European Journal of Echocardiography 2004 5(1):68-71; doi:10.1016/S1525-2167(03)00040-4
© 2004 by European Society of Cardiology
Copyright © 2003, The European Society of Cardiology
Anatomical basis for acquired intracardiac shunt postaortic valve replacement: Doppler echocardiographic diagnosis
S Al Ahmari,
J Malouf,
F Al Atawi,
H Schaff and
K Chandrasekaran*
Cardiovascular Division, Echocardiography Laboratory, Mayo Clinic, 200 First Street SW, Gonda 6-138 NW, Rochester, MN 55905, USA
* Corresponding author. Tel: +1-507-284-3581; fax: +1-507-284-3968.
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Abstract
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We report a case of postoperative intracardiac shunts across
the membranous septum detected by Doppler echocardiography and
discuss the anatomical basis for the development of such a complication.
Iatrogenic intracardiac shunts are uncommon and have been recognized
after aortic and mitral valve surgery.
2–5 The early detection
and treatment of such a complication can prevent subsequent
adverse hemodynamic effects and long-term sequelae.
1,6 We report
a case of intracardiac shunts from the left ventricle outflow
tract (LVOT) across the membranous septum into the right atrium
(RA), right ventricle (RV) and left atrium (LA) following a
redo aortic valve replacement. The lesion was detected by transthoracic
Doppler echocardiography (TTDE).
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1. Case report
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An 82-year-old male who had undergone a coronary artery bypass
and tissue aortic valve replacement in 1997, followed by mitral
valve annuloplasty in 1998, was treated for uncomplicated infective
endocardities (IE) in February 2000 with prolonged antibiotic
course and in June 2002 he was evaluated for exertional shortness
of breath. He denied orthopnea, nocturnal dyspnea, or fevers.
Physical examination of this afebrile elderly patient was unremarkable
except for a 3/6 ejection systolic murmur over the aortic area
radiating to the carotids and a holodiastolic murmur along the
right sternal border. There was no peripheral stigma of IE.
Laboratory results were normal. ECG revealed sinus rhythm, first-degree
heart block and an old inferior infarct. Transthoracic echocardiogram
showed moderately enlarged left ventricle with decreased systolic
function, EF 35%. The aortic tissue valve was thickened, with
decreased cusp excursion and without obvious vegetation or flail.
Color flow Doppler demonstrated severe prosthetic regurgitation.
The degree of regurgitation has increased from moderate to severe
compared to previous examination. The estimated pulmonary systolic
pressure was 61 mmHg. The patient underwent aortic valve replacement
with a 23 Carpenteer Edwards tissue valve, and the postoperative
course was uneventful. Transthoracic echocardiogram performed
prior to discharge showed improved LV function with an EF of
50%, and normal function of the aortic tissue prosthesis. However,
there was a highly turbulent color flow jet from the LVOT across
the membranous septum into the RA and RV straddling the septal
leaflet of the tricuspid valve on the parasternal short-axis
view (
Fig. 1). The peak velocity of the jet, from the LVOT to
RA, was 6 m/s (
Fig. 2). In the apical four-chamber view another
jet was seen entering the LA from the LVOT just beneath the
aortic prosthesis (
Fig. 3). The RV was not enlarged and the
Doppler estimated RV systolic pressure was 46 mmHg. The calculated
shunt fraction was not significant (QP/QS ratio of 1.2). The
patient was discharged with instruction for early follow up.
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Figure 1 (A) Parasternal short-axis view showing two jets straddling the septal leaflet of the tricuspid valve (TV), one into the RA and one into the RV. (B) Cross-sectional anatomy of the membranous septum (MS) denoted by the two asterisks at the level of the LVOT where it is divided into superior atrioventricular (AV) and inferior inter-ventricular (IV) portions.
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Figure 2 (A) Color flow Doppler from the apical four-chamber view showing an eccentric jet from the LVOT into RA directed toward the right atrial free wall. (B) CW Doppler demonstrates a peak velocity of the LVOT–RA systolic shunt to be 6 m/s.
