Case Presentation: A 35-year-old man presented to ED with sudden onset weakness on left hand. He denied fever, dizziness, headache, and similar symptoms in the past. He doesn’t take any medication. He had upper respiratory symptoms two weeks ago and resolved. He has not received influenza and COVID-19 vaccine. Examination showed diminished power (4/5) in left hand. His initial blood tests including CBC, CMP were normal. Test for Influenza A, B, COVID-19 by PCR, HIV and syphilis were negative. The only abnormal finding was elevated troponin (0.26, normal < 0.01ng/dl). CT scan of head was normal. He was admitted for stroke workup. MRI of the brain (Fig 1) showed focal cortical infarction of right lateral and frontal lobe. Echocardiogram (Fig 2) showed apical thrombus. Cardiac MRI confirmed apical thrombus and showed patchy myocardial enhancement throughout the left ventricle suggestive of myocarditis. The cause of myocarditis was thought to be viral because of recent viral URI. Apixaban for anticoagulation and atorvastatin for secondary prevention was initiated. Factor V laden, protein C, protein S, antiphospholipid antibody, prothrombin antibody, ANA, and rheumatic factor were normal. Repeat cardiac MRI in four month showed complete resolution of the thrombus. He was treated with apixaban for 6 months and then with aspirin 81 mg daily.
Discussion: Myocarditis is Inflammation of myocardium resulting from infections, drugs, toxins or abnormal immunoreactivity. In developed countries viral infection is the leading cause. Myocarditis can result from direct damage by virus or virus associated immune response [1]. 80% of patients reported prodromal symptoms weeks prior to acute myocarditis including fever, myalgias, and fatigue [2]. Symptoms of acute phase include chest pain, dyspnea, fatigue, palpitations, and syncope. Fulminant myocarditis is severe heart failure with cardiogenic shock. Complications of myocarditis are heart failure, ventricular arrythmias and myocardial necrosis. LV thrombus and cardioembolic stoke are rare complications. A case of giant cell myocarditis with LV thrombus was reported by Whitehead NJ et al. [3].Biopsy is gold standard for diagnosis of myocarditis [4]. In our case MRI confirmed the diagnosis and biopsy was not performed as he did not have heart failure. His recent URI suggested viral myocarditis. Other causes including drug, toxins, and autoimmune conditions were ruled out. Coagulation studies were normal. LV wall motion dyskinesia and blood statis are likely cause of the thrombus [5]. No studies have shown association between coagulopathy and viral myocarditis. Management of myocarditis is symptomatic. NSAIDs should be avoided as they impede myocardial healing and exacerbate inflammation. Immunosuppressive therapy is recommended only in giant cell, eosinophilic, and autoimmune myocarditis. Patients with heart failure should receive goal directed medical therapy [6]. Current guidelines recommend treating LV thrombus with vitamin K antagonist or DOACs for 3 to 6 months [7].
Conclusions: Viral infection is the most common cause of myocarditis in developed countries. The symptoms vary greatly. LV thrombus is a rare complication of myocarditis. The mechanism of formation of thrombus is poorly understood and warrants further studies. Management of myocarditis is symptomatic. Guidelines are not established on routine use anticoagulant in myocarditis, but presence of LV thrombus needs anticoagulation for 3 to 6 months.
