Giant cell myocarditis in a patient presenting with pulmonary embolism and biventricular failure: a case report
CCCF ePoster library. Wouters J. Oct 4, 2017; 198111; 105
Dr. Joris Wouters
Dr. Joris Wouters
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Abstract
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Giant cell myocarditis in a patient presenting with pulmonary embolism and biventricular failure: a case report

Wouters, J 1; Convens, C 2; Lauwers, M.H. 1;  Machado Tironi, R 1

1 Dept. Anesthesia, ZNA Jan Palfijn, Merksem, Belgium

2 Dept. Cardiology, ZNA Middelheim, Antwerp, Belgium

 


Introduction
A 43-year-old man presented to our emergency department with complaints of worsening chest pain, progressive dyspnea and exercise intolerance for 2 weeks. His medical history only showed epilepsy, treated with valproate. Clinical examination showed  a transient swelling and pain of the left leg and foot. He had been treated by his general practitioner with amoxicillin clavulanic acid, followed by moxifloxacin and methylprednisolon, without improvement of symptoms.

Electrocardiogram on admission showed sinus rhythm with normal PQ interval,  left anterior fascicular block and incomplete right bundle branch block with atypical ST-depression in the precordial leads. Laboratory examination revealed mild inflammation (CRP 17 mg/l), myocardial injury (troponin I: 7.8 ng/ml), elevated D-dimers (7,1 µg/ml)  and hepatic congestion.  CT angiography was positive for pulmonary embolism (Figure 1). There were multiple bilateral thrombi on segmental and subsegmental level. Bilateral pleural effusions were present. Therapeutic anticoagulation was started (nadroparine 0.8cc 2x/day subcutaneously) and patient was transferred to the ICU. Transthoracic echocardiography showed biventricular failure with left and right intraventricular thrombi and right heart overload. Coronary angiography was performed and revealed no signs of obstructive coronary artery disease. Duplex ultrasonography could not demonstrate the presence of a deep venous thrombosis at any site.

Treatment was initially supportive and consisted of  therapeutic anticoagulation and oxygen therapy. There were no signs of organ hypoperfusion and thus no need for the use of inotropics or vasopressors. Because of the rapidly progressing heart failure, suspicion was high for myocarditis and further diagnostics were performed. Autoimmune and serological tests were taken and a MRI investigation was planned. MRI showed signs of myocarditis (Figure 2). Cardiac function further declined, evolving to cardiogenic shock with multiple organ failure despite thrombolysis, inotropic and vasoactive support. There were three epidoses of sustained ventricular tachycardia with succesfull electrical reconversion. Mechanical circulatory support was placed and an endomyocardial biopsy was performed, which confirmed the diagnosis of giant cell myocarditis (GCM) (Figure 3). Ultimately patient received combined heart and kidney transplantation. The patient had a complete recovery and was dismissed from the hospital 41 days after admission.
Conclusion
GCM, first described in 1905 [1], is rare and frequently fatal. The presentation of a subacute myocarditis, and a rapid decline in ejection fraction despite medical therapy, should raise the possibility of GCM.
Endomyocardial biopsy plays an important role in early diagnosis. The pathology of GCM is characterized by multifocal or diffuse, predominantly CD8-positive lymphocytic infiltrates, eosinophils, and multinucleated giant cells [2].
Treatment  consists of standard heart failure therapy. Immunosuppressive therapy with calcineurin inhibitors and corticosteroids is recommended, regardless of ventricular function [3] [4]. Mechanical circulatory support (MCS) is a valid option to support patients with GCM. It has been been utilized as bridge to recovery or bridge to transplantation [5] [6]. Despite combined immunosuppression, there is a high percentage of patients who require cardiac transplantation [3].
 

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