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'Pseudo-prolapse' in mitral regurgitation post myocarditis

Session Clinical case poster session 2

Speaker Audry Lee

Event : EuroEcho 2018

  • Topic : imaging
  • Sub-topic : Echocardiography: Valve Disease
  • Session type : Poster Session

Authors : A S Y Lee (Singapore,SG), MR Amanullah (Singapore,SG), A Law (Singapore,SG), HC Tang (Singapore,SG), SH Ewe (Singapore,SG), LY Teo (Singapore,SG)

A S Y Lee1 , MR Amanullah1 , A Law1 , HC Tang1 , SH Ewe1 , LY Teo1 , 1National Heart Centre Singapore - Singapore - Singapore ,

European Heart Journal - Cardiovascular Imaging ( 2019 ) 20 ( Supplement 1 ), i392

A 33 year old with pre-eclampsia and HELLP syndrome was found to have stillbirth at 22 weeks. This was complicated by acute pulmonary edema requiring intubation and mechanical ventilation. She had had a previous mid-trimester miscarriage.

Troponin T of 2589 (normal: <30ng/l) and NT-proBNP were elevated. Transthoracic echocardiogram revealed an LV ejection fraction of 35%. Coronary angiogram was normal. Cardiac MRI showed myocardial oedema and sub-epicardial late-gadolinium enhancement in the mid-anterior and inferolateral walls, fulfilling criteria for myocarditis. She declined endomyocardial biopsy.

Lupus anticoagulant antibody and anti-cardiolipin IgM were positive. Obstetric antiphospholipid syndrome with acute myocarditis was diagnosed. She was treated with pulsed methylprednisolone, cyclophosphamide, diuresis, beta blockade, an ACE inhibitor and ivabradine with initial improvement.

In spite of ongoing diuresis, she developed a further episode of acute pulmonary oedema 20 days later, requiring intubation. Echocardiogram was notable for new severe secondary mitral regurgitation with a restricted posterior leaflet. She received an intra-aortic balloon pump and intravenous venodilators for afterload reduction. She made gradual improvement with diuresis.

At five months review, she had NYHA class 2 symptoms in spite of optimal heart failure therapy and LVEF recovery. Repeat echocardiogram now showed increased mitral regurgitation, with what appeared to be anterior mitral leaflet prolapse, in addition to her restricted posterior leaflet.

We postulate that the severe secondary mitral regurgitation is due to localized LV remodeling following her episode of myocarditis, resulting in tethering and restriction of the posterior leaflet with pseudo-prolapse of the anterior leaflet.

Her cardiac MRI demonstrated late gadolinium enhancement in the sub-epicardial inferolateral wall suggestive of myocardial necrosis, which could have led to localized LV remodeling and subsequent posterior leaflet tethering.

In spite of normalization of her LV systolic function, her mitral regurgitation worsened after later development of anterior leaflet ‘pseudo-prolapse’, with a more prominent posteriorly directed regurgitant jet.

The term ‘pseudo-prolapse’ has been more commonly used in secondary ischaemic mitral regurgitation1, to refer to the free edge of the anterior leaflet riding above the free edge of the posterior, without true prolapse in overriding the plane of the mitral annulus. This is thought to be due to the restricted motion of the posterior leaflet, as opposed to true Carpentier II-type anterior leaflet prolapse.

This is the only case report we are aware of in which severe mitral regurgitation post-myocarditis can be attributed to pseudo-prolapse of the mitral leaflet. The management of her severe mitral regurgitation is controversial as it is unclear if surgical or percutaneous intervention would result in clinical improvement.

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