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A case of myocarditis revealing a diagnosis of Eosinophilic granulomatosis with polyangiitis
Session:
Prémio Melhor Caso Clínico
Speaker:
Rita Amador
Congress:
CPC 2022
Topic:
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Theme:
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Subtheme:
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Session Type:
Prémios
FP Number:
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Authors:
Rita Amador; Christopher Strong; Nazar Ilchyshyn; Matilde Fraga; Catarina Brízido; Ana Rita Bello; Ana Catarina Gomes; Ana Catarina Albuquerque; Maria Helena Lourenço; Pedro Freitas; António Tralhão
Abstract
<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Background: </strong></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare systemic eosinophil-rich necrotizing vasculitis affecting small to medium sized vessels. Although symptomatic cardiovascular involvement occurs in up to a third of cases, overt heart failure due to fulminant myocarditis is an infrequent complication.</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Case presentation:</strong></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">A 55-year-old female with a prior history of asthma, allergic rhinitis, nasal polyps and polyarthritis presented to the emergency room with acute chest pain, fatigue, nausea and vomiting. Upon admission she was hypotensive, tachycardic and capillary refill time was prolonged. Blood lactate was elevated and urinary output was preserved. The 12-lead electrocardiogram showed sinus rhythm and a QS pattern from V2 to V4 leads and a transthoracic echocardiogram disclosed a LVEF of 35% with diffuse hypokinesia, no right ventricular dysfunction and a moderate pericardial effusion. Cardiac troponin was elevated (2184 ng/L). In a few hours she progressed into SCAI (Society for Cardiovascular Angiography and Interventions) C cardiogenic shock requiring noradrenaline and dobutamine support. Emergent coronary angiography was performed revealing no significant epicardial stenoses. She was then referred to our Cardiac Intensive Care Unit for further workup and anticipating the need for mechanical circulatory support. </span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"> Cardiac magnetic resonance was consistent with acute myocarditis (see Figure 1A for details). Right ventricular endomyocardial biopsy demonstrated findings suggestive of necrotizing eosinophilic myocarditis (Figure 1B). Significant extracardiac findings included perilobular inflammation involving the inferior pulmonary lobes bilaterally on chest computed tomography, peripheral eosinophilia (1900 cells/µL) and elevated erythrocyte sedimentation rate (82 mm/h). </span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">This constellation of features was highly suggestive of EGPA, indeed fulfilling the American College of Rheumatology classification criteria. She was started on high dose iv methylprednisolone pulses for 3 days, followed by 1 mg/kg/day of oral prednisolone, combined with a two-month intermittent cyclophosphamide scheme, after which she began to improve. Vasopressor and inotropic support were subsequently weaned and low-dose neurohormonal blockade was introduced, allowing step-down to the Cardiology ward.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Conclusion:</strong></span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Necrotizing eosinophilic myocarditis is a rare but potentially severe complication of EGPA. In this case, aggressive immunosuppression resulted in clinical improvement, precluding the need for mechanical circulatory support. A multimodality approach including endomyocardial biopsy was key to rapid diagnosis, histological phenotyping and initiation of disease modifying therapies.</span></span></p>
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