Persistent myocarditis succescfully treated with Immunoadsorption

Suhaib Aldughaim (Aschaffenburg)1, A. Gradascevic (Aschaffenburg)1, W. Pistner (Mainaschaff)2, B. Stürmer (Aschaffenburg)1, F. Geis (Aschaffenburg)1, D. Raaz-Schrauder (Aschaffenburg)1, D. Frank (Kiel)3, M. Rosenberg (Aschaffenburg)1, S. Büttner (Aschaffenburg)1

1Klinikum Aschaffenburg Medizinische Klinik I Aschaffenburg, Deutschland; 2Gemeinschaftspraxis Kardiologie & Pneumologie Mainaschaff, Deutschland; 3Universitätsklinikum Schleswig-Holstein Innere Medizin III mit den Schwerpunkten Kardiologie, Angiologie und internistische Intensivmedizin Kiel, Deutschland



Myocarditis is a rare serious disease, characterized by an inflammation of the heart muscle. While infections are reported to be the most common cause of myocarditis, autoimmunity with cardiac antibodies has been described in the development of the disease. Although acute myocarditis usually resolves, sudden cardiac death has been implicated as a possible outcome. Persistent myocarditis can lead to cardiac dysfunction up to end-stage dilatative cardiomyopathy, especially if cardiac antibodies are present. Elimination of these antibodies by immunoadsorption (IA) has shown promising results, with significant improvement in cardiac performance. 


Case description 

The 50-year-old man with a history of bronchial asthma and ex nicotine abuse was admitted intubated to our intensive care unit after a successful resuscitation due to ventricular fibrillation. The patient complained of recurring chest pain on exertion since the COVID-19 infection 5 months ago. 

Coronary artery disease and spontaneous coronary artery dissection were ruled out by coronary angiography. An echocardiogram showed a preserved left ventricular ejection fraction with no signs of valvular heart disease. CT-Scan of the thorax region showed mediastinal and bilateral hilar lymphadenopathy. Cardiac MRI revealed severe myocarditis with atypical distribution pattern with a normal left ventricular size and preserved left ventricular ejection fraction. The myocardial biopsy showed no evidence of an acute or persistent infection, it revealed mild chronic myocardial damage with focal fibrosis without evidence of significant lymphocytic infiltration, consistent with myocarditis that had occurred in the past. A heart failure therapy with candesartan and bisoprolol was introduced. After successful weaning, the patient was discharged to rehab with a LifeVest wearable defibrillator. 

A follow-up MRI scan after 3 months showed persistent active myocarditis with now slightly reduced left ventricular ejection fraction (EF 46%). The serological tests for sarcoidosis and the CD4/CD8 quotient were unremarkable. Analysis of cardiac antibodies showed a positive result for B1-, B2- and M2-autoantibodies. 

We started immunosuppressive therapy with prednisolone (1 mg/kg body weight for 4 weeks, then 0,33 mg/kg body weight for 5 months) and azathioprine (2 mg/kg body weight for 6 months) followed by a cycle of five immunoadsorption (IA) treatments every second day, treating 2.5 times the plasma volume per session. A further follow-up MRI scan 3 months after IA revealed no evidence of further active myocarditis. Myocardial scarring was noted anteriorly, anteroseptally, inferiorly, and inferiolaterally, and the left ventricular ejection fraction was still slightly reduced (EF 49%). A subcutaneous implantable cardioverter-defibrillator (S-ICD) was implanted. 



Since progression of persistent myocarditis to dilated cardiomyopathy is considered likely and seems to occur more frequently in the presence of cardiac antibodies, our patient showed no signs of myocarditis and no further deterioration of LVEF 6 months after induction of IA. Several studies showed that the removal of these antibodies led to a recovery of left ventricular function and a better clinical outcome. Therefore, the analysis of cardiac antibodies in non-infectious persistent myocarditis could help to identify a group of patients in whom IA could be a promising option. 

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