Clinical
Investigation
Osman Tansel Darcin, MD
Tahir Yagdi, MD
Yuksel Atay, MD
Cagatay Engin, MD
Erturk Levent, MD
Suat Buket, MD
Emin Alp Alayunt, MD
C
Key words: Aortic valve
stenosis/surgery; cardiac
surgical procedures; heart
septal defects, ventricular;
myectomy; retrospective
studies; ventricular outflow
obstruction/surgery
From: Departments of
Cardiovascular Surgery
(Drs. Darcin, Yagdi, Atay,
Engin, Buket, and Alayunt)
and Pediatric Cardiology
(Dr. Levent), Ege University
Hospital, Izmir, Turkey
Address for reprints:
Yuksel Atay, MD,
Ege University Medical
Faculty, Department of
Cardiovascular Surgery,
Bornova–Izmir 35100,
Turkey
E-mail:
yatay @med.ege.edu.tr
© 2003 by the Texas Heart ®
Institute, Houston
286 Discrete Subaortic Stenosis: Surgical Outcomes
Discrete
Subaortic Stenosis
Surgical Outcomes and Follow-Up Results
Discrete subaortic stenosis, which is an obstructing lesion of the left ventricular outflow
tract, remains a surgical challenge. The recurrence rate is high despite sufficient conven-
tional resection.
We retrospectively reviewed the results of surgery for discrete subaortic stenosis at
our institution from September 1995 through March 2001. Twenty-one patients with
this lesion underwent surgical treatment during this period. Excision of the fibromus-
cular membrane with myectomy was performed in all of the patients. Follow-up in all
patients ranged from 7 to 67 months (mean follow-up period, 39.57 ± 15.46 months).
The mean systolic gradient between the left ventricle and the aorta decreased from
59.23 ± 35.38 mmHg preoperatively to 9.47 ± 9.91 mmHg postoperatively. There was
no instance of heart block that required a permanent pacemaker, nor of bacterial en-
docarditis. There was no early or late postoperative death. A 22nd patient, who had 3+
aortic regurgitation, required aortic valve replacement and was excluded from the
study. Two of the patients (9.5%) underwent reoperation because of recurrent gradi-
ent and residual ventricular septal defect.
Our results suggest that fibromuscular membrane excision combined with myecto-
my in patients with discrete subaortic stenosis produces sufficient relief of obstruction
with low morbidity. (Tex Heart Inst J 2003;30:286-92)
ongenital obstruction of the left ventricular outflow tract (LVOT) affects
approximately 3% to 10% of individuals with congenital heart disease,
and discrete subaortic membrane accounts for 8% to 10% of all cases of
LVOT obstruction in children.1-3 This last condition presents as a membranous or
fibromuscular ring below the aortic valve, either in isolation or in association with
other congenital anomalies such as ventricular septal defect, patent ductus arterio-
sus, coarctation of the aorta, bicuspid aortic valve, abnormal left ventricular (LV)
papillary muscle, atrioventricular septal defect, and persistent superior left vena
cava. The condition is rarely diagnosed antenatally or in infancy but often mani-
fests in the 1st decade of life with features of progressive LVOT obstruction, LV hy-
pertrophy and dysfunction, or aortic regurgitation. The jet from the narrowed
subaortic tract damages the aortic cusps and causes regurgitation; this damage may
also render the aortic valve prone to infective endocarditis.4
Treatment is usually surgical. Despite adequate resection, there is a substantial re-
currence rate among patients who have undergone operation for discrete membra-
nous subaortic stenosis (DSS). Although membranectomy, with or without septal
myotomy or myectomy, has been the accepted method of treating fixed subaortic
stenosis, there are still controversies concerning operative methods and uncertain-
ties concerning the recurrence of subaortic obstruction and the development of
aortic insufficiency after repair. Our usual approach to DSS is membrane excision
with resection of the septal myocardium. In this study, we aimed to evaluate our
surgical results.
Patients and Methods
Data Collection. All patients who underwent surgical treatment of DSS at our in-
stitution from September 1995 through March 2001 were included in this study.
Patients with significant valvular aortic stenosis, tunnel LVOT obstruction, or idio-
pathic hypertrophic cardiomyopathy were excluded. One patient who underwent
