Vol 81, No 11 (2023)
Clinical vignette
Published online: 2023-10-02

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Clinical vignette

Subacute pericarditis following calcified ischemic apical aneurysm rupture and pseudoaneurysm formation

David Sá Couto*12Mariana Santos*12Maria Trêpa134Severo Torres12Patrícia Rodrigues1–4
1Department of Cardiology, Centro Hospitalar Universitário de Santo António (CHUdSA), Porto, Portugal
2ICBAS — School of Medicine and Biomedical Sciences, University of Porto, Porto, Portugal
3UMIB — Unit for Multidisciplinary Research in Biomedicine, ICBAS — School of Medicine and Biomedical Sciences, University of Porto, Porto, Portugal
4ITR— Laboratory for Integrative and Translational Research in Population Health, Porto, Portugal
*Both authors equally contributed to the study

Correspondence to:

David Sá Couto da Maia Romão, MD,

Department of Cardiology,

Centro Hospitalar Universitário de Santo António,

Largo do Prof. Abel Salazar,

4099–001, Porto, Portugal,

phone: +351 222 077 500,

e-mail: david.sa.couto@gmail.com

Copyright by the Author(s), 2023

DOI: 10.33963/v.kp.97150

Received: July 1, 2023

Accepted: August 24, 2023

Early publication date: October 2, 2023

We present a case of a 78-year-old diabetic male with multivessel coronary artery disease and a history of non-revascularized anterior myocardial infarction (15 years earlier), with severe left ventricular systolic dysfunction and apical aneurysm developed at that time. He had a single-chamber, apical cardioverter-defibrillator implanted soon after as a primary prevention strategy.

He presented with a two-week history of fatigue, weight loss, and fever. On admission, he was hemodynamically stable, febrile, with elevated inflammatory markers. Chest X-ray showed mild left pleural effusion (Supplementary material, Figure S1) and an electrocardiogram revealed sinus rhythm, PR segment depression, and anterior QS complexes (Supplementary material, Figure S1, S2).

Considering the systemic inflammatory syndrome, the patient underwent a thoraco-abdominopelvic computed tomography scan showing an enlarged left ventricle with a large intracavitary thrombus and an aneurysmatic and calcified apical wall, with two regions of apparent discontinuity, communicating with the saccular cavities also filled with thrombus, suggesting pseudoaneurysms (Figure 1). Echocardiography also showed mild pericardial effusion (Supplementary material, Videos S1 and S2). Further investigation excluded infectious, autoimmune, and neoplastic causes. Antigranulocyte scintigraphy demonstrated isolated high uptake in the pericardium, apical wall, and pseudoaneurysms.

Figure 1. Contrast-enhanced computed tomography: multiplanar reconstruction images, projecting 2-chamber (A), 3-chamber (B), 4-chamber (C), and 5-chamber (D) views, and a modified plane (E). The left ventricular (LV) apex is aneurysmatic, with a very thin and calcified wall (red arrow) and contains a large thrombus (27 × 49 mm). There are 2 regions of apparent discontinuity of the calcified apical LV wall in relationship with 2 globular sacs that protrude within the pericardium, with a hypodense lumen (red and white asterisks). There is minimal pericardial effusion. These images suggest a contained rupture of the LV apex (or pseudoaneurysms) filled with thrombus, a probable late sequel of myocardial infarction

Although speculative, the subacute (two-week) presentation of a systemic inflammatory syndrome, with the exclusion of infectious, neoplastic, or autoimmune causes, allied with the cardiac and nuclear imaging findings, supported a working diagnosis of pericardium contained myocardial apical wall rupture with pseudoaneurysm formation and probable hemopericardium.

Therapeutic decisions were made by the Heart Team. The patient was considered inoperable due to unacceptable surgical risk. Pericardiocentesis was not pursued due to the risk of increased bleeding into the pericardial space (which precluded a definite etiological diagnosis of the effusion). Anticoagulation was not initiated because, despite a large apical thrombus, the contained free ventricular wall rupture posed a significant bleeding risk.

Considering this, we followed a conser­vative treatment of the pericarditis, with high-dose acetylsalicylic acid and colchicine. This strategy was successful in reducing inflammatory markers and bringing down fever, which made the working diagnosis more likely. Magnetic resonance imaging (MRI) was not performed since it would not have impacted management decisions and the device was not MRI conditional.

The patient was eventually discharged, under an anti-inflammatory tapering scheme and palliative care, when clinical status and pericardial effusion stability were evidenced. We later found that he suffered sudden death three weeks after discharge. Its cause is unknown but probably related to pseudoaneurysm rupture and cardiac tamponade.

We presented a patient with a late mechanical complication of myocardial infarction and its rare presentation as subacute hemopericarditis. The thin calcified wall of the left ventricular apex was a ticking time bomb, and it could have presented itself earlier as sudden cardiac death. However, contained ruptures can be clinically silent, or they can present as mild unspecific clinical scenarios, including pericarditis [1]. Overall, contained ventricular wall with pseudoaneurysm formation has a poor prognosis if not subject to surgical repair. Patient management is often challenging and requires multidisciplinary and case-by-case analysis [2, 3]. In this case, due to anatomical and clinical conditions, the patient was not suitable for surgery, thus conservative management was pursued with knowledge of its probable unfavorable outcome.

Supplementary material

Supplementary material is available at https://journals.viamedica.pl/kardiologia_polska.

Article information

Conflict of interest: None declared.

Funding: The publication of this article was funded by UMIB Unit for Multidisciplinary Research in Biomedicine, ICBAS School of Medicine and Biomedical Sciences, University of Porto, Porto, Portugal. Reference: UIDB/00215/2020; UIDP/00215/2020; LA/P/0064/2020 to David Sá Couto and Patrícia Rodrigues.

Open access: This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, which allows downloading and sharing articles with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially. For commercial use, please contact the journal office at kardiologiapolska@ptkardio.pl.

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