Spectacular and unexpected a rare case of a giant thrombosed left ventricular aneurysm after silent myocardial infarction - challenging differential diagnosis of true or false aneurysms

Madan Raj Poudel (Bielefeld)1, D. Lawin (Bielefeld)1, C. Köster (Bielefeld)1, A. I. Diaconescu (Bielefeld)1, S. Schulze Lammers (Bielefeld)1, A. Teren (Bielefeld)1, M. Skasa (Bielefeld)1, J. Gummert (Bad Oeynhausen)2, T. Lawrenz (Bielefeld)1, J. Kramer (Bielefeld)1, E. Stellbrink (Bielefeld)1, T. Gilis-Januszewski (Bad Oeynhausen)2, D. Stoyanova (Bad Oeynhausen)2, C. Stellbrink (Bielefeld)1

1Universitätsklinikum OWL Klinik für Kardiologie und intern. Intensivmedizin Bielefeld, Deutschland; 2Herz- und Diabeteszentrum NRW Klinik für Thorax- und Kardiovaskularchirurgie Bad Oeynhausen, Deutschland


 Background:  Left ventricular free wall rupture (LVFWR) is a rare complication of acute myocardial infarction (MI). LVFWR may be restricted by pseudoaneurysm (PA) formation presenting as aneurysmal dilatation of the LV wall on transthoracic echocardiography (TTE). In contrast to a true LV aneurysm,  (PA) is bound only by the pericardium without any myocardial tissue whereas a true aneurysm (TA) is a bulging of scarred myocardium. The diagnostic differentiation between TA and PA is challenging.

Case Description: A 64-year-old male presented with mild heart failure symptoms in rehabilitation after orthopedic surgery. The electrocardiogram revealed Q waves in the anterior leads and prior unknown left bundle branch block. The patient reported a single syncopal episode with mild chest pain several months ago but did not undergo any cardiac evaluation. TTE including contrast and cardiac computed tomography (CCT) were indicative of a giant PA with rupture of the posterolateral LV wall. Coronary angiography revealed 3-vessel disease with chronic subtotal occlusion of the left anterior descending artery, significant stenosis of the Ramus interventricular posterior and significant stenosis and peripheral total occlusion of the left circumflex artery which was presumed to be the responsible vessel for the infarction and subsequent PA formation. The patient was referred for surgical treatment because of the high risk of PA free perforation. Cardiac surgery and histology confirmed the diagnosis of a TA with a huge thrombus, which was managed with pericardial patch repair. The patient was discharged after 1 week to the cardiac rehabilitation in good condition without any neurological disorder. LV function was preserved in TTE.

Discussion and conclusion: LV aneurysm is one of the most common causes and one of the most serious mechanical complications of acute MI. TA may lead to congestive heart failure, embolic events, and may also give rise to ventricular arrhythmias. PA occurs after FWR and is covered by adherent pericardium or scar tissue. Notably, there are no endocardial or myocardial cells in the PA and there is a narrow neck diameter. Mostly TA and PA are detected incidentally by TTE or other imaging modalities, but the differentiation is sometimes challenging. Echocardiography and CT have generally low diagnostic accuracy to discriminate between  true and false aneurysms. Large thrombus mass, undifferentiated myocardial border and the lateral localization provide conflicting deterministic information despite broad-based neck aneurysm.PA requires urgent surgical resection because of the likelihood of complete rupture with pericardial tamponade, while TA can often be managed conservatively. In our case, PA presentation was unusual late after infarct, in an uncommon location at the posterolateral wall in close proximity to the mitral annulus and with a wide neck. Surgery indeed revealed a TA as the sac wall contained thinned myocardium.Multimodality Imaging with late gadolinium enhancement magnetic resonance imaging resolution may accurately discriminate fibrotic tissue from healthy myocardium, blood pool, and thrombus.


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