aortic valve replacement combined with aortoventriculoplasty was excluded from
Volume 30, Number 4, 2003
the study. All patients were evaluated preoperatively
and monitored for variable periods postoperatively.
All patients or their families signed informed consents
for investigation during the study period. The case
histories of all patients, including patient and primary
physician interviews and medical records, were exam-
ined retrospectively. We compiled information on
each patient’s age, sex, previous cardiac operation or
coexisting cardiac anomaly (if any), physical signs and
symptoms, electrocardiography, chest radiography,
echocardiography, and cardiac catheterization. Echo-
cardiography was performed preoperatively and at
regular postoperative intervals (Fig. 1). All complica-
tions and reoperations were noted.
All echocardiographic and angiocardiographic stud-
ies were conducted by the same pediatric cardiologist
(EL). The maximal instantaneous gradient across the
LVOT was calculated from the peak spectral Doppler
velocity using the modified Bernoulli equation.5 Aor-
tic regurgitation was characterized as follows: 0, no
aortic regurgitation; 1, trivial (thin regurgitant jet seen
at the valve leaflets, no left ventricular distention or
diastolic retrograde aortic flow in the descending aor-
A nary bypass under moderate systemic hypothermia.
B cardiopulmonary bypass time was 68 ± 41 minutes,
Fig. 1 A) Parasternal long-axis view of the left ventricular
outflow tract shows a subaortic discrete membrane (arrow).
B) Postoperative parasternal long-axis view in the same
patient demonstrates relief of the subaortic stenosis.
Texas Heart Institute Journal
ta); 2, mild (slightly broader jet limited to the LVOT,
no ventricular enlargement, minimal or no retrograde
flow in the descending aorta, pressure half time = 400
ms); 3, moderate (broad regurgitant jet extending into
left ventricle, mild ventricular enlargement, holodia-
stolic retrograde aortic flow in the descending aorta,
pressure half time 200–400 ms); and 4, severe (wide
regurgitant jet extending deep into the left ventricle,
marked left ventricular enlargement, holodiastolic
retrograde flow in the descending aorta, pressure half
time <200 ms). Cardiac catheterization was per-
formed in 9 patients in whom no satisfactory images
could be obtained on echocardiography. The peak
gradient across the left ventricle–aorta was measured
by catheter pull-back and by monitoring pressures in
both chambers.
Surgical Procedure. Indications for surgery varied
but included left ventricle–aorta gradient that exceed-
ed 30 mmHg, coexisting cardiac lesions that required
operation, and echocardiographic or angiographic ev-
idence of new or progressive aortic regurgitation. All
operations were performed by the same pediatric car-
diac surgeon (EAA) at the department of cardiac sur-
gery in Ege University Hospital. All operations were
performed with the patient on standard cardiopulmo-
Myocardial protection was achieved by means of cold
blood cardioplegia—antegrade, retrograde, or both.
After cardiopulmonary bypass was instituted, the aor-
ta was opened by an oblique aortotomy that was ex-
tended into the noncoronary sinus. After carefully
retracting the leaflets of the aortic valve, surgeons
could see the subaortic membrane (Fig. 2). They cir-
cumferentially excised both the obstructing discrete
membrane and the adjacent hypertrophied muscle.
Great care was exercised to avoid injury to the con-
duction tissue between the right and noncoronary
cusps and the anterior leaflet of the mitral valve, to
which the membrane occasionally adheres. The mean
and the mean cross-clamp time was 30 ± 17 minutes.
Statistical Analysis. Results are expressed as a range,
with the mean ± SE. Group means were compared
with Student’s t-test on SPSS software (SPSS Inc.;
Chicago, Ill); a P value of less than 0.05 was consid-
ered significant.
Results
Preoperative Data. From September 1995 through
March 2001, 21 patients with DSS underwent resec-
tion of discrete subaortic stenosis alone or as part of a
more comprehensive surgical procedure. The group
comprised 9 female and 12 male patients who ranged
in age from 27 months to 61 years (mean age, 12.64
± 16.19 years). Three patients (14.3%) had under-
Discrete Subaortic Stenosis: Surgical Outcomes 287

