Loeffler Endocarditis Mimicking Apical Hypertrophic Cardiomyopathy
A 35-year-old woman presenting with left-side weakness visited our emergency room. She was previously healthy and did not have any clinical risk factors for cerebral vascular disease. Multiple embolic cerebral infarctions were found in her brain through magnetic resonance imaging (MRI). An ECG showed ST depression and T-wave inversion in all of the precordial leads (Figure 1). An abnormal eosinophil count (2718 per 1 μL) and elevated erythrocyte sedimentation rate (58 mm/h) were reported in her blood test; otherwise, her blood test was normal. Her cardiac enzyme level was within normal limits. Transthoracic echocardiography was performed (Figure 2 and online-only Data Supplement Movies I and II), and apical hypertrophy suggesting apical cardiomyopathy was initially reported.
Further workup for the eosinophilia, including parasitic disease, did not give any additional information. She was admitted to the neurology department and treated with anticoagulation. She complained of recurrent chest discomfort after admission, and cardiac computed tomography was performed for workup. Coronary arteries were normal, but a low attenuated endomyocardial lesion in the left ventricular apex was reported (Figure 3). Cardiac MRI depicted apical thrombus (nonenhancing lesion) with endocardial enhancement after administration of gadopentetate dimeglumine, suggesting Loeffler endocarditis1,2 (Figure 4). Reevaluation of the apex by transthoracic echocardiography after zooming and focus adjustment showed the different echogenic layering in the apical segment (Figure 5 and online-only Data Supplement Movies III and IV).
She was finally diagnosed with Loeffler endocarditis and started on high-dose steroid therapy (prednisolone 60 mg twice a day). Her chest discomfort disappeared the day after initiation of steroid therapy, and her ECG and eosinophil count became rapidly normalized (Figure 6). One month later, both the cardiac MRI (Figure 7) and echocardiography (Figure 8 and online-only Data Supplement Movies V and VI) showed an improvement in the left ventricular apical lesion.
Apical thrombus in Loeffler endocarditis is not associated with apical wall motion abnormality; therefore, Loeffler endocarditis with a small lesion in the early stage can be hard to diagnose and is sometimes confused with apical hypertrophy such as in our case. Because the early pathology of Loeffler endocarditis is eosinophilic thrombus with inflammation, cardiac MRI with delayed enhanced imaging can clearly demonstrate apical thrombus without enhancement from endomyocardium with high-signal-intensity plane.1,2 Therefore, if the diagnosis of Loeffler endocarditis is under suspicion, contrast-enhanced cardiac MRI will be very informative. Our case also shows that the endomyocardial lesion in the early stage of Loeffler endocarditis can be regressed by optimal medical therapy.
The online-only Data Supplement is available at http://circ.ahajournals.org/cgi/content/full/120/1/82/DC1.