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Figure 3 (A) Color flow Doppler from the apical four-chamber view showing the two shunts into the LA (arrowhead) and into the RA (arrow). (B) Anatomy of the membranous septum (between the two asterisks) divided by the septal leaflet of the tricuspid valve into superior atrioventricular (AV) and inferior inter-ventricular (IV) portions.
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2. Discussion
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The congenital form of LV to RA communication accounts for less
than 1% of all congenital heart disease and was first classified
by Gerbode et al.
7 Acquired communications are recognized as
a complication of IE, myocardial infarction and cardiac trauma
8–10 and albeit far less frequently, as complication of aortic or
mitral valve surgery. Jackson et al. reviewed a series of 310
patients with aortic valve replacement and found two cases of
postoperative iatrogenic shunts.
6 Both patients developed heart
failure, one at 6 months and the other at 1 year and were found
to have intracardiac shunts on cardiac catheterization. Similar
observation of a membranous defect following aortic valve replacement
has been reported at autopsy.
11
The membranous portion of the ventricular septum is intricately related to aortic, mitral, and tricuspid valves in addition to RA, right and left ventricles.12 The thin membranous septum, which is about 3 mm in thickness, lies posterior to the aortic root (non-coronary cusp), and to the left ventricular outflow tract. The septal leaflet of the tricuspid valve straddle the right side of the membranous septum dividing it into two portions, superior atrioventricular and inferior inter-ventricular portions. The atrioventricular portion is between the RA and left ventricular outflow tract (LVOT) and the inter-ventricular portion is between the two-ventricle (Fig. 1). The membranous septum separates the aortic root and the LVOT on one side and the RA and RV on the other side. This anatomical arrangement explains the developmental course of fistula communication from the LVOT to either RV or RA or from the aortic root to the RV. Additionally, the membranous part of the ventricular septum lies posterior to the posteromedial commissure of the mitral valve adjoining the LA. During aortic or mitral valve surgery, aggressive debridement of calcific aortic or mitral valve annuli, and in some cases, inclusion of the septum in the suture line, may result in injury causing ischemic necrosis and gradual weakening of the septum and formation of fistulae.13,14
The clinical presentation may vary based on the magnitude of the shunt. Large shunts are associated with failure of hemodynamic improvement immediately after aortic or mitral valve surgery.1 Small shunts, as in our case, are initially asymptotic and the associated murmur may be the only clue. Progressive enlargement of the defect with the resultant increase in shunt may lead to heart failure weeks or months after surgery.6 With the wide application of intraoperative echocardiography these defects can be diagnosed promptly. While the communication into RA or LA can be detected easily, the communication into anteriorly located RV can be at times difficult to image due to the intervening aortic prosthesis. The two-dimensional echocardiogram may show the fistulous tract if it is large, whereas color Doppler will invariably show the left to right shunt and the spectral Doppler can estimate the systolic gradient. The color Doppler jet from the LVOT to RA should be differentiated from an eccentric tricuspid regurgitation jet. The tricuspid regurgitation usually has a lower peak velocity unless there is severe pulmonary hypertension, whereas the shunt from LVOT to RA will usually be higher and directed toward the right atrial free wall. The hemodynamic consequences of significant shunts are readily determined by the surface echocardiography and include the assessment of RV size and function. Determination of shunt fraction and pulmonary artery pressure will quantify the hemodynamic burden on the pulmonary circulation. Obtaining this information from an echo obviates the need for cardiac catheterization indicated in early case reports.2,6,13
Surgical trauma to membranous septal tissue, already weakened from previous valve operations and previous IE, rendered our patient usceptible for developing this complication. Since the patient had no symptoms and the shunt was not significant, conservative management with bacterial endocarditis prophylaxis and frequent clinical and echocardiographic monitoring was decided.
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References
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Abstract
1. Case report