Case report
A 52-year-old man was referred to our institute with progressively increasing symptoms of dyspnea for 2 weeks. He revealed a history of anterior MI 2 years ago and received medical treatment then, which resulted in reduced symptoms.
Physical examination indicated blood pressure of 139/96 mmHg, heart rate of 86 beats/min and a respiratory rate of 18/min. An electrocardiogram (ECG) showed sinus tachycardia and ST-segment elevation in leads V1-V5 . Laboratory examinations revealed highly elevated levels of creatine kinase isozyme CK-MB (98 U/L, normal, 0–25 U/L) and troponin I (0.178 ng/mL; normal range, <0.045 ng/mL). Coronary angiography revealed a 90% occlusion of the proximal anterior descending coronary artery (Figure 1A).
The patient prepared to be treated by percutaneous transluminal coronary intervention (PCI). However, transthoracic echocardiography (TTE) revealed a small chamber (39 mm×25 mm in size) attached to the apical wall with  a free-floating isoechoic band (Figure 1B-D, Supplemental Videos 1-3), except for  left cardiac enlargement (LAD 43mm, LVEDD 55mm), reduced ejection fraction (LVEF 40%) and abnormal motion of extensive anterior wall. Intro-myocardial dissection hematoma caused by myocardial infarction was on the top of our differential diagnosis. Furthermore, an apical aneurysm with mural thrombus was not excluded.
To identify the diagnosis, a left heart contrast echocardiography and magnetic resonance imaging (MRI) were performed. The left heart contrast echocardiogram showed that there was no entry of contrast agents into the small chamber (Figure 1E, Supplemental video 4). In the meanwhile, CMRI demonstrated a slightly short T1 and long T2 abnormal signal (37 mm×29 mm in size) located in the apex (Figure 1F-G) and first pass perfusion MRI showed that the abnormal signal had no enhancement (Figure 1H).
The preoperative diagnosis was an thrombosed LV aneurysm. The patient underwent apical aneurysm resection and thromboembolectomy under general anaesthesia and cardiopulmonary bypass. The apical thrombus was removed and the apical aneurysm was sutured (Figure 2A-B). A histopathological evaluation of excised tissue with haematoxylin and eosin staining revealed the presence of the thrombus (Figure 2C). The patient recovered well and no compli­cations, for example serious arrhythmia, occurred. At the 3‑month follow‑up, the patient showed no obvious signs of heart failure. An ultrasonic cardiogram showed that the LV aneurysm had disappeared.