Unusual Site of Left Ventricular Thrombus after Acute Myocardial Infarction.

Left ventricular (LV) thrombus formation is a frequent complication in patients with acute anterior myocardial infarction (MI). Its incidence is lower with inferior wall MI. Risk factors for the development of LV thrombus are consistently irrespective of infarct treatment and include large infarct size, severe apical akinesia or dyskinesia LV aneurysm, and anterior MI.

INTRODUCTION

Left ventricular thrombus (LVT) is one of the most common complications of myocardial infarction (MI). The incidence of LVT in patients with acute anterior MIs in the prethrombolytic era is ranged from 20% to 40% and with a non anterior acute myocardial infarction (AMI) and the risk of LVT was <5%.[1] Although controversial, in the contemporary era of routine early revascularization and more aggressive anticoagulation, the incidence of LVT complicating as an anterior AMI is likely reduced and is currently estimated at 5-15%.[2] The risk factors for the development of LVT are consistently irrespective of infarct treatment and include large infarct size, severe apical akinesia, or dyskinesia left ventricular (LV) aneurysm, and anterior MI.[34] Two-dimensional transthoracic echocardiography is the imaging modality used most often for assessing the presence, shape, and size of an LV mural thrombus with an excellent specificity of 85-90% and sensitivity of 95%.[5]

CASE REPORT

Here, we report a case of 40-year-old male patient who is presented in emergency department with the complaint of substernal chest pain radiating to left arm and back associated with sweating for the last 1½ day, there was no history of dyspnea, palpitation, any limb weakness, or any history suggestive of transient ischemic attack and peripheral embolization. Hemodynamically he was stable, and other systemic examinations were normal. His 12-lead electrocardiogram was suggestive of inferior wall MI [Figure 1]. His total leukocyte and eosinophil counts were normal, prothrombin time/International Normalized Ratio and activated partial thromboplastin time were normal, and other tests for hypercoagulable states were planned for the follow-up evaluation. A transthoracic echocardiogram was performed bedside which revealed hypokinesia of basal, mid inferior, and inferoseptal wall [Figure 2 and Video 1]. Surprisingly, it also revealed a mobile mass which is the most probably thrombus attached to hypokinetic inferobasal septum just near the LV outflow tract (LVOT) [Figure 3 and Video 2]. Considering the possibility that this mass was high risk for embolism, we planned for coronary angiogram followed by the surgical extraction of possible thrombus. However, unfortunately, despite the proper counseling and explanation of the risk of embolism, the patient refused for further intervention and got discharged against medical advice.

Figure 1

Electrocardiogram showing ST elevation leads II, III. aVF suggestive of inferior wall MI

Figure 2

Short axis view – small arrows showing hypokinesia of basal inferior septum, large arrow indicates left ventricle probable thrombus

Figure 3

Apical four chambers view – arrow showing left ventricle mass probably thrombus attached to basal septum

DISCUSSION

The mass formation at the LVOT is a rare phenomenon. The possible etiologies of a cardiac mass include tumor, thrombus, and vegetation. Thrombi formation at basal interventricular septum near LVOT is extremely rare as it is a region of high-velocity blood flow. Traditionally, the causes of LVT formation after acute ST-segment elevation MI include segmental dysfunction of the infracted myocardium resulting in the stasis of blood, endocardial tissue inflammation that provides a thrombogenic surface and a hypercoagulable state.[67] The higher mortality has been reported in patients with LV thrombi after infarction, especially when these develop within the first 48 h after infarction.[8] The treatment for cardiac mass is a prompt surgical resection of the mass with the patients placed on cardiopulmonary bypass. Immediate postoperative mortality in the most series ranges from 0% to 7.5%.[9] Therefore, better understanding of the circumstances in which LV thrombosis occurs may influence the patient management. In our case, thrombus formed at the very unusual site and could lead to dreaded complication for the patient. The possible etiology of thrombus formation, in our case, is hypokinesia of basal septum due to MI, but the presence of a subtle septal rupture which is not detectable on echocardiography could not be ruled out.

CONCLUSION

Thrombus around LVOT is extremely rare and might be a fatal complication after AMI.

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Conflicts of interest

There are no conflicts of interest.