 13 vs. 3.6 ± 1.5
days, P= 0.028), and longer hospital stay (23 ± 22 vs. 14 ± 5 days, P= 0.004).
There was one late death related to a reoperation for pulmonary arterioplasty
and residual ventricular septal defect in the palliated group. We conclude that
repair of AVSD/TOF can be achieved with low mortality. In this series initial
palliation with a shunt resulted in a more complex post-operative course and
carried a higher reoperative rate, mainly due to pulmonary artery
complications. Primary repair of AVSD/TOF at the time of symptomatic
presentation is superior to initial palliation followed by repair.
*By invitation
23. THE MODIFIED NORWOOD PROCEDURE FOR
HYPOPLASTIC LEFT HEART SYNDROME: EARLY TO INTERMEDIATE RESULTS OF 120 PATIENTS.
William J. Brawn, F.R.C.S.*Kozo
Ishino, M.D.*, Oliver Stumper, M.D.*, Joseph V. De Giovanni, F.R.C.P.*, Eric D.
Silove, F.R.C.P.*, John G.C. Wright, F.R.C.P.* and Babulal Sethia, F.R.C.S.*
Birmingham, England
Sponsored by: Marc de Leval,
M.D., London, England
Discussant: Roger B.B. Mee,
M.B., Ch.B., Cleveland, Ohio
Background: Classical
first-stage Norwood repair of hypoplastic left heart syndrome (HLHS) utilizes
homograft patch enlargement to obtain an unobstructed aorta and coronary
arteries. Because of possible disadvantages of the homograft such as lack of
growth, degeneration and calcification, and homograft availability, we have
tried to repair the aorta without patch supplementation.
Method and Results: Between
February 1993 and September 1997, 120 patients, aged 0 to 47 days (median, 4
days) and weighing 1.7 to 4.4 kg (median, 3.1 kg) underwent first-stage
palliation for HLHS. The ascending aortic diameter ranged from 1.5 to 8 mm
(median, 3.0 mm). Eight patients had an anomalous right subclavian artery
(ARSCA) arising from the descending aorta In 95 patients (Group I), all ductal
tissue was excised, the descending aorta anastomosed to the aortic arch which
had been opened back to the ascending aorta, then to this confluence was
anastomosed the proximal main pulmonary artery. In the remaining 25 patients
(Group II), continuity of the aortic arch was maintained and the repair was
performed with a Damus anastomosis. The size of the systemic-to-pulmonary shunt
was 3.5 mm (70), 3 nun (48), and 4 mm (2). Circulatory arrest time ranged from
19 to 105 Min (median, 54 Min). A homograft patch was necessary for the arch
reconstruction in a total of 18 patients (15.0%); 9 Group I patients (9.5%) and
9 Group II (36.0%) (p< 0.01). There were 82 hospital survivors (68.3%); 69
Group I (72.6%) and 13 Group II (52.0%) (p<0.05); 71 patients without patch
(69.6%) and 11 with patch (61.1%) (p = NS). By multiple logistic regression,
risk factor for hospital death included ascending aortic diameter ≤ 2 MM
(p = 0.1018) and the ARSCA (p = 0.039). There were 6 late deaths. Sixteen of 71
patients (22.5%) who underwent second-stage palliation had developed neo-aortic
arch obstruction with a peak gradient > 10 mmHg; 14 Group I (19.4%) and 2
Group II (22.2%) (p = NS); 15 without patch (23.1%) and one with patch (16.7%)
(p = NS). Overall survivals were 56.7% at 1 year and 55.0% at 2 years.
Conclusion: The modified
Norwood procedure without the use of exogeneous material does not result in an
increased incidence of neo-aortic arch obstruction and may allow better
long-term growth of the neo-aorta.
1973-74 AATS Graham Fellow
*By invitation
24. POST-ISCHEMIC HYPERTHERMIA EXACERBATES
NEUROLOGICAL INJURY FOLLOWING DEEP HYPOTHERMIC CIRCULATORY ARREST.
Dominique Shum-Tim, M.D.*, Mitsugi
Nagashima, M.D.*, Toshiharu Shin'oka, M.D.*, Jan Bucerius, M.D.*, Georg
Nollert, M.D.*, Hart G.W. Lidov, M.D.*, Adre du Plessis, M.D.*, Peter C.
Laussen, M.D.* and Richard A. Jonas, M.D.*
Boston, Massachusetts
Discussant: Julie A. Swain,
M.D., Lexington, Kentucky
Background: Aggressive
surface warming is common practice in the pediatric intensive care unit; also,
fever is commonly seen after cardiopulmonary bypass (CPB). Recent rodent data
emphasizes the protective effect of mild (2-3°C) hypothermia after cerebral
ischemia. The purpose of this study was to evaluate different temperature
regulation strategies after deep hypothermic circulatory arrest (DHCA) using a
survival piglet model. Methods: Fifteen piglets (9.1 ± 1.1 kg)
were randomized into 3 groups (n = 5/group) and a small temperature probe was
inserted in the superficial temporal cortex. All groups underwent 100 min. of
DHCA at 15°C and 40 min. of reperfusion with a Hct of 25% during CPB. Brain
temperature was maintained at 34°C for 24 hr after coming off CPB in Gp I, 37°C
in Gp II, and 39°C in Gp III, respectively. The cerebral redox state was
determined by near infrared spectroscopy (NIRS) during and 3 hr after CPB.
Neurobehavioral recovery was evaluated daily for 3 days after extubation in a
blinded fashion by neurological deficit score (NDS; 0 = normal, 500 = brain
death) and overall performance capacities (OPC; 1 = normal, 5 = brain death).
