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.