Abstract 4365350: Fulminant Myocarditis and Pulmonary Tuberculosis Presenting as Inferolateral ST-elevation myocardial infarction: A Case Report

Background: Fulminant myocarditis can present as ST-elevation myocardial infarction (STEMI) and requires early recognition and distinct management. We report a rare case of fulminant myocarditis and pulmonary tuberculosis (TB) presenting as inferolateral STEMI, complicated by biventricular failure and cardiogenic shock. Case: A 76-year-old male presented with 3 days of chest pain and infero-lateral ST elevations (Figure 1). Emergent cardiac catheterization revealed 70% calcified left main disease without plaque rupture or thrombus (Figure 2). IVUS confirmed stable disease. Echocardiogram showed LVEF 45%; an intra-aortic balloon pump (IABP) was placed, and surgery was deferred pending ticagrelor washout. Over the next 3 days, the patient’s condition worsened with rising troponin, LVEF decline to 10%, right ventricular failure, and complete heart block. The clinical picture was inconsistent with coronary anatomy, prompting suspicion for myocarditis. Endomyocardial biopsy and temporary pacing were performed. Due to worsening cardiogenic shock, mechanical circulatory support with Impella 5.5 was initiated. Immediately after Impella, the patient developed ventricular tachycardia and suction alarms due to right sided failure, therefore a veno-arterial Venoarterial Extracorporeal Membrane Oxygenation (ECMO) was initiated. Biopsy confirmed lymphohistiocytic myocarditis with immunophenotype supported the diagnosis of tuberculous myocarditis (Figure 3); respiratory cultures grew Mycobacterium tuberculosis. Despite treatment with corticosteroids, IVIG, inhaled nitric oxide, and antitubercular treatment, the patient failed to improve and expired. Conclusion: This case emphasizes the need to consider myocarditis in patients presenting with STEMI-like ECGs and rapid progression to biventricular dysfunction unexplained by coronary findings. While tuberculosis in general is a slowly progressing disease, this case shows rate manifestation which presents as rapidly progressive tubercular fulminant myocarditis. Tuberculosis cases are on the rise due to global travel and immunosuppression therapy; therefore, the index of suspicion should be high. Early recognition and aggressive mechanical support with Impella and ECMO, and immunosuppressive and targeted therapies are critical in these rare presentations.

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Journal
Circulation
Published
2025-11-03
DOI
https://doi.org/10.1161/circ.152.suppl_3.4365350
Primary Topic
Viral Infections and Immunology Research
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article
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article

Abstract 4365350: Fulminant Myocarditis and Pulmonary Tuberculosis Presenting as Inferolateral ST-elevation myocardial infarction: A Case Report

Samaneh Zoghi, Agustín E. Ure, Pushkal Jadaun, Surabhi Atreja
Circulation
Viral Infections and Immunology Research
article

Abstract 4365350: Fulminant Myocarditis and Pulmonary Tuberculosis Presenting as Inferolateral ST-elevation myocardial infarction: A Case Report

Samaneh Zoghi, Agustín E. Ure, Pushkal Jadaun, Surabhi Atreja
article en

Abstract

Background: Fulminant myocarditis can present as ST-elevation myocardial infarction (STEMI) and requires early recognition and distinct management. We report a rare case of fulminant myocarditis and pulmonary tuberculosis (TB) presenting as inferolateral STEMI, complicated by biventricular failure and cardiogenic shock. Case: A 76-year-old male presented with 3 days of chest pain and infero-lateral ST elevations (Figure 1). Emergent cardiac catheterization revealed 70% calcified left main disease without plaque rupture or thrombus (Figure 2). IVUS confirmed stable disease. Echocardiogram showed LVEF 45%; an intra-aortic balloon pump (IABP) was placed, and surgery was deferred pending ticagrelor washout. Over the next 3 days, the patient’s condition worsened with rising troponin, LVEF decline to 10%, right ventricular failure, and complete heart block. The clinical picture was inconsistent with coronary anatomy, prompting suspicion for myocarditis. Endomyocardial biopsy and temporary pacing were performed. Due to worsening cardiogenic shock, mechanical circulatory support with Impella 5.5 was initiated. Immediately after Impella, the patient developed ventricular tachycardia and suction alarms due to right sided failure, therefore a veno-arterial Venoarterial Extracorporeal Membrane Oxygenation (ECMO) was initiated. Biopsy confirmed lymphohistiocytic myocarditis with immunophenotype supported the diagnosis of tuberculous myocarditis (Figure 3); respiratory cultures grew Mycobacterium tuberculosis. Despite treatment with corticosteroids, IVIG, inhaled nitric oxide, and antitubercular treatment, the patient failed to improve and expired. Conclusion: This case emphasizes the need to consider myocarditis in patients presenting with STEMI-like ECGs and rapid progression to biventricular dysfunction unexplained by coronary findings. While tuberculosis in general is a slowly progressing disease, this case shows rate manifestation which presents as rapidly progressive tubercular fulminant myocarditis. Tuberculosis cases are on the rise due to global travel and immunosuppression therapy; therefore, the index of suspicion should be high. Early recognition and aggressive mechanical support with Impella and ECMO, and immunosuppressive and targeted therapies are critical in these rare presentations.

CirculationVol. 152(Suppl_3)
University of California Davis Medical Center (US)
Openalex Percentile: Top 52%
Viral Infections and Immunology Research
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