Body weight gain and total body water content indicated by electrobioimpedance
were evaluated at 3 hr, 24 hr, and 4 days post-operatively. Brain was fixed in
situ on day 4 and the hemisphere contralateral to the probe was examined and
scored for ischemic injury (0 = normal, 5 = necrosis) in a blinded fashion. Results:
All results are expressed as mean or percentage ± SD. P-value <0.05 is
considered significant. One animal in Gp III died on day 3 due to severe
neurological impairment. There were no differences in % body weight gain and
bioimpedance after CPB. At 24 hr, Gp III animals had significant changes in
weight line break (Gp 1= 109.3± 1.7%, Gp II = 113.6 ±6.3%, and Gp III = 117.9 ±
3.4%; p<0.05 Gp I vs III) and bioimpedance (Gp I = 83.9 ± 12.5%, Gp II =
74.0 ± 9.6%, and Gp III = 62.9 ± 10.8%; p<0.05 Gp I vs III) suggesting total
body edema. There were no significant differences in NIRS signals throughout CPB.
Recoveries of NDS, OPC, histology and NIRS were significantly worse in
hyperthermic Gp III. There was a trend towards reduced injury in Gp I (see
table).
|
Table
|
NDS
|
OPC
|
Histology (POD 4)
|
Oxy-Hb
|
Deoxy-Hb
|
Cyt. a,«3
|
|
|
|
|
cortex
|
hippocampus
|
caudate
|
2hr off CPB
|
2hr off CPB
|
2hr off CPB
|
|
GpI
|
30.0±28.3
|
1.0±0.0
|
0.0 ± 0.0
|
0.0 ±0.0
|
0.8 ± 1.0
|
22.7±12.5
|
-28.7±9.0
|
3.9±0.6
|
|
GpII
|
87.0±59.4
|
1.4±06
|
1.0±1.2
|
0.0 ± 0.0§
|
0.8 ± 1.0
|
9.9±8.4
|
-10.1±20.6
|
05±2.1§
|
|
GplII
|
186.0±131*
|
2.8±1.3#
|
2.8 ± 1 8#
|
2.4 ± 0.9#
|
2.2 ±1 8
|
-13.5±12.1*
|
25.3±16.4*
|
-3.9±2.3*
|
|
p <
0.05 Gp I vs III by ANOVA and Bonferroni, #p< 0.05 Gp I vs III by
Mann-Whitney u tests
§ p <
0.05 Gp II vs III
|
Conclusions: Mild
post-ischemic hyperthermia significantly exacerbates functional and structural
neurological injury after DHCA. Fever and active warming above 37°C should be
avoided after DHCA. A mild degree of hypothermia may reduce cerebral injury
after prolonged DHCA.
*By invitation
25. IS IT NECESSARY ROUTINELY TO
FENESTRATE AN EXTRACARDIAC FONTAN?
LeNardo D. Thompson, M.D.*, Edwin
Petrossian, M.D.*, Doff B. McElhinney, M.S.*, Natalia A. Abrikosova, M.S.*,
Andrew J. Parry, M.D.*, V. Mohan Reddy, M.D.* and Frank L. Hanley, M.D.
San Francisco, California
Discussant: John E. Mayer,
M.D., Boston, Massachusetts
Fenestration (FEN) of a Fontan connection has been
proposed as a means of improving outcomes of single ventricle palliation by
allowing partial decompression of the Fontan pathway. The benefit of FEN is
likely to be greatest in the early postoperative period, when pts may
experience increased pulmonary vascular resistance and decreased systolic and
diastolic cardiac function due to the effects of cardiopulmonary bypass (CPB),
aortic cross-clamping (ACC), and positive pressure ventilation. However, there
are potential drawbacks to FEN, including arterial desaturation, complications
of a right-left shunt, and the need for another procedure to close the
communication, suggesting that routine use may not be in the best interest of
all pts. The utility of FEN with the extracardiac conduit Fontan operation has
not been determined. Since 1992, 60 pts have undergone a modification of the
Fontan procedure in which an extracardiac inferior cavopulmonary conduit is
used in combination with a previously staged bidirectional Glenn anastomosis.
FEN was performed selectively in 32 pts (54%). Among the last 25 pts, FEN was
used in only 6 (24%). In 7 pts, a FEN was placed or clipped in the early
postoperative period without CPB. CPB time did not differ between the 2 groups
(108 vs 122 rain), but significantly fewer non-fenestrated than fenestrated pts
had ACC (3 vs 8; p<0.05). There were no operative deaths. Prolonged (>2
wks) pleural drainage occurred in 12 pts, 8 with FEN and 4 without. Fontan and
common atrial pressures 1 day after surgery did not differ between
non-fenestrated and fenestrated pts (13.1 vs 12.6 mmHg and 4.8 vs 5.8 mmHg,
respectively). At followup ranging to 5 yrs, there were 2 late deaths and no
pts developed protein losing enteropathy. These data suggest that there is no
difference in outcome between pts who undergo the extracardiac conduit Fontan
procedure with and without FEN. The extracardiac Fortran operation has a number
of advantages that minimize the need for and utility of FEN, including
avoidance of ACC, shorter duration of CPB, and a more streamlined hydrodynamic
connection. These factors help optimize ventricular and pulmonary vascular
function in the early postoperative period, which contributes to improved
hemodynamics. Moreover, when necessary, a FEN can be placed or revised without
return to CPB, which allows for more accurate and practical assessment of the
need for FEN after the Fontan connection has been completed. We conclude that
FEN is of no benefit in the majority of Fontan pts when an extracardiac conduit
technique as described is used, and therefore FEN should not be performed
routinely.
