Background: Myocarditis is the inflammation of cardiac muscle with variable presentations mimicking heart failure, myocardial infarction, arrhythmias/heart block. Epicardial and/or pericardial involvement can lead to... [ view full abstract ]
Background: Myocarditis is the inflammation of cardiac muscle with variable presentations mimicking heart failure, myocardial infarction, arrhythmias/heart block. Epicardial and/or pericardial involvement can lead to effusions and pleuritic chest pain. Its etiology can be categorized by infectious and noninfectious causes, with viruses being the most common among infectious etiologies. Noninfectious causes include autoimmune disorders such as systemic lupus erythematosus and drug-related hypersensitivity myocarditis. Definitive diagnosis is established by endomyocardial biopsy.
Case Description: A 71 year old man with history of chronic atrial fibrillation and renal disease presented to our intensive care unit after sustaining a fall at home, where he was found down by his daughter several hours later. He was febrile, tachycardic, tachypneic, and normotensive upon presentation, with the primary complaint of lethargy. EKG demonstrated prominent ST elevations in leads II, III, aVF and serum troponins were elevated at 23.18. He received a drug eluting stent in his right coronary artery for what was deemed as critical stenosis and his cardiac catheterization also showed a chronically occluded left anterior descending artery with collateral flow. The patient’s course was further complicated by coagulopathy and renal failure, although he experienced improvement of initial symptoms. Regardless, his ST elevations never normalized and his troponin exceeded 100 ng/dl; he also developed tachyarrythmias and new chest pain on hospital day 5. Repeat catheterization lead to stenting of his left anterior descending artery. Echocardiogram revealed LVEF of 42.3% with inferior and distal RV free wall infarction with the concern of a contained free wall rupture. His clinical status deteriorated with eventual endotracheal intubation and placement of an intra-aortic balloon pump. He eventually succumbed to his illness and passed on hospital day 7. Postmortem biopsy revealed lymphohistiocytic myocarditis.
Discussion: Early identification of myocarditis can be challenging especially in the setting of concurrent coronary artery disease. Lymphocytic myocarditis can be subclinical and progress to dilated cardiomyopathy (or recovery), or as described here in fulminant cardiac failure. Fulminant lymphocytic myocarditis is classified by biopsy-proven myocarditis, severe hemodynamic compromise, rapid onset of symptoms, and fever. Treatment is targeted towards acute heart failure, suppression of arrhythmias, pharmacologic and mechanical circulatory support, and even cardiac transplantation. Evidence to support routine use of antiviral agents, immunosuppressive agents, or IVIG is currently lacking. This case illustrates the importance of keeping a broad differential diagnosis in the setting of worsening cardiac disease in a critically ill patient.
