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, Austriajutta.bergler-klein@meduniwien.ac.at

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)

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

Transthoracic Echocardiography

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Transthoracic Echocardiography

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Transthoracic Echocardiography Report

Left ventricle• 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 • Mildly thickened cusps• Normal transaortic aortic gradient: mean 19 mmHg; Peak 39 mmHg• Trivial paravalvular regurgitation

Transthoracic Echocardiography II

Severe functional mitral regurgitation (MR) • 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).

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

Turbulent PDA Jet visualized in parasternal short axis view:V. contracta 7 mm, pulmonary artery dilated 25mm

CW Doppler spectrum of the PDA flow: Maximal Velocity 5.8 m/s, end-diastolic velocity 3 m/s, ductus size 6 mm

Significant left-to-right shunt Qp : Qs = 1:1.5

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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

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

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.

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

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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