Abstract 13769: Too Early, Too Late: A 38-Year-Old Man with Cardiogenic Shock
A 38-year-old man with a history of autoimmune lymphoproliferative syndrome was transferred to our hospital with progressive fatigue and shortness of breath after returning from a camping trip in the Pacific Northwest. His hematologic disorder had previously been treated with a splenectomy, multiple courses of steroids, and rituximab injections. On admission the patient was found to be in decompensated heart failure and complete heart block. He developed high fevers and hemodynamic collapse, ultimately requiring extracorporeal life support for clinical stabilization. The diagnosis of fulminant myocarditis was established after myocardial biopsy demonstrated an inflammatory infiltrate with myocyte necrosis. A broad infectious and autoimmune workup was notable for a positive enterovirus serum PCR assay. Despite supportive measures, profound biventricular systolic dysfunction developed. As the patient was a poor candidate for long-term mechanical circulatory support due to right ventricular failure and recurrent ventricular arrhythmias, cardiac transplantation was pursued. Catastrophic hypoxic brain injury occurred at the time of transplant and the patient died after care was withdrawn. Examination of the patient's explanted heart unexpectedly revealed severe atherosclerotic coronary artery disease and a remote myocardial infarction in addition to active myocarditis. By prematurely accepting viral myocarditis as the sole etiology of the patient's heart failure, the contributory role of atherosclerosis in his cardiovascular deterioration and neurologic injury was not appreciated until after the therapeutic window had closed. This patient's presentation highlights the differential diagnosis of myocarditis in the setting of immunosuppression, recent wilderness exposure, and prior autoimmune disease. Consideration of the patient's cardiogenic shock in the context of his underlying lymphoproliferative syndrome yields insight into the role of autoimmunity in the pathogenesis of viral myocarditis. Finally, the clinical cardiologist is reminded of the need to fully exclude common causes of common diseases, especially when an atypical diagnosis is suspected.
- © 2011 by American Heart Association, Inc.