4:35 p.m. EXECUTIVE
SESSION (Limited to Members)
Ballroom B, Hynes Convention
Center
6:30 p.m. MEMBER RECEPTION
Museum of Science
*By invitation
1:45 p.m. SIMULTANEOUS SCIENTIFIC SESSION B
ADULT CARDIAC SURGERY
Ballroom B, Hynes Convention
Center
Moderators: Bruce W. Lytle, M.D.
Marko I. Turina, M.D.
26. DISENTANGLING PENETRATING ULCER AND
INTRAMURAL HEMATOMA OF THE THORACIC AORTA FROM CLASSIC TYPE A AND B
DISSECTIONS.
Michael A. Coady, M.D.*, John A.
Rizzo, Ph.D.*, Graeme L. Hammond, M.D., Lee J. Goldstein, B.A.*, Gary S. Kopf,
M.D. and John A. Elefteriades, M.D.
New Haven, Connecticut
Discussant: Nicholas T.
Kouchoukos, M.D., St. Louis, Missouri
Classic type A and B aortic dissections have been well
described, however, less is known about the natural history of penetrating
atherosclerotic ulcers (PU) and intramural hematomas (IMH) of the thoracic
aorta. PU are atherosclerotic plaques which disrupt the internal elastic
lamina, burrow deeply through the intima into the aortic media, and cause a
localized intramedial dissection. The diagnosis is made on CT scan by
demonstration of a contrast-filled outpouching in the aorta in the absence of a
dissection flap or a false lumen. Patients with IMH have a hematoma in the
media but have no evidence of an atheromatous ulcer on imaging studies, and an
intimal tear is not visualized. The objective of this study is to determine the
natural history of PU and IMH and assess appropriate therapeutic correlates of
the natural history. Data on 198 patients with aortic dissection (86 type A and
112 type B) treated at our institution from 1985 to 1997 were analyzed. The
aortic dissection database includes 431 imaging studies (MRI, CT, and ECHO). Of
the 198 patients, 27 individuals (13.6%) were found to have either a PU or IMH
by CT/MRI imaging studies, intraoperative findings, or pathology reports. For
PU and IMH, 5 cases (18.5%) were located in the ascending aorta, and the remaining
22 (81.5%) were in the descending aorta.
A chart review was conducted in all patients with type A
and type B dissections, PU, and IMH to evaluate rates of rupture and further
define the natural history. The follow-up period ranged from 2 to 107 months,
with a mean of 26.2 months. Sixteen of the 27 patients with PU or IMH (59.3%)
had malignant courses (7 patients (25.9%) went on to require aortic replacement
and another 9 (33.3%) died of aortic rupture prior to surgery). Results of
univariate analyses are summarized in the table and figure below. Patients with
PU and IMH, in comparison to type A or B thoracic aortic dissections, affect an
older age population, present with larger aortic diameters, occur primarily in
the descending aorta, are associated more often with a prior diagnosed or
treated AAA. The risk of aortic rupture is higher in patients with PU and IMH
(9/27, 33.3%) than in patients with type A (6/86, 6.97%) (p<0.0003) or type
B (4/1 12, 3.57%) aortic dissection (p<0.0001). One year survival is less
for patients with penetrating ulcers (71%), as opposed to patients with type A
(90%) or B dissections (90%) (p<0.05).
|
|
Penetrating Ulcer/ Intramural
Hematoma
|
Type
Dissection
|
Type B
Dissection
|
|
Patients
|
27 (15m, 12 f)
|
86 (61m, 25 f)
|
1 12 (70 m, 42 f)
|
|
Age
|
73.9 years ± 8.2*
|
52.7 years ±17.6
|
67.1 years ± 13.3*
|
|
Initial
Aortic Size
|
6.45 cm ± 1.9
|
5.63 cm ± 1.5
|
5.4 cm ± 1.6
|
|
Prior AAA
|
8 (29.6%)
|
8 (9.3%)**
|
35 (31.2%)**
|
|
|
Table
reports means ± standard deviation, *p = 0.01, p < 0.0001, **p = 0.001
|

We conclude that accurate recognition at initial
presentation is critical for optimal clinical management of these patients. PU
and IMH presenting acutely must be differentiated from classic acute
dissections. For PU and IMH, the prognosis is more serious than with classic
acute aortic dissection. Surgical treatment should be considered strongly at
presentation.
*By invitation
27. RUPTURE OF CHRONIC TYPE B DISSECTING
ANEURYSMS: A NATURAL HISTORY STUDY.
Tatu Juvonen, M.D.*, M. Arisan
Erigan, M.D., Jan D. Galla, M.D.*, Steven L. Lansman, M.D., Jock N. McCullough,
M.D.*, Khanh H. Nguyen, M.D.*, David Spielvogel, M.D.*, James J. Klein, M.D.*, Carol A. Bodian, Dr.PH.* and Randall B. Griepp, M.D.
New York, New York
Discussant: D. Craig Miller,
M.D., Stanford, California
In an attempt to identify risk factors for rupture and to
improve management of patients with type B dissection who survive the acute
phase without operation, we have studied 59 patients using serial
computer-generated 3-dimensional CT scans. Patients were included if they did
not undergo surgery during the acute phase of a documented type B dissection,
and had at least two CT scans a minimum of three months apart thereafter. The
median duration of followup was 4.4 years (range 0.3-9.1), and the median
interval between scans was 204 days (98-655) in the unoperated group and 258
(61-443) days in those who ruptured.
During followup, four patients
died of causes unrelated to the aneurysm, and nine patients underwent elective
aneurysm resection because of large aneurysm size, rapid expansion, or
development of symptoms: they are not considered further. Eleven patients (19%)
experienced rupture, and 35 remain alive without operation or rupture. Possible
risk factors for rupture and various dimensional parameters are shown below:
the data for patients with rupture are from their last CT scans, and the data
for patients still in nonoperative followup are from their penultimate studies.
