LVT is most commonly found in myocardial infraction, low ejection fraction, LV aneurysms, and ventricular wall akinesis or dyskinesis4, 5. The thrombus formation refers to Virchow's triad: blood stasis, endothelial injury, and hypercoagulability6. McCarthy et al. reported that in unselected patients, the incidence of LVT detected by TTE is 0.1%. Most LV thrombi are formed within 2 weeks. However, some occur even more later, especially in the patients with LV systolic dysfunction6. Cullen JG et al. reported that systemic embolism was found in patients even with calcified thrombi7.
Post-myocardial infraction has been demonstrated as the most common risk factor for the development of LVT in the previous studies, and heart failure, alcohol abuse, and tobacco use has also been documented1, 8. In this case, the patient has a history of drinking and smoking for over 10 years. Approximately two years ago, the patient was completely drunk and transferred to the emergency room for rescuing care. CAG showed myocardial bridge in middle of RCA with 70% systolic stenosis, which was in concordance with the ECG examination. MRI and myocardial perfusion scintigraphy demonstrated left ventricular aneurysm with apical thrombus. Montone RA et al. reported that coronary spasm with MB is the independent risk factor of myocardial infarction and non-obstructive coronary arteries9. In this case, we speculated that MB in RCA, alcohol and tobacco abuse contributed to myocardial infraction. Essential thrombocytopenia (ET) is another important incentive that we should take into account, which have been demonstrated to be responsible for the onset of acute myocardial infarction10, 11. In this case, the patient's complete blood cell count showed platelet count was 435x109/L. Further test was carried out, gene mutation of JAK2 V617F, JAK2 exon 12, MPL, CALR was not detected in this patient, which have ruled out the possibility of ET.
LVT remains a severe complication associated with a high risk of systemic embolism. According to the latest guidelines12, 13, several anticoagulation therapies are introduced. The current standard therapy for LVT is chronic warfarin therapy for at least 3months. Recently, direct oral anticoagulants (DOACs) are introduced3, 14. The therapeutic dilemmas are: which one is the best? How long the treatment course should take? What's the dose? Several studies have suggested that even following strict anticoagulant treatment, the prognosis of patients is frustrated 15, 16. Lattuca et al. demonstrated that prolonged anticoagulation therapy duration could reduce the occurrence of major adverse cardiovascular events, but the bleeding complications raised15.
Surgical treatment is another considerable option for patients with LVT, especially for those with giant or hypermobile LVT or recurrent systemic emboli developed undergoing anticoagulant therapy2, 17. Lee et al. reported that the rate of post-treatment thromboembolism in operative treatment group is less than anticoagulation and antiplatelet group18.
Although surgical intervention has some intrinsic risks, patients would benefit from it. We highlight that for the patients with giant or hypermobile LVT or recurrent systemic emboli, surgical treatment should be a priority.