A were corrected concomitantly at the time of DDS
B period and was treated medically with complete re-
Fig. 2 Intraoperative views of A) subaortic discrete mem-
brane (arrow) and B) left ventricular outflow tract after
membranectomy.
gone a previous cardiac surgical procedure: ventricular
septal defect (VSD) closure in 1; coexisting VSD clo-
sure and right ventricular outflow tract (RVOT) ste-
nosis repair in 1; and coexisting atrial septal defect
(ASD) and VSD closure in 1.
Eight patients (38.1%) were noted to be sympto-
matic: 4 patients showed diminished exercise toler-
ance, 1 had palpitations, and 1 had syncopal episodes.
The remaining 13 patients (61.9%) were asympto-
matic. On physical examination, all 21 patients re-
vealed systolic ejection murmurs, and 15 had diastolic
murmurs of aortic regurgitation. The left ventricle–
aorta gradient ranged from 14 to 155 mmHg (the
mean gradient was 59.23 ± 35.38 mmHg). Eleven
patients had 1+ aortic regurgitation, and 4 patients
had 2+ aortic regurgitation. Two patients had mild
mitral insufficiency. No patient had endocarditis pre-
operatively.
Of the 21 patients, 15 (71.4%) had coexisting car-
diac lesions. Of these, 6 patients had a VSD, 3 had
RVOT stenosis, 2 had a patent foramen ovale (PFO),
2 had persistent left superior vena cava (LSVC), and 2
had mild mitral insufficiency. All conditions but the
288 Discrete Subaortic Stenosis: Surgical Outcomes
persistent LSVC and the mild mitral insufficiency
surgery. The 2 patients with mild mitral insufficiency
did not require concomitant surgical correction. The
remaining 7 patients (33.3%) had isolated DSS, as
summarized in Table I.
Postoperative Findings. The patients underwent
postoperative follow-up that included physical exami-
nation and echocardiography. Follow-up results were
available for all patients, and length of follow-up
ranged from 7 to 67 months (mean, 39.57 ± 15.46
months). Two patients (9.5%) developed nonfatal
cardiac arrhythmia during the perioperative period
and were treated successfully. One patient (4.8%) de-
veloped acute pancreatitis during the postoperative
covery. Bundle branch block developed in 8 patients
during the postoperative period. No patient devel-
oped endocarditis or heart block that required a pace-
maker. There were no early or late postoperative
deaths. The early postoperative echocardiographic re-
sults showed that the membrane was completely re-
moved in all patients. At late follow-up, the systolic
gradient between the left ventricle and the aorta
ranged from 0 to 38 mmHg (mean gradient, 9.47 ±
9.91 mmHg), which was significantly lower than the
preoperative values (P <0.001) (Fig. 3). Aortic regur-
gitation was also evaluated by means of echocardi-
ography during the postoperative period. It decreased
in 8 patients (38.1%) and progressed in 4 patients
(19%). The aortic competence in the remaining 9 pa-
tients (42.9%) was unchanged. Two patients (9.5%)
required reoperation: 1 patient had recurrent DSS,
and 1 patient required closure of a recurrent ventricu-
lar septal defect, which had been repaired at the time
of DSS resection.
Symptoms of the patients were relieved completely
during the early postoperative period, except for pal-
pitation in 1 patient, which resolved with medical
therapy.
Discussion
Discrete subaortic stenosis is a manifestation of a geo-
metric anatomic alteration in the LVOT. This endo-
cardial abnormality involves not only the subaortic
ridge but also the leaf lets of the adjacent valves.1
Although substantial pressure gradient and aortic re-
gurgitation are the main indications for surgery, con-
troversy persists about the timing of surgical repair
and the surgical technique.3,5
Unlike valvular aortic stenosis, DSS seems to be ac-
quired, because it is almost never present at birth. It is
believed that obstruction in this instance is a conse-
quence of some abnormality of ventricular motion,
growth, hypertrophy, or a combination of these fac-
Volume 30, Number 4, 2003
TABLE I. Summary of Patient Data