Data in the table are medians or percents; p values were derived using the
Wilcoxon rank sum test for quantitative data, and Fisher's exact test for
categorical data.
|
Risk
Factors
|
No
Operation or Rupture
|
Rupture
|
p
value
|
|
|
(n = 35)
|
(n =
11)
|
|
|
Age
(years)
|
67
|
73
|
0.05
|
|
Years
since dissection
|
3.0
|
3.4
|
NS
|
|
Male(%)
|
63
|
46
|
NS
|
|
Pain(%)
|
26
|
55
|
0.14
|
|
COPD(%)
|
14
|
46
|
0.04
|
|
Smoking
(%)
|
54
|
64
|
NS
|
|
Hypertension
(%)
|
69
|
73
|
NS
|
|
False
lumen open (%)
|
59
|
71
|
NS
|
|
Aortic
Dimensions (3dCT)
|
|
|
|
|
Descending diameter (cm)
|
4.7
|
5.4
|
0.05
|
|
Descending volume (cm3)
|
268
|
285
|
NS
|
|
Abdominal diameter (cm)
|
3.7
|
4.7
|
0.02
|
|
Abdominal volume (cm3)
|
97
|
171
|
0.03
|
Patients in whom aortic rupture occurred were
significantly older, and they were significantly more apt to have a history of
COPD when compared with those without rupture; they were also somewhat more
likely to have complained of pain at the time of their last visit. In addition,
the size and extent of the aneurysm appears to have significant predictive
value: patients who subsequently experienced rupture had significantly larger
descending aortic and abdominal aortic diameters and a significantly larger
abdominal aortic volume than were observed in patients whose aneurysms remained
intact. These data indicate that older patients with larger and more extensive
aneurysms following acute type B dissections, especially if they have a history
of COPD, are significantly more likely to experience rupture than younger
patients with smaller chronic type B aneurysms. The presence of a persistently
patent false lumen does not appear to increase the risk of rupture. Overall, our
data from patients who have entered the chronic phase of type B dissection
reveal a pattern which bears a striking resemblance to the natural history of
patients with nondissecting aneurysms, suggesting that operative guidelines for
patients with chronic type B dissections should be similar to those for
patients with other types of chronic descending thoracic and thoracoabdominal
aneurysms.
*By invitation
28. SURGERY FOR ASCENDING AORTIC AND ARCH
ANEURYSM: ANTEGRADE AORTIC PERFUSION AVOID NEUROLOGICAL COMPLICATIONS.
Francesco Musumeci, M.D.*,
Giovanni Casali, M.D.*, Frank Dunstan, Ph.D.*, Antonino Marullo, M.D.* and
William J. Penny, M.D.*
Cardiff, Wales
Sponsored by: Lawrence H. Cohn,
M.D., Boston, Massachusetts
Discussant: G. Michael Deeb,
M.D., Ann Arbor, Michigan
Background. Femoral
arterial cannulation is commonly used for cardiopulmonary bypass (CPB) with
ascending aortic (AAo) and arch aneurysm. Retrograde cerebral embolization,
retrograde aortic dissection and lower limb ischaemia are well recognized
complications. In order to minimize these events, since 1991 we have used
direct cannulation of the aneurysmal AAo for CPB. This paper reviews our
experience and the effectiveness of antegrade aortic perfusion in reducing
postoperative neurological events.
Methods. Between
December 1991 and June 1997, 84 consecutive pts (50 males; age range 6 to 83
(median 54) yrs) were operated on. Twenty-four (26.4%) were older than 70 yrs.
All pts were evaluated by preoperative CT or MRI and perioperative echocardiography.
The aneurysm involved the AAo only in 39 pts and in 45 extended also to the
aortic arch. When replacing the AAo, the aortic root was also replaced in 71
pts, 9 had root remodelling and 4 aortic valve replacement. In addition, 45 pts
had arch replacement (partial 19, total 24, elephant trunk 2). Direct
cannulation of the aneurysmal AAo and bicaval venous return was used for CPB.
Cerebral protection was achieved with hypothermic circulatory arrest to a
temperature of 15 to 28°C. Continuous retrograde cerebral perfusion (RCP)
through the superior vena cava was used in 24 pts when circulatory arrest time
was longer than 30 min. All pts had a short period of RCP for de-airing prior
to re-establishing CPB. The arterial cannula was repositioned within the distal
sutureline, proximal to the innominate artery. Median circulatory arrest, cross
clamp and CPB time were 19 (range, 8 to 53) min, 89 (range, 48 to 1 64) min and
122 (range, 82 to 206) min, respectively.
Results. Two pts
aged 74 and 76 died in hospital (2.5%) due to respiratory (1) and renal (1)
failure. Post-operative complications were bleeding (3) and prolonged
ventilatory support (4). No cerebral or peripheral embolic complications
occurred. At a mean follow up of 29 (3 to 69) months, there were 3 late deaths.
The estimated 4 yr survival rate is 93% (SE 7%).
Conclusion. Direct
cannulation of the aneurysmal AAo is a simple and safe alternative to femoral
artery cannulation. Antegrade flow throughout the procedure associated with a
period of RCP at the end of circulatory arrest was not associated with
neurological embolic events. These excellent results suggest that this
technique is worthy of further evaluation in a prospective manner.
2.45 p.m. INTERMISSION
- VISIT EXHIBITS
*By invitation
3:15 p.m. SIMULTANEOUS SCIENTIFIC SESSION B
ADULT CARDIAC SURGERY
Ballroom B, Hynes Convention
Center
Moderators: Bruce W. Lytle, M.D.
Marko I. Turina, M.D.
