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Severe Coronary Artery Disease Disguised as Myocarditis

Serum troponin is a marker of cardiac myocyte damage that is typically used to assess for myocardial infarction in the setting of acute coronary syndrome. However, many conditions, including cardiomyopathy, pulmonary embolism, or myocarditis, can cause an elevation in serum troponin. The most common...

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Detalles Bibliográficos
Autores principales: Tandon, Varun, Kumar, Manish, Mosebach, Christian M, Tandon, Aysha A
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488449/
https://www.ncbi.nlm.nih.gov/pubmed/31058042
http://dx.doi.org/10.7759/cureus.4159
Descripción
Sumario:Serum troponin is a marker of cardiac myocyte damage that is typically used to assess for myocardial infarction in the setting of acute coronary syndrome. However, many conditions, including cardiomyopathy, pulmonary embolism, or myocarditis, can cause an elevation in serum troponin. The most common use of this tool is to determine whether acute coronary syndrome (ACS) is occurring, but other differentials include cardiomyopathy, pulmonary embolism, and even acute heart failure. We present the case of a patient who presented with symptoms consistent with viral myocarditis but ultimately was found to have severe coronary artery disease (CAD). A 33-year-old Caucasian male with no cardiac risk factors other than a five-pack year smoking history, presented with progressively worsening upper respiratory symptoms, including sore throat and a non-productive cough that began a few weeks ago. These symptoms were associated with fevers, and 24 hours prior to admission, he developed intermittent chest pain at rest, radiating to the back, worsening in the supine position. In the emergency room (ER), the patient was found to have an elevated serum troponin of 15.61 ng/L (normal <0.05 ng/L). The electrocardiogram (EKG) showed T-wave inversions in the lateral leads. Based on his presentation and age, there was a high suspicion of viral myocarditis. However, non-ST elevation myocardial infarction (NSTEMI) had not yet been ruled out and the patient was started on started on a heparin infusion per the ACS protocol. A transthoracic echocardiogram showed wall motion abnormalities with low-normal left ventricular ejection fraction. A coronary angiogram showed severe CAD and he underwent staged a percutaneous coronary intervention with the resolution of symptoms. CAD and viral myocarditis, at times, can share common presenting symptoms, EKG changes, and laboratory findings. Out of all possible diagnoses, an elevation in serum troponin correlates to an MI up to 60% of the time. Myocarditis is the second leading cause of troponin elevation and accounts for 25% of cases. We highlight this case to discuss the importance of maintaining a broad differential and pursuing complete work-up when treating younger patients with chest pain and elevated serum troponin who lack typical risk factors for CAD.