Preoperative Data Postoperative Data

LV–Ao LV–Ao Grad. at

Pt. Gradient Associated Follow-Up Late Follow-Up Endo-
No. Age/Sex (mmHg) AI Procedures (mo) (mmHg) AI carditis Reoperation

1 4 y 3 mo/M 14 1+ VSD closure, 7 0 1+ No Yes (recur-

resection, rent DSS)
RVOT stenosis

2 5 y/M 85 1+ PDA ligation 52 38 2+ No No

3 12 y/F 51 1+ PFO closure 52 11 1+ No No

4 6 y/M 46 0 None 42 0 0 No No

5 2 y 3 mo/F 18 0 VSD closure 47 7 1+

6 7 y/F 62 1+ VSD closure 63 10 0

7 4 y/M 90 1+ Resection, 21 5 0 No No
RVOT stenosis

8 5 y/F 65 0 None 58 15 1+ No No

9 11 y/M 35 1+ None 31 0 0 No No

10 19 y/M 95 2+ None 38 0 2+ No No

11 5 y/F 73 2+ Persistent LSVC 42 12 1+ No No

12 5 y/F 15 2+ VSD closure 27 5 2+ No No

13 56 y/M 120 1+ None 67 30 0 No No

14 4 y/F 60 1+ None 42 13 0 No No

15 9 y/M 38 1+ VSD closure, 27 0 0 No Yes (recur-

resection, rent VSD)
RVOT stenosis

16 5 y/M 35 1+ PDA ligation 48 10 1+ No No

17 5 y/M 50 0 Persistent LSVC 24 10 1+ No No

18 61 y/F 55 2+ None 33 10 2+ No No

19 25 y/M 22 0 VSD closure 56 5 0 No No

20 5 y/M 60 1+ None 24 0 0 No No

21 10 y/F 155 0 PFO closure 30 18 0 No No

AI = aortic insufficiency; Ao = aorta; DSS = discrete subaortic stenosis; F = female; Grad. = gradient; LSVC = left superior vena
cava; LV = left ventricle; M = male; PDA = patent ductus arteriosus; PFO = patent foramen ovale; RVOT = right ventricular out-
flow tract; VSD = ventricular septal defect

tors.1,3,4,6 -8 An abnormal angle between the muscular
and conical ventricular septum appears to be an im-
portant causative factor, but a definitive cause has not
been established.9-11
Various theories about the cause of DSS—congeni-
tal, inflammatory, genetic, and acquired—have been
proposed.3,12 Some investigators have considered the
disease to be a form of cardiomyopathy,13 and there
are patients with DSS who develop an unusually pro-
found LV myocardial hypertrophic response. More
often, however, there appears to be no global cardio-
myopathic component. In the vast majority of cases,
LV hypertrophy regresses after relief of the outflow
obstruction, as would be expected in a patient with
valvular aortic stenosis. We are convinced that DSS
has multifactorial causes.
Discrete subaortic stenosis is sometimes associated
with various other cardiac malformations1- 4, 7,8 that
must be monitored and treated surgically when neces-
sary. Chung and colleagues14 reviewed the cases of 8
patients, aged 1 to 8 years, who had VSD in combi-
nation with various other cardiac lesions, but no evi-