29. MITRAL VALVE REPAIR FOR DEGENERATIVE
DISEASE.
A. Marc Gillinov, M.D.*, Delos M.
Cosgrove, M.D., John H. Arnold, M.D.*, Nicholas G. Smedira, M.D.*, Joseph F.
Sabik, M.D.*, Patrick M. McCarthy, M.D., Craig R. Saunders, M.D.*, Bruce W.
Lytle, M.D., Robert W. Stewart, M.D.* and Floyd D. Loop, M.D.
Cleveland, Ohio
Discussant: Lawrence H. Cohn,
M.D., Boston, Massachusetts
Objective Degenerative
mitral valve disease has become the most common cause of mitral insufficiency
in the United States. Mitral valve repair is applicable to the majority of
these patients and has become the procedure of choice. This study was
undertaken to define the operative risk and to determine risk factors for late
mortality and reoperation.
Patients and Methods From
1985 to 1996, 1,101 consecutive patients (pts) had primary isolated mitral
valve repair for valvular insufficiency caused by degenerative disease. Mean
age was 58 ±12 years; 64% were male. Preoperative degree of mitral
regurgitation was 3.6 ± 0.9. Results There were 4 hospital deaths
(0.4%). Long-term followup was available in 1,089 pts (99%), with 4,319
pt-years of follow-up available for analysis. Eight-year actuarial survival was
84% and 8-year freedom from cardiac death was 94%. Univariate analysis
identified moderate or severe left ventricular dysfunction (p<0.001), older
age (p<0.001), chordal shortening (p<0.001) and earlier year of surgery
(p<0.001) and annulopasty alone (p = 0.001) as risk factors for late
mortality. At 8 years, freedom from thromboembolism was 92%, from endocarditis
99%, from anticoagulant-related hemorrhage 99%, and from reoperation 94%. Of
the 30 pts who required reoperation for late mitral valve dysfunction, 15 (50%)
repairs failed secondary to progressive degenerative disease. Univariate
analysis identified chordal shortening (p<0.02), earlier year of surgery
(p<0.001), and annuloplasty alone (p<0.001) as risk factors for
reoperation.
Conclusions For patients
with degenerative mitral valve disease, valve repair is associated with (1)
very low operative mortality rates, and (2) low rates of valve related
morbidity and mortality. (3) Isolated annuloplasty and chordal shortening
jeopardize late results.
*By invitation
30. IMPACT OF CORONARY ARTERY DISEASE AND
AGE ON LATE SURVIVAL IN PATIENTS UNDERGOING BIOPROSTHETIC AORTIC VALVE
REPLACEMENT.
Gideon Cohen, M.D.*, Tirone E.
David, M.D., Christopher M. Feindel, M.D., Joan Ivano, MSc.*, Michael Borger,
M.D.* and Susan Armstrong, MSc.*
Toronto, Ontario, Canada
Discussant: Robert W. Emery,
M.D., Minneapolis, Minnesota
Prolonged lifespan in a progressively aging population
will likely increase the incidence of aortic valve disease and the demand for
aortic valve replacement (AYR) well into the new millennium. To ensure maximal
event-free survival, age and lifestyle are routinely considered upon prosthetic
valve selection (tissue vs. mechanical). The presence of concomitant coronary
artery disease (CAD), however, may be overlooked in the decision-making
process. METHODS: Data were prospectively collected on 670 patients undergoing
bioprosthetic Hancock II AYR between 1982 and 1994. Follow-up was conducted
during a four month period in 1996 by clinic visit or telephone interview. All
events were verified. Longitudinal survival and freedom from reoperation were
evaluated univariately by Kaplan-Meier analysis and multivariately by Cox
regression.

RESULTS: Follow-up was 99.7%
complete at 69 ± 40 mos (median 66 mos; range 0.1-168 mos) with 75% of patients
having follow-up of at least 93 mos. Mean patient age was 65 ± 12 yrs (median:
68 yrs; range: 18-86 yrs). Survival was significantly different by Kaplan-Meier
analysis for both age <65 (71 ± 4% at 12 yrs) vs age > 65 (36 ± 7%, p =
0.0004) and no CAD (65 ± 4% at 12 yrs) vs CAD (35 ± 8%, p<0.0001). When both
variables were combined, patients <65 years of age with no CAD demonstrated
the best long-term survival, patients <65 years with CAD or patients
≥ 65 years without CAD demonstrated intermediate long-term survival, and
patients ≥ 65 years with CAD demonstrated the poorest long-term survival
(p<0.0001). After adjusting for gender, the Cox regression coefficient for
age ≥ 65 was 0.62 ±0.17 (risk ratio 1.86) and for CAD, 0.50 ±0.16 (risk
ratio 1.86). Only 24 patients required reoperation for primary tissue failure
(PTF). CAD did not univariately nor multivariately influence the need for
reoperation. At 12 yrs, freedom from reoperation for PTF was 83 ± 5% for those
<65 yrs and 98 ± 1% for those ≥ 65 yrs (p = 0.006). Age ≥ 65 was
associated with a reduced risk for reoperation: Cox regression coefficient
-1.24 ± 0.5 (risk ratio 0.29).
CONCLUSIONS: Long-term survival following AYR is highly
dependent upon age and the presence of concomitant CAD. Thus, patients greater
than 65 years of age with CAD are ideal candidates for a bioprosthetic valve.
In patients greater than 65 years without CAD, the benefit of a bioprosthesis
is less clear. Age has an independent effect on the durability of the porcine
bioprosthesis. Although older patients with CAD are unlikely to require
reoperation for bioprosthetic failure, older patients without CAD and all
younger patients may require reoperation for this purpose.
