Key result
Cardiac magnetic resonance imaging clearly demonstrated endocardial fibrosis, tissue inflammation, and apical ventricular hypertrophy, obviating the need for biopsy to confirm Loeffler's endocarditis.
Why the study?
Does cardiac MRI improve the diagnosis of endomyocardial fibrosis compared to transthoracic echocardiography in a patient with rheumatoid arthritis?
Case Report (n=1)
No
Does cardiac MRI improve the diagnosis of endomyocardial fibrosis compared to transthoracic echocardiography in a patient with rheumatoid arthritis?
Cardiac MRI is a highly useful, non-invasive tool for diagnosing endomyocardial fibrosis (Loeffler's endocarditis), potentially obviating the need for endomyocardial biopsy.
May support noninvasive CMR diagnosis of Loeffler's endocarditis; hypothesis-generating and requires prospective validation before changing practice.
Loeffler's endocarditis and cardiac manifestations of the hypereosinophilic syndrome (HES) are rare and difficult to diagnose. We report a case of in a 36 year-old female with a history of rheumatoid arthritis with disabling dyspnea. The transthoracic echocardiogram demonstrated normal systolic cardiac functions and a left ventricular apical thrombus. However, using cardiovascular magnetic resonance (CMR) with inversion-recovery (IR) delayed enhancement, and cine steady-state free precession (SSFP) sequences, we were able to clearly demonstrate endocardial fibrosis, tissue inflammation, apical ventricular hypertrophy, and LV thrombus that correlate with clinical findings. We believe cardiac MRI is more useful than transthoracic echocardiography in the diagnosis and management of HES and ultimately it obviated the need for biopsy to confirm the diagnosis.
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Kharabish et al. (2014) conducted a case report in Endomyocardial fibrosis (Loeffler's endocarditis) (n=1). Cardiac Magnetic Resonance (CMR) vs. Transthoracic echocardiography was evaluated on Detection of cardiac manifestations of hypereosinophilic syndrome. Cardiac magnetic resonance imaging clearly demonstrated endocardial fibrosis, tissue inflammation, and apical ventricular hypertrophy, obviating the need for biopsy to confirm Loeffler's endocarditis.
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