Texas Heart Institute Journal Discrete Subaortic Stenosis: Surgical Outcomes 289

Fig. 3 Postoperative changes in left ventricle–aorta (LV–Ao)
peak gradient.
dence of DSS. They operated on 6 of these patients
for the associated lesions, but none required closure of
the VSD. In 6 of the 8 patients, the VSD closed spon-
taneously, and in the remaining 2 there was a small
residual VSD. Subsequent serial echocardiography
showed evidence of a subaortic membrane, which was
confirmed by catheterization and then by surgical re-
section in 5 patients. They concluded that DSS might
develop in patients with small or spontaneously closed
VSDs. Rayburn and associates3 recorded 3 cases of
VSD in their DSS patients and closed all of the de-
fects. We encountered 6 cases of VSD in our patients
who had DSS, and we closed all of the ventricular
defects during resection of the fibromuscular mem-
brane. We also resected 3 stenoses of the RVOT, li-
gated 2 patent ducti arteriosi (PDAs), and closed 2
PFOs. Discrete subaortic stenosis can sometimes re-
quire direct procedures to enlarge the LVOT, especi-
ally when DSS coexists with the diffuse type of LVOT
stenosis. Such a procedure is generally conducted as
an aortoventriculoplasty.1,15 We performed it in the
patient who underwent aortic valve replacement and
was subsequently excluded from this study.
Although the most common symptom in patients
with DSS is diminished exercise tolerance, they may
also have syncope or angina pectoris.1,3,4 It should be
remembered that most patients are asymptomatic,
even in the presence of important gradients that in-
dicate surgery.1,3,8 Rayburn and colleagues3 confirmed
that 70% of their patients had no symptoms, but the
proportion varies from series to series. Kuralay and co-
workers16 reported that 64.4% of their patients had
exertional dyspnea. In our series, 8 patients (38.1%)
were noted to be symptomatic, and the remaining 13
(61.9%) were asymptomatic.
Apart from congenital cardiac abnormalities, ac-
quired aortic insufficiency is the most common lesion
found in association with DSS, and it can of course
290 Discrete Subaortic Stenosis: Surgical Outcomes
be progressive. The aortic regurgitation appears to be
due to thick fibrous tissue on the left ventricular sur-
face of the valve leaf lets. The fibrosis is caused by
repetitive trauma from a jet of blood through the
stenosis or by the proliferation of the fibroelastic
membrane itself. This fibrous tissue can play an im-
portant role in the retraction of the valve leaflets.17 Al-
though an important study found no benefit in early
surgery and a higher prevalence of aortic regurgitation
in surgically treated patients,18 we think that early sur-
gery may preserve the integrity of the aortic valve in
such a manner as to avoid later valve replacement.
Aortic insufficiency can progress postoperatively de-
spite relief of the LVOT stenosis of DSS, but our op-
erative results and early follow-up tend to support the
conclusion that worsening of the regurgitation in DSS
can be slowed or stopped with adequate resection of
DSS. This has been affirmed by various other stud-
ies.3-5,15,16
Although DSS has been treated surgically for many
years,1, 7 the optimal operative management and the
timing of surgery remain controversial.5,12 Many au-
thors have suggested surgery for patients who have left
ventricle–aorta gradients that exceed 30 mmHg or a
coexisting cardiac defect that requires surgical correc-
tion,1,5,8 while others advocate surgical resection for
DSS of any degree because of concerns about the de-
velopmental role that subaortic stenosis may play in
aortic insufficiency.12,18 This earlier intervention for
DSS can prevent the development of abnormal mus-
cular hypertrophy and can reduce the occurrence of
aortic regurgitation. It also protects patients from bac-
terial endocarditis.1-3,5, 7
The optimal surgical method for patients with DSS
is debatable.3,5 Although some surgeons prefer enu-
cleation of the discrete membrane and in selected pa-
tients its fibromuscular ridge,8 many others believe
that a routine myectomy is adequate to eliminate re-
currence. The latter, however, confirm that surgery is
not sufficient without resection of hypertrophied
muscle.5,19 We too resected adjacent hypertrophied
muscle during resection of fibrous membrane in all of
our patients. Limited septal muscle resection can re-
