They are as follows: 1) thickened myocardium with a 2-layered structure consisting of a thin compacted epicardial layer [C] and a much thicker, noncompacted endocardial layer [N] or trabecular meshwork with deep endomyocardial spaces (N/C ratio > 2.0 at end-systole);

2) predominant location of the pathology in the mid-lateral, mid-inferior, and apical areas; 3) color Doppler evidence of deep intertrabecular recesses filled with blood from the LV cavity; and 4) absence of coexisting cardiac abnormalities (in isolated LVNC). There have been many reports of coexistent congenital cardiac disorders, including atrial septal defect, ventricular septal defect, Inhibitors,research,lifescience,medical pulmonary stenosis, anomalous pulmonary venous connection, Ebstein’s anomaly, and a bicuspid aortic valve.3-6) However, only Inhibitors,research,lifescience,medical a few cases of LVNC with LV aneurysm have been reported.10-12) The mechanism of aneurysm is uncertain. Sato et al.10) proposed impaired microcirculation of noncompacted and compacted layers as the mechanism of aneurysm formation in LVNC. However,

in our patient, the epicardial coronary arteries appeared normal on coronary computed tomography angiography and Inhibitors,research,lifescience,medical selleck chem Ceritinib neither perfusion defects nor delayed enhancement were seen on cardiac MRI. We therefore thought that our patient’s aneurysm might be congenital rather than degenerative change of LVNC. The classical triad of complications with LVNC is heart failure, ventricular arrhythmia, and systemic embolic events.8) Because there are limited data regarding treatment of this condition, it is recommended that clinical complications be managed according to the current guidelines for each clinical complication. Our but patient presented with 2 embolic events: stroke Inhibitors,research,lifescience,medical and renal infarction. The prevalence of systemic embolic

events in patients Inhibitors,research,lifescience,medical with LVNC varied in reports. Based on the high rate of embolic events reported in long-term follow-up data, Oechslin et al.8) recommended anticoagulant therapy for these patients, independent of ventricular systolic function. However, Oechslin and Jenni9) recently recommended anticoagulation therapy for patients with impaired systolic function (LV ejection fraction < 40%) Anacetrapib because deep intertrabecular recesses and slow blood flow might increase the risk of thrombus formation. Our patient had a thrombus in an apical LV aneurysm. We believed that the apical thrombus was the embolic source of her presentation with renal infarction and that the apical aneurysm with slow blood flow was a risk factor for recurrent embolic events. Therefore, we suggest that anticoagulation therapy might be needed in patients with LVNC with coexisting LV aneurysm, even in the absence of systolic dysfunction or atrial fibrillation. In conclusion, we described a rare case of LVNC with LV aneurysm presenting as recurrent thromboembolic events.