Friedli, Bernhard C.

Hufschmid, Urs

Vontobel, Jan

Zellweger, Michael J.

European Heart Journal

Jan Vontobel

Urs Hufschmid

Michael J. Zellweger

Bernhard C. Friedli

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Ventricular septal defect originating from an apical left ventricular pseudoaneurysm

Bern Open Repository and Information System (BORIS)

CARDIOVASCULAR FLASHLIGHT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .doi:10.1093/eurheartj/eht518Online publish-ahead-of-print 25 December 2013Ventricular septal defect originating from an apical left ventricularpseudoaneurysmJan Vontobel1, Urs Hufschmid1, Michael J. Zellweger2, and Bernhard C. Friedli1*1Cardiology, Department of Internal Medicine, Cantonal Hospital Baden, CH-5404 Baden, Switzerland and 2Department of Cardiology, University Hospital, Basel, Switzerland* Corresponding author. Tel: +41 56 486 26 36, Fax: +41 56 486 26 37, Email: bernhard.friedli@hin.chWe report the case of a 63-year-old man with anapical trabecular ventricular septal defect (VSD)with a restrictive unidirectional left-to-rightshunt (peak gradient 80 mmHg), originatingfrom a perfused, dyskinetic apical pseudoaneur-ysm (PA; 38 × 31 mm) primarily diagnosed bytransthoracic echocardiography (Panels A–C ).The communication between the left ventricular(LV) cavity and the PA was narrow (8 × 10 mm).The pulmonary artery pressure was normal.Cardiac magnetic resonance imaging confirmedthe LV apical lesions (the PA containing no muscu-lar tissue; arrows in Panels D and E, arrow heads inPanel E) with a small shunt volume (Qp/Qs 1.15), aslightly hypertrophied right ventricle with goodfunction and no signs of volume overload of theLV (LVEF 59%). A 12-lead ECG was normal andergometry showed excellent exercise capacityand no ischaemia.Pseudoaneurysms normally are the result ofhealed myocardial free wall rupture after myocar-dial infarction. Additional causes include local orsystemic inflammation, trauma, or cardiomyop-athies. Despite extensive diagnostic work-up,the patient surprisingly did not show any ofthem [normal late gadolinium enhancement images (Panel F), no significant coronary artery disease (CAD) at coronary angiography(Panels G– I )]. The patient’s history without trauma, prolonged infective illness, and a cardiac murmur diagnosed at the age of 20 suggestedcongenital aetiology of both the PA and the VSD. The risk of myocardial rupture remains up to speculation. Transcatheter closure andcardiac surgery were therapeutic options, but the patient refused both. In an asymptomatic patient without CAD, a small restrictiveVSD and a long history of cardiac murmur, a close clinical follow-up seemed to be the most reasonable approach.Supplementary material is available at European Heart Journal online.Published on behalf of the European Society of Cardiology. All rights reserved.& The Author 2013. For permissions please email: journals.permissions@oup.comCardiovascular flashlight 1159

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Ventricular septal defect originating from an apical left ventricular pseudoaneurysm

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