lieve obstruction of the LVOT in some patients, but a
more aggressive approach must be taken when the
pathologic condition requires it. Some of the residual
perioperative left ventricular–aortic gradients in pa-
tients with discrete subaortic stenosis undergoing
repairs are dynamic and transient, and are probably
related to increased sympathetic activity following
surgery. However, persistent dynamic obstruction was
found in 44% of patients after removal of discrete
subaortic obstruction.13 Several groups have reported
the need for repeat myectomy to relieve obstruction
after the successful removal of subaortic membrane.
Because the fibrous tissue that retracts the aortic valve
Volume 30, Number 4, 2003
leaflets remains, there can be no improvement in the
aortic regurgitation after surgery. Radical excision of
all diseased tissue, which attains a minimal early post-
operative gradient, may reduce the occurrence of late
aortic regurgitation.20 However, this more aggressive
approach increases the risk of iatrogenic damage to
the conduction tissue, ventricular septum (VSD), and
mitral valve. Kuralay and coworkers16 have reported
fewer complications, such as conduction tissue injury,
when myectomy is guided by transesophageal echo-
cardiography. We believe that the risk of developing
heart block that requires permanent pacing is mini-
mal when the surgeon takes great care to avoid injury
to the conduction tissue between the right and non-
coronary cusps.
Early results after surgery for DSS are usually good.
The left ventricle–aorta gradient was decreased signif-
icantly in many studies similar to ours.3,5, 7,8,19, 21 Two of
our patients had residual gradients of 30 mmHg or
greater, but no progression was seen in early follow-
up. The failure to eliminate their residual gradients
may be due to incomplete resection of the hypertro-
phied myocardium. In recent series,9,11 postoperative
aortic regurgitation has decreased substantially. Al-
though the rate of bacterial endocarditis22, 23 was rela-
tively high in older reports, it too has decreased in
recent studies.3 In most of the series, the rates of peri-
operative mortality and cardiac-related late death have
been low.5,15, 21 Jahangiri and associates15 affirmed that
they had no postoperative early or late deaths in their
patients who had undergone surgery for subaortic
stenosis. Postoperative complications and recurrences
are also low in these patients. The residual gradients
that are seen in some patients (including 2 of our own)
may be due to insufficient resection of the fibromus-
cular diaphragm and the coexisting hypertrophied
muscle that together cause dynamic outflow obstruc-
tion.5,8 Complete heart block and bundle branch block
can follow extensive muscle resection.24, 25 In our proce-
dure, we routinely resected hypertrophied myocardi-
um. We had 1 patient (4.8%) with a residual gradient
that required reoperation, and no patient with heart
block that required a permanent pacemaker. Eight of
our patients (5 of whom had undergone concomitant
VSD closure) developed bundle branch block postop-
eratively. Bacterial endocarditis has been considered
an important risk attendant upon DSS, especially in
former series.1,3,5, 7,8, 22 We encountered no bacterial en-
docarditis in our patients, as some authors did.24, 25
Although DSS is a well-known cardiac anomaly
that is seen in both children and adults, there is no
agreement about its surgical management.5,8,12,18 As our
experience shows, membranectomy together with
routine myectomy and (when necessary) a more ag-
gressive approach seems to yield acceptable morbidi-
ty, mortality, and recurrence rates, compared with series
Texas Heart Institute Journal
that have used only membranectomy. However, our
follow-up period was relatively short, and our con-
cept has never been tested in a prospective, random-
ized trial. Due to the infrequent occurrence of this
disease, our conclusions are drawn from retrospective
study. We must await the long-term results in these
same patients before our approach can be justified. In
conclusion, we believe that a larger number of pa-
tients, longer follow-up by the pediatric cardiologist,
and close collaboration with the pediatric cardiac sur-
geon will be necessary to support this management.
References
1. Kirklin JW, Barratt-Boyes BG. Cardiac surgery: morpholo-