*By invitation
31. CRYOPRESERVED HOMOGRAFT VALVES IN THE
PULMONARY POSITION - RISK ANALYSIS FOR LATE FAILURE.
Christopher J. Knott-Craig,
M.D.*, Kazuo Niwaya, M.D.*, Ronald C. Elkins, M.D, Mary M. Lane, Ph.D.*, K.
Chandrasekaran, M.D.* and Kent E. Ward, M.D.*
Oklahoma City, Oklahoma
Discussant: Gordon K. Danielson, Jr., M.D.,
Rochester, Minnesota
To examine their durability, and factors associated with
late failure, we reviewed our entire experience (1986-1997) with 369 hospital
survivors in whom cryopreserved homografts (aortic n = 37, pulmonary n = 332)
were used in the "pulmonary" position. Mean age was 18.5 ± 15.7 years (range 2
days -62 years). Operations included Ross operation (n = 273), Tetralogy of
Fallot (n = 48), truncus arteriosus (n = 22), transposition of great arteries
(n = 16), others (n=10). Median follow-up was 3.3 years (range 0.1-10.8 yrs)
and recent echocardiographic evaluation was complete for 97% pts. Reoperation
occurred in 7.3% (27/369), and failure (reoperation, gradient ≥ 40mmHg)
in 12.7% (47/369) pts. Freedom from reoperation at 8 years was 83 ± 4%, and
freedom from failure was 72±4%; for aortic versus pulmonary homografts, this
was 38 ± 11% vs 77 ± 14% (p = 0.001). For pts <3 yrs at operation (n = 41)
this was 34 ± 12% vs 75±5% for older pts (p = 0.0002). Multivariate analysis
identified (i) younger age of homograft donors, (ii) aortic homografts, (iii)
non-Ross operation, and (iv) later year of operation as risk factors for
homograft failure (all p<0.005).
Homografts are the replacement conduit of choice for the
pulmonary position. Pulmonary homografts are more durable than aortic
homografts, and both fail earlier in young children. Residual pulmonary
vascular abnormalities adversely impact the long-term durability of the conduit.
1989-90 AATS Graham Fellow
*By invitation
32. A 20-YEAR EXPERIENCE WITH CARDIAC
RETRANSPLANTATION.
Ranjit John, M.D.*, Jonathan Chen,
M.D.*, Alan Weinberg, M.S.*, Mehmet C. Oz, M.D., Silviu Itescu, M.D.*, Eric A.
Rose, M.D. and Niloo M. Edwards, M.D.*
New York, New York
Discussant: William A.
Baumgartner, M.D., Baltimore, Maryland
Retransplantation is the only currently available
treatment for severe myocardial dysfunction in cardiac allograft recipients.
However, the allocation of scarce organs to patients who have previously
received a transplant is a controversial issue. We, retrospectively, reviewed
our experience with patients undergoing cardiac retransplantation. Between 1977
- October 1997, 952 patients underwent cardiac transplantation for the
treatment of end stage heart disease. Of these, 43 patients underwent
retransplantation for cardiac failure resulting from transplant coronary artery
disease, rejection and early graft failure. The mean age of these patients at
primary transplantation was 37.2 years (range 2 -58 years, SD ± 16.7) and mean
age at retransplantation was 41.6 years (range 5-64 years, SD ± 16.6). The
interval between primary and retransplantation ranged from < 1 day to 11.4
years (mean 4.4 years). There was no significant difference in actuarial
survival by Kaplan Meier analysis at 1, 2 and 5 years between patients
undergoing primary and retransplantation -76%, 71% and 60% versus 66%, 66% and
45% respectively (p = 0.213). However, the actuarial survival of retransplant
patients from the time of the first transplant was 91%, 88% and 74% at 1, 2 and
5 years respectively. A univariate analysis of various risk factors affecting
outcome after cardiac retransplantation was performed. The variables evaluated
included the decade of transplantation, ages at primary and retransplantation,
indications for primary and retransplantation, interval between transplants,
HLA matching, recipient and donor demographic variables and the presence of
pretransplant anti-HLA IgG and IgM antibodies. A shorter duration between
transplants (p = 0.003) and older age at transplantation (p = 0.04) were
identified as risk factors for poorer outcome after retransplantation. In
conclusion, cardiac retransplantation can be performed with low morbidity and
mortality and satisfactory long term outcome. However, patient characteristics
and preoperative variables should assist in the rational application of
retransplantation to ensure optimal utilization of donor organs.
4:35 p.m. EXECUTIVE
SESSION (Limited to Members)
Ballroom B, Hynes Convention
Center
6:30 p.m. MEMBER RECEPTION
Museum of Science
1994-96 AATS Robert E. Gross Research Scholar
*By invitation
1:45 p.m. SIMULTANEOUS SCIENTIFIC SESSION C
GENERAL THORACIC SURGERY
Ballroom C, Hynes
Convention Center
Moderators: Andre C.H. Duranceau, M.D.
Victor F. Trastek, M.D.
33. RESECTION MARGINS, N2 STATUS AND CELL
TYPE DETERMINE SURVIVAL IN TRIMODALITY THERAPY OF MALIGNANT PLEURAL
MESOTHELIOMA (MPM): RESULTS IN 183 PATIENTS.
David J. Sugarbaker, M.D., Raja M.
Flores, M.D.*, Michael T. Jaklitsch, M.D.*, William G. Richards, Ph.D.*,
Malcolm M. DeCamp, M.D.*, Scott J. Swanson, M.D.*, Raphael Bueno, M.D.* and
Steven J. Mentzer, M.D.
