SCMR 22nd Annual Scientific Sessions
Description of Clinical Presentation: 61 year old woman with a past medical history of stroke complicated by seizures, hypertension, and diabetes initially presented with generalized weakness and left-sided shaking movements. This prompted the initiation of lamotrigine for management of seizures. She subsequently developed chest pain which was aggravated by laying flat and alleviated by sitting forward. Physical exam was notable for a morbilliform rash over the extremities and trunk. Laboratory data was notable for positive troponin (peak 1.9 ng/ml, normal <0.01), eosinophilia (peak 14%), and transaminitis (peak AST 827, ALT 624) with normal bilirubin. Transthoracic echocardiogram showed an left ventricular ejection fraction (LVEF) of 45% with global hypokinesis, which was decreased from an LVEF of 59% two months prior. Cardiac magnetic resonance (CMR) imaging was pursued to differentiate between non ischemic versus ischemic patterns of left ventricular fibrosis.
Diagnostic Techniques and Their Most Important Findings: CMR images were obtained on a 1.5T magnet. Steady state free precession cine images demonstrated mildly depressed LVEF of 46%, and global hypokinesis which was more severe in the apical septum. Standard T2 weighted images suggested hyperintensity of the entire interventricular septum (Fig 1), although subendocardial involvement was difficult to interpret. Delayed enhancement images were obtained, showing circumferential subendocardial late gadolinium enhancement (LGE), in addition to diffuse enhancement of the pericardium (Fig 2). In order to discriminate subendocardial edema, repeat T2 images were obtained and reconstructed into T2 maps, which confirmed subendocardial edema in the apical septum (Fig 3).
Learning Points from this Case:
The patient’s clinical presentation of rash, eosinophilia and transaminitis after the initiation of lamotrigine were consistent with DRESS syndrome. Myocarditis was suspected in the setting of chest pain and positive troponin, and was confirmed by the typical pattern of circumferential subendocardial LGE1. Pericardial enhancement also suggested a component of pericarditis. Although circumferential LGE can also be seen in the setting of endomyocardial fibrosis and cardiac amyloidosis, these processes were considered unlikely given the acuity of the patient’s presentation and adequate nulling of the myocardium. T2 imaging also supported active inflammation. The patient was started on steroids and lamotrigine was discontinued with subsequent resolution of symptoms and improvement of EF to 56% on follow up echocardiogram. This case is an interesting example of the delayed enhancement pattern and T2 signal characteristics of eosinophilic myopericarditis in the clinical setting of DRESS syndrome.