Case Presentation: A 32-year-old man with untreated hypertension for 5 years, presented with 4 hours of sharp substernal chest pain. The pain woke him up from sleep and was present at rest and on exertion. The pain lasted 30 seconds and then decreased in severity, without any identifiable alleviating factors. He received aspirin and ondansetron injection and the pain resolved. Further questioning revealed a history of hypertension and tobacco abuse. He denied a recent upper respiratory illness, kidney disease, diabetes, or hypercoagulability disorders. His family history included myocardial infarction in grandfather and uncle after the age of 60.
He had intermittent bradycardia with an otherwise unremarkable physical exam. Cardiac exam did not show a murmur and had a regular rhythm. PMI was not displaced and no heave was palpated. The white blood cell count and hemoglobin were with normal limits. The patient had diffuse ST segment elevations and PR depressions, with a troponin 7.8 on admission. Serial EKGs showed ST elevations in leads II/III/AVF and a peak troponin of 14. Lipid panel, TSH were normal. Urine drug screen was positive for nicotine and marijuana. The transthoracic echocardiogram (TTE) showed an EF greater than 55% without a pericardial effusion. Due to a high level of suspicion for pericardial disease, a cardiac MRI was obtained. Results were notable for transmural to near transmural delayed enhancement involving the inferior wall and inferoseptal wall of the mid and basilar left ventricle consistent with an ischemic process. Cardiac catheterization lab revealed a non-intervenable 100% stenosis of the mid RCA due to fibrosis. Aggressive medical management was recommended with aspirin, clopidogrel, high dose statin, ace inhibitor and counseling on smoking cessation.

Discussion: Chest pain is a frequent complaint encountered by hospitalists. The history, physical exam, and laboratory evaluation often guide the work-up and allow hospitalists to narrow the broad differential diagnosis in chest pain.

Since pericarditis or myocarditis was initially high on the differential given the young age of this patient, he was initially treated with high dose aspirin and colchicine. However with an elevated troponin and his risk factors of coronary artery disease, acute coronary syndrome (ACS) remained high on the differential. This patient was also initially begun on heparin drip, ACE-I, high dose statin. Due to the dual concern for pericarditis or myocarditis and ACS, an elegant test to non-invasively decide between the two is a contrast-enhanced cardiac MRI. The MRI has the ability to assess for inflammation in and around the heart in the myocardium and pericardium and allows a clear visualization of the anatomy. The contrast-enhanced element added the ischemic dimension to the assessment with rest and stress portions of the testing.
In the case of this patient, Cardiac MRI was an optimal test that helped elucidate the underlying cause for the initial subjective symptoms and the large ischemic territory that was ultimately corroborated by anatomical findings seen on catheterization.

Conclusions: This case is an instance of appropriate use of Cardiac MRI at obtaining a diagnosis that changes management and direction of treatment. Cardiac MRI will improve the speed at which clinicians will be able to assess non-invasively both ACS and pericardial disease more quickly leading to faster treatments. With the wider availability of cardiac MRI, hospitalists should consider the use of this test to improve patient care.