A 67-year-old female presented with syncope and was found to have left ventricular volume overload. Transthoracic echocardiography revealed a patent ductus arteriosus causing a left-to-right shunt, elevating pulmonary pressures and resulting in functional mitral and tricuspid regurgitation. While the PDA may have been an incidental finding, it was thought to be the primary cause of left ventricular volume overload. The patient was referred for percutaneous closure of the PDA to treat her symptoms.

1. An Unusual Cause of Left
Ventricular Volume
Overload after Aortic Valve
Replacement
Philipp Emanuel Bartko, MD and
Jutta Bergler-Klein, MD, Prof.
Med. Univ. of Vienna, Dept. Of
Cardiology, Vienna, Austria
jutta.bergler-klein@meduniwien.ac.at

2. Clinical Presentation and Medical History
 67 year old female admitted with syncope
 Past medical history
• Hypertension
• Transient ischemic attack (no stroke at MRI, chronic
microangiopathy and leukencephalopathy, carotid stenosis <50%)
• Aortic valve replacement (bioprosthetic Carpentier-Edwards
Perimount Magna 21 mm) in 2006 for severe symptomatic aortic
stenosis
 She complains of recurrent dizziness and pre-syncope,
exercise intolerance and dyspnoea on exertion (NYHA
class II-III)

3. Clinical and Biological Examination
 Physical examination:
• 150 cm, 45 kg, body surface area 1.37m²
• Blood pressure 119/47 mmHg
• Loud systolic and diastolic continuous heart murmur at left intercostal
space 2-3
• Apical heave
• No cyanosis
 ECG
• Sinus rhythm 80 bpm
• LV hypertrophy
• 24h Holter ECG: no significant arrhythmias or conduction disorder
 Biology
• Normal creatinine, CRP levels
• High NT-proBNP 1749 pg/ml

4. Transthoracic Echocardiography
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5. Transthoracic Echocardiography
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Watch video
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6. Transthoracic Echocardiography Report
 Left ventricle
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•
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Hyperdynamic with ejection fraction 84%
No regional wall motion abnormalities
Borderline LV enlargement [EDV 102ml; LVEDD 50 mm (36.5 mm/m²)],
LVESD 30 mm (22 mm/m²),
Moderate LV hypertrophy
 Left atrium
•
Moderately enlarged (diameter 56 mm, volume 46 ml (34 ml/m²)
 Bioprosthetic aortic valve
•
•
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Mildly thickened cusps
Normal transaortic aortic gradient: mean 19 mmHg; Peak 39 mmHg
Trivial paravalvular regurgitation

7. Transthoracic Echocardiography II
 Severe functional mitral regurgitation (MR)
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•
•
•
Central jet through the whole coaptation line
Vena contracta =10mm
PISA: Effective regurgitant orifice 0.2 cm² and regurgitant volume 43 ml
(possible underestimation due to ellipsoidal geometry of flow convergence)
Severe mitral annular dilatation (39 mm in apical 4 chamber view)
 Severe functional tricuspid regurgitation
 Vena contracta 8 mm
 High systolic pulmonary artery pressure: tricuspid velocity 3.8 m/s, estimated
sPAP ~67mmHg, enlarged inferior vena cava dilated (20mm, <50% respiratory
variation).

8. A Closer Look at the Pulmonary Trunk:
Patent Ductus Arteriosus
Turbulent continuous colour Doppler flow from the aorta
through the patent ductus arteriosus to the pulmonary artery
Watch video
CW Doppler spectrum of the PDA flow:
Turbulent PDA Jet visualized in
Maximal Velocity 5.8 m/s, end-diastolic
parasternal short axis view:
velocity 3 m/s, ductus size 6 mm
V. contracta 7 mm, pulmonary artery
dilated 25mm
Significant left-to-right shunt
Qp : Qs = 1:1.5

9. Patent Ductus Arteriosus
 Persistent communication between the proximal left
pulmonary artery and the descending aorta distal to left
subclavian artery: in adults usually isolated finding
 Results in left to right shunt, and LV volume overload
 Depending on PDA size, pulmonary artery pressure is
elevated
 Either: LV volume overload (leading to left heart failure), or
pulmonary arterial hypertension with RV pressure overload
(leading to right heart failure) may be predominant
 Eisenmenger syndrome may result in very large PDA
 PDA should be closed in patients with signs of LV Volume
overload (ESC, Class I C)
 Baumgartner H, Bonhoeffer P, De Groot NM et al. ESC guidelines for the management of
grown-up congenital heart disease. Eur Heart J 2010;31:2915-57
 Schneider DJ, Moore JW. Patent ductus arteriosus. Circulation 2006;114(17):1873-82

10. In this Case: Chicken or Egg?
 PDA was considered the predominant cause for LV volume
overload in this patient, with functional mitral regurgitation
as a consequence of mitral annular dilatation, establishing a
vicious circle with additional elevation of sPAP and positive
feedback mechanisms of mitral regurgitation.
 Alternatively, PDA might be an incidental finding and
predominant mitral regurgitation the primary cause for LV
volume overload and elevated sPAP. However, the mitral
leaflets of this patient were only mildly thickened, therefore
mitral regurgitation was most likely functional in origin.
 Patient was referred for percutaneous PDA closure

11. Further Considerations -I
 Consider indexed values for chamber quantification in
patients with small body surface area
 Ventricular dilation is a response to volume overload.
However, not every patient may respond with the same
extent of myocardial dilation to volume load. In this
case, the patient had previous severe aortic stenosis with
aortic valve replacement, and hypertension. A left ventricle
previously adapted to chronic pressure overload (with
consecutive hypertrophy, increasing diastolic stiffness and
myocardial fibrosis) may not dilate as excessively as might
be expected.
 It was surprising that PDA was not diagnosed during the
previous aortic valve replacement.

12. Further Considerations -II
 Moderately sized, unrepaired PDA may be tolerated for many
years without symptoms, and may become clinically
significant when acquired conditions such as valvular or
ischemic heart disease, or chronic obstructive pulmonary
disease or pneumonia are superimposed.
 In adults, calcification of the PDA may cause a problem for
surgical closure.
 Device closure is the method of choice, even if other cardiac
surgery is indicated due to further concomitant cardiac
lesions, and can be successfully performed in the vast
majority of adults with very low complication rates.
 Baumgartner H, Bonhoeffer P, De Groot NM et al. ESC guidelines for the management of
grown-up congenital heart disease (new version 2010). Eur Heart J 2010;31:2915-2957
 Zabal C, García-Montes JA, Buendía-Hernández A, et al Percutaneous closure of hypertensive
ductus arteriosus. Heart 2010;96:625–9

13. Summary
 Patent Ductus Arteriosus is a rare cause of LV volume
overload and functional MR in adults.
 Magnetic resonance imaging or CT angiography can aid in
additional quantification of LV volumes, and evaluation of
pulmonary artery anatomy.
 Cardiac catheterization is indicated when PAP is high on
echocardiography for estimation of pulmonary pressure and
resistance if closure is considered.
 Closure of PDA should be considered in LV volume overload,
or in pulmonary arterial hypertension with PAP still below
2/3 of systemic pressure, or pulmonary vascular resistance
<2/3 of systemic vascular resistance.
 Transcatheter device closure is the preferred technique.

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