Boston, Massachusetts
Discussant: Larry R. Kaiser,
M.D., Philadelphia, Pennsylvania
Objectives: We review our
experience with extrapleural pneumonectomy (EPP) in the multimodality
management of MPM. Methods: From 1980 to 1997, 183 consecutive patients
underwent trimodality therapy involving EPP followed by adjuvant chemotherapy
and radiotherapy. Standardized systematic pathologic analysis was undertaken.
Results: The cohort included 43 women and 140 men with a mean age of 51yrs
(range 31- 76) and a median followup interval of 13 months. Overall survival
was 36% at 2 yrs and 14% at 5 yrs (median 17 mo). There were seven
perioperative deaths (3.8% mortality). Factors affecting long-term survival
were evaluated in 176 patients surviving surgery (among these, survival was 38%
at 2 yrs and 15% at 5 yrs; median 19 mo). As indicated in the table below, lack
of N2 nodal involvement, negative resection margins and epithelial histology
were associated with improved survival. Factorial grouping by N2 status and
resection margins significantly stratified survival among all patients
surviving surgery (p<0.02), and among those with epithelial histology
(p<0.02). Thirty-one patients with epithelial tumors, negative resection
margins and without N2 involvement had a 51 mo median survival (68% 2-yr. 46%
5-yr). A clinico-pathologic staging system previously published stratified
survival (p< 0.05; see table).
|
Epithelial
Mixed/Sarcom.
|
103
73
|
52%
16%
|
21%
0%
|
26
13
|
0.0001
|
|
Margins
(+)
Margins
(-)
|
110
66
|
33%
44%
|
9%
25%
|
15
23
|
0.02
|
|
N2(+)
N2(-)
|
40
136
|
23%
42%
|
0%
17%
|
14
21
|
0.004
|
|
Epithel.
N2(+)
Epithel.
N2(-)
|
21
82
|
38%
56%
|
0%
24%
|
20
34
|
0.052
|
|
Epithel.
N2(+) Marg(+)
Epithel.
N2(+) Marg(-)
Epithel.
N2(-) Marg(-)
Epithel.
N2(-) Marg(-)
|
12
9
51
31
|
29%
43%
49%
68%
|
0%
0%
14%
46%
|
14
22
22
51
|
0.013
|
|
Stage I
Stage II
Stage III
|
66
41
69
|
53%
44%
17%
|
20% 14%
14%
|
25
20
16
|
0.048
|
These data support the following conclusions: 1)
Multimodality therapy including EPP is feasible in selected patients with MPM,
2) Microscopic resection margins affect long-term survival, pointing to the
need for further investigation of local-regional control strategies, 3)
Mediastinoscopy to evaluate N2 nodes is recommended, and 4) Patients with
epithelial, margin-negative, N2-negative resection enjoy long-term survival.
*By invitation
34. INDUCTION CHEMOTHERAPY FOR T4
CENTRALLY LOCATED NON SMALL CELL LUNG CANCER.
Erino A. Rendina, M.D.*, Federico
Venuta, M.D.*, Tiziano De Giacomo, M.D.*, A. Maria Ciccone, M.D.* Giorgio Furio
Coloni, M.D.* and Costante Ricci, M.D.*
Rome, Italy
Sponsored by: G. Alexander
Patterson, M.D., St. Louis, Missouri
Discussant: L. Penfield Faber,
M.D., Chicago, Illinois
We employed induction
chemotherapy in a prospective, single institution clinical trial intended to
achieve resectability in patients with centrally located, irresectable T4
NSCLC. Other types of T4 (pleural effusion, N3) were excluded. Between January
1990 and April 1996 we enrolled 57 patients with histologically confirmed
NSCLC. They all underwent Computed Tomography (CT), bronchoscopy, bone scan and
in selected cases Magnetic Resonance (MR). Eligibility criteria for T4 were:
Clinical [Superior Vena Cava Syndrome (9 patients), vocal cord paralysis (6
patients), dysphagia from esophageal involvement (1 patient)]; Radiological (CT
and MR evidence of infiltration - 10 patients); Bronchoscopic (tracheal
infiltration - 11 patients); Thoracoscopic (histologically proved mediastinal
infiltration - 20 patients). Mediastinoscopy was employed in 38 patients. N2
was histologically confirmed in 40 patients. After 3 cycles of cisplatin (120
mg/m2), vinblastine (4 mg/m2), mitomycin (2 mg/m2)
patients were reevaluated: 42 (73%) (36 males. 6 females: age range 42-75
years; mean 58 years) responded to therapy and underwent thoracotomy; 11 did
not respond and 4 had major toxicity. Thirty-six patients (85%) had complete
resection. We performed 4 exploratory thoracotomies, 6 pneumo-nectomies, 32
lobectomies (20 associated with reconstruction of hilar-mediastinal
structures). Pathologically, 4 patients had T4, 6 had T3, 24 had T2, 3 had T1
and 5 had T0. Thirteen patients had N2, 15 had N1 and 14 had N0. Overall, 4
patients had no histological evidence of disease. We had 2 bronchopleural
fistulas with 1 death, 5 other major complications and 9 cases of delayed lung
reexpansion. Adjuvant chemo and/or radiotherapy was administered to N2 and N1 patients.
After a follow up of 15 to 76 months (mean 26 months), 25 patients died of
cancer and 2 died of unrelated causes: 14 are alive and free of disease and 1
is alive with disease. Survival at 1 and 4 years is 69% and 26% (median
survival 25 months). In conclusion, of the initial group of 57 patients, 42
(73%) underwent exploration with a 4 year survival of 26%, and 36 (63%) had
complete resection. Our data indicate that induction chemotherapy is effective
for downstaging and surgical reconvertion of centrally located, irresectable T4
NSCLC. Survival is promising but it remains to be confirmed in larger series of
patients and phase III trials.
*By invitation
35. THE PROGRESSION OF INTESTINAL
METAPLASIA IN GASTROESOPHAGEAL REFLUX DISEASE.
