Lymphocytic Myocarditis in a Previously Healthy Male Leading to Orthotopic Heart Transplantation

Document Type

Conference Proceeding - Restricted Access

Publication Date

5-9-2025

Abstract

Lymphocytic Myocarditis (LM) is the infiltration of lymphocytes into myocardial tissue. LM has a prevalence of 22 cases per 100,000 people. Prevalence is higher in males, and the median age of onset is 44. Viral infections such as Parvovirus B19, Human Herpesvirus 6 or enteroviruses are the most common cause of LM. Complications of autoimmune conditions also lead to LM. After infiltration of the myocardium, lymphocytes cause inflammation and myocyte damage with resultant fibrosis leading to heart failure. Diagnosis is confirmed using endomyocardial biopsy. Standard heart failure treatment protocols are often initiated along with support of Extracorporeal Membrane Oxygenation (ECMO) (1.2% of cases) and/or cardiac assist devices to maintain cardiopulmonary stability. While most cases resolve spontaneously, severe cases with refractory heart failure require transplant (8% of cases).

A 23-year-old man presented to urgent care with complaints of worsening shortness of breath, fatigue, body aches, and dizziness that started 4 days prior. He had no past medical or surgical history and took no medications. At baseline, he was very active. He denied drug use other than intermittent marijuana. EKG at urgent care showed intraventricular conduction block. He was admitted to the hospital where labs showed ProBNP 1375 pg/ml (elevated), Troponin 3,830 ng/L (elevated), Lactate 1.8 mmol/L, Hb 12.0 g/dl, and no leukocytosis. Respiratory panel for Influenza A&B, RSV, and COVID-19 was negative. Initial cardiac echo demonstrated LVEF 53% with basal to mid-septal hypokinesis. On hospital day 2, endomyocardial biopsy was performed to rule out giant cell myocarditis. The pathology resulted on day 6 and showed lymphocyte-mediated myocardial destruction with no giant cells or granulomas, confirming the LM diagnosis.

Pulmonary artery catheterization (cardiac index of 1.68 ml/min/m2 and mixed venous saturation of 47%) and repeat cardiac echo indicated severe heart failure, for which the patient was placed on VA ECMO on day 2. On day 3, the patient went into Ventricular Tachycardia and was treated with amiodarone, lidocaine load, and lidocaine infusion. Percutaneous ventricular assist device (PVAD) placement was complicated by pulseless right lower extremity, leading to consult for distal perfusion cannula. Hospital days 4-11 saw management of arrhythmias while awaiting organ availability. On day 12, the patient underwent orthotopic heart transplant, decannulation from ECMO, and PVAD removal. The procedure was well tolerated and on day 13 the patient was extubated. On day 14, cardiac echo measuring allograft function showed LVEF 65% and normal RV function. On day 17, the patient was undergoing routine de-escalation of critical care with multiple catheters and surgical tubes removed. His course is ongoing as of this writing.

This case highlights the essential features and management of LM, a relatively rare cause of severe refractory heart failure. The clinical course discussed here demonstrates how rapidly LM can progress from the time of presentation. Prompt management and diagnosis are required for optimal care. As in this case, LM with refractory heart failure may require progression to complex management, device support, and ultimately transplantation.

Comments

2025 Research Day Corewell Health West, Grand Rapids, MI, May 9, 2025. Abstract 1715

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