gy, diagnostic criteria, natural history, techniques, results,
and indications. 2nd ed. Vol 2. New York: Churchill Living-
stone; 1993. p. 1212-24.
2. Hoffman JI, Christianson R. Congenital heart disease in a
cohort of 19,502 births with long-term follow-up. Am J
Cardiol 1978;42(4):641-7.
3. Rayburn ST, Netherland DE, Heath BJ. Discrete membra-
nous subaortic stenosis: improved results after resection and
myectomy. Ann Thorac Surg 1997;64:105-9.
4. Kleinert S, Ott DA, Geva T. Critical discrete subaortic sten-
osis in the newborn period. Am Heart J 1993;125:1187-9.
5. Lupinetti FM, Pridjian AK, Callow LB, Crowley DC, Beek-
man RH, Bove EL. Optimum treatment of discrete subaor-
tic stenosis. Ann Thorac Surg 1992;54:467-71.
6. Sullivan ID, Gooch VM. Echocardiography. In: Stark J, de
Leval M, editors. Surgery for congenital heart defects. 2nd
ed. Philadelphia: WB Saunders; 1994. p. 59-84.
7. de Leval M. Surgery of the left ventricular outflow tract. In:
Stark J, de Leval M, editors. Surgery for congenital heart de-
fects. 2nd ed. Philadelphia: WB Saunders; 1994. p. 511-37.
8. Rohlicek CV, del Pino SF, Hosking M, Miro J, Cote JM,
Finley J. Natural history and surgical outcomes for isolated
discrete subaortic stenosis in children. Heart 1999;82(6):
708-13.
9. Gewillig M, Daenen W, Dumoulin M, Van der Hauwaert
L. Rheologic genesis of discrete subvalvular aortic stenosis: a
Doppler echocardiographic study. J Am Coll Cardiol 1992;
19:818-24.
10. Kleinert S, Geva T. Echocardiographic morphometry and
geometry of the left ventricular outflow tract in fixed sub-
aortic stenosis. J Am Coll Cardiol 1993;22:1501-8.
11. Cape EG, Vanauker MD, Sigfusson G, Tacy TA, del Nido
PJ. Potential role of mechanical stress in the etiology of pe-
diatric heart disease: septal shear stress in subaortic stenosis.
J Am Coll Cardiol 1997;30:247-54.
12. Douville EC, Sade RM, Crawford FA Jr, Wiles HB. Subval-
var aortic stenosis: timing of operation. Ann Thorac Surg
1990;50:29-34.
13. Somerville J, Stone S, Ross D. Fate of patients with fixed
subaortic stenosis after surgical removal. Br Heart J 1980;
43:629-47.
14. Chung KJ, Fulton DR, Kreidberg MB, Payne DD, Cleve-
land RJ. Combined discrete subaortic stenosis and ventric-
ular septal defect in infants and children. Am J Cardiol
1984;53(10):1429-32.
15. Jahangiri M, Nicholson IA, del Nido PJ, Mayer JE, Jonas
RA. Surgical management of complex and tunnel-like
subaortic stenosis. Eur J Cardiothorac Surg 2000;17:637-
42.
Discrete Subaortic Stenosis: Surgical Outcomes 291
16. Kuralay E, Ozal E, Bingol H, Cingoz F, Tatar H. Discrete
subaortic stenosis: assessing adequacy of myectomy by
transesophageal echocardiography. J Card Surg 1999;14(5):
348-53.
17. Feigl A, Feigl D, Lucas RV Jr, Edwards JE. Involvement of
the aortic valve cusps in discrete subaortic stenosis. Pediatr
Cardiol 1984;5:185-9.
18. Oliver JM, Gonzalez A, Gallego P, Sanchez-Recalde A, Ben-
ito F, Mesa JM. Discrete subaortic stenosis in adults: in-
creased prevalence and slow rate of progression of the
obstruction and aortic regurgitation. J Am Coll Cardiol
2001;38:835-42.
19. Wright GB, Keane JF, Nadas AS, Bernhard WF, Castaneda
AR. Fixed subaortic stenosis in the young: medical and sur-
gical course in 83 patients. Am J Cardiol 1983;52:830-5.
20. Parry AJ, Kovalchin JP, Suda K, McElhinney DB, Wudel J,
Silverman NH, et al. Resection of subaortic stenosis; can a
more aggressive approach be justified? Eur J Cardiothorac
Surg 1999;15:631-8.
292 Discrete Subaortic Stenosis: Surgical Outcomes
21. Jaumin P, Rubay J, Lintermans J, Arena V, Matta A, Goe-
nen M, et al. Surgical treatment of subvalvular aortic steno-
sis. Long-term results. J Cardiovasc Surg (Torino) 1990;31:
31-5.
22. Gupta KG, Loya YS, Sharma S. Discrete subaortic stenosis:
a study of 20 cases. Indian Heart J 1994;46(4):157-60.
23. Matsuyama N, Asada K, Kondo K, Minohara S, Hasegawa
S, Sawada Y, et al. Surgical treatment of discrete subaortic
stenosis in an adult. Jpn Circ J 1998;62(1):69-71.
24. Brown J, Stevens L, Lynch L, Caldwell R, Girod D, Hur-
witz R, et al. Surgery for discrete subvalvular aortic stenosis:
actuarial survival, hemodynamic results, and acquired aortic
regurgitation. Ann Thorac Surg 1985;40:151-5.
25. Jones M, Barnhart GR, Morrow AG. Late results after op-
erations for left ventricular outflow tract obstruction. Am J
Cardiol 1982;50:569-79.
Volume 30, Number 4, 2003