Stefan Oberg, M.D.*, Jeffrey H.
Peters, M.D.*, Peter F. Crookes, M.D.*, John J. Nigro, M.D.*, Jorg Theisen,
M.D.*, Jeffrey A. Hagen, M.D.* and Tom R. DeMeester, M.D.
Los Angeles, California
Discussant: Victor F. Trastek,
M.D., Rochester, Minnesota
It is currently suggested that Barrett's esophagus appears
abruptly and once present does not increase in length. This widely quoted but
unproven hypothesis is based on data from patients with traditional, long
segment Barrett's esophagus with endstage gastroesophageal reflux disease
(GERD). Increasingly it is recognized that shorter segments of intestinal
metaplasia are part of the same underlying disease process. The aim of the
present study was to relate physiologic abnormalities of GERD to increasing
lengths of intestinal metaplasia.
One hundred thirty consecutive patients with symptoms
suggestive of GERD and intestinal metaplasia of the cardia or esophagus on
biopsy during upper endoscopy, were studied by esophageal motility and 24 hour
pH and bilirubin monitoring. Duration of symptoms was documented. Standard
measures of lower esophageal sphincter (LES) function, esophageal acid and
bilirubin exposure, and lower esophageal peristaltic amplitude were assessed.
Patients were divided into three groups based on the extent of intestinal
metaplasia: Cardiac intestinal metaplasia (CIM) where the intestinal metaplasia
was detected on biopsy in an endoscopically normal appearing cardia, short
segment Barrett's Esophagus (SSBE) group with intestinal metaplasia in the
tubular esophagus less than 3cm, and patients with long segment Barrett's
Esophagus (LSBE).
|
|
CIM (n = 30)
|
SSBE (n = 32)
|
LSBE (n = 68)
|
|
Duration
of GERD symptoms (years)
|
10.0 (5-15)
|
10.0 (3-15)
|
17(10-23)*
|
|
% time
esophageal pH < 4
|
6.5 (3.3-8.4)
|
10.0 (5.5-16.4)*
|
21.3(13.2-41.1)*
|
|
% time
esophageal bilirubin abs. > 0.2
|
1.6 (0.0-12.8)
|
14.8 (1.7-25.4)
|
16.9 (4.3-30.5)*
|
|
LES
resting pressure (mmHg)
|
6.6 (3.5-11.8)
|
5.2 (2.3-10.2)
|
3.2(1.2-7.4)
|
|
LES
abdominal length (cm)
|
1.0 (0.4-1.4)
|
0.6 (0.2-1.2)
|
0.2 (0.0-0.8)
|
|
Prevalence
of defective LES (%)
|
58.6
|
65.9
|
87.5*
|
|
Esophageal
contraction amplitude (mmHg)
|
64.5 (39.2-98.5)
|
56.5 (38.8-83.7)
|
51.0 (35.0-74.0)*
|
|
Values
expressed as medians (IQR) * p < 0.05 vs all other groups, P < 0.05 vs
CIM
|
Length of intestinal metaplasia was strongly correlated
with the degree of esophageal acid exposure (r = 0.71, p = 0.0001), and
inversely with the LES pressure (r = -0.26, p = 0.003). Patients with long
segment Barrett's esophagus had a longer duration of symptoms than those with
short segment or cardia metaplasia only. The LSBE group demonstrated the
greatest degree of physiologic derangement and the CIM group the least.
The results of this study suggests that longer segments of
IM are associated with longer duration of reflux symptoms and increased
severity of reflux disease. Intestinal metaplasia at the cardia is
characterized by the same physiologic abnormalities as traditional Barrett's
esophagus, although of lesser degree. This raises the possibility that shorter
segments of intestinal metaplasia may progress to longer segments as the
antireflux mechanism deteriorates.
2:45 p.m. INTERMISSION - VISIT EXHIBITS
*By invitation
3:15 p.m. SIMULTANEOUS SCIENTIFIC SESSION C
GENERAL THORACIC SURGERY
Ballroom C, Hynes
Convention Center
Moderators: Andre C.H. Duranceau, M.D.
Victor F. Trastek, M.D.
36. PLEURAL SPACE IRRIGATION AND MODIFIED
CLAGGETT PROCEDURE FOR THE TREATMENT OF EARLY POSTPNEUMONECTOMY EMPYEMA.
Farid Gharagozloo, M.D.*, Gregory
D. Trachiotis, M.D.*, Andrew J. Wolfe, M.D.*, Kevin M. DuBree, P.A.C.* and
James L. Cox, M.D.
Washington, DC
Discussant: Peter C. Pairolero,
M.D., Rochester, Minnesota
The incidence of postpneumonectomy empyema is 5 - 10%.
Approximately half of postpneumonectomy empyemas occur within 2 to 4 weeks of
pneumonectomy. A bronchopleural fistula is found in more than 80% of the
patients. The classic treatment of postpneumonectomy empyema includes
parenteral antibiotics, drainage of the pleural space, removal of necrotic
tissue, and open pleural packing for many weeks followed by obliteration of the
empyema space with antibiotic fluid or muscle. This approach results in
prolonged hospitalization, repeated operations, and significant morbidity. In a
five year period we treated 22 patients with early postpneumonectomy empyema.
All patients had a bronchopleural fistula. The patient profile and predisposing
factors were:
Sex
|
Age
|
Pleural Space
|
Bronchiectasis
|
PreOp Radiation
|
|
16M/16F
|
62 ± 5
|
18R/4L
|
2
|
3
|
|
|
|
Malnutrition
|
Steroid Therapy
|
Obstructive Pneumonitis
|
|
|
|
2
|
3
|
12
|