Journal of The Indian Academy of Echocardiography & Cardiovascular Imaging

: 2021  |  Volume : 5  |  Issue : 2  |  Page : 173--176

Left Ventricular Thrombosis in a Case of Acute Inferior Wall Myocardial Infarction

Anil Kumar Singhi1, Sandip Sardar2, Dilip Kumar3,  
1 Department of Pediatric Cardiology, Medica Super Speciality Hospital, Kolkata, West Bengal, India
2 Department of Cardiothoracic Surgery, Jagannath Gupta Institute of Medical Sciences and Hospital, Kolkata, West Bengal, India
3 Department of Cardiology, Medica Institute of Cardiac Sciences, Medica Super Speciality Hospital, Kolkata, West Bengal, India

Correspondence Address:
Dr. Anil Kumar Singhi
Senior Consultant Pediatric Cardiologist, Medica Super Speciality Hospital, Mukundapur, Kolkata - 700 099, West Bengal


Left ventricular (LV) thrombosis is caused by multiple etiological factors. Acute anterior wall myocardial infarction tops the list. Acute inferior wall infarction is not commonly associated with LV thrombus formation. A rare case of LV thrombus formation at LV apex due to acute inferior wall myocardial infarction is described in a young adult with successful resolution on medical therapy. Appropriate cardiac imaging is the key in correct diagnosis and treatment.

How to cite this article:
Singhi AK, Sardar S, Kumar D. Left Ventricular Thrombosis in a Case of Acute Inferior Wall Myocardial Infarction.J Indian Acad Echocardiogr Cardiovasc Imaging 2021;5:173-176

How to cite this URL:
Singhi AK, Sardar S, Kumar D. Left Ventricular Thrombosis in a Case of Acute Inferior Wall Myocardial Infarction. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2021 [cited 2022 Jan 27 ];5:173-176
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Full Text


Acute myocardial infarction (MI) can lead to left ventricular thrombosis (LVT). Anterior wall MI is the most common cause of LVT. The occurrence of LVT is very rare in a case of inferior wall MI. We report a young adult who presented with acute inferior wall MI and also had a large left ventricular (LV) thrombus.

 Case Report

A 43-year-old male, nondiabetic and nonhypertensive, had an episode of acute left-sided chest pain. The electrocardiogram showed ST segment elevation in the inferior leads suggestive of acute inferior wall MI. He was admitted to a tertiary care hospital for the management of acute coronary syndrome. His cardiac troponin T was elevated. The unconjugated bilirubin was elevated (2.3 mg%) with mild elevation of liver enzymes. The renal function was normal. Echocardiogram done on admission revealed mildly hypokinetic mid and basal inferior septum. The LV ejection fraction (LVEF) was 53%. There was a large pedunculated mass at the LV apex attached to the interventricular septum. The elongated mass was well visualized from apical four-chamber view and the anatomy was further delineated in parasternal long-axis and short-axis views [Figure 1]a,[Figure 1]b,[Figure 1]c,[Figure 1]d and [Video 1]. Coronary angiogram showed the left coronary artery normally dividing into left anterior descending (LAD) and left circumflex (LCx) arteries. The LAD was a type III vessel with evidence of mild plaque in the mid part. The LCx showed no significant disease [Figure 2]a,[Figure 2]b,[Figure 2]c and [Video 2]. The right coronary artery (RCA) was dominant and it had large thrombus in the proximal and mid part of the artery. There was evidence of spasm in the proximal part of RCA [Figure 2]d and [Figure 2]e and [Video 2]. Thrombosuction was done with Stentys AC aspiration catheter (Stentys SA, Paris, France). Loading dose glycoprotein IIb/IIIa receptor blocker was given along with intracoronary bolus dose (7.5 mg) of recombinant tissue plasminogen activator (Reteplase). At the end of the procedure, the RCA showed Thrombolysis In Myocardial Infarction III flow up to distal part [Figure 2]f and [Video 2]. He was started on subcutaneous low molecular weight heparin along with clopidogrel, rosuvastatin, and telmisartan. Heparin was later switched to oral warfarin maintaining optimal prothrombin time and international normalized ratio. He remained stable during hospital stay and the LV thrombus remained the same on echocardiogram. Cardiac magnetic resonance (CMR) imaging done on the 5th day showed 37 mm × 17 mm mass at the LV apex attached to the interventricular septum. The lesion was faintly hyperintense in turbo T2-weighted spin echo TSE (T1)/TSE (T2) sequence and hypointense in true fast imaging with steady-state free precession (TRUFI) sequence. The lesion was poorly enhancing in contrast-enhanced CMR. It had fluttering movements with cardiac pulsations suggestive of clot. There was no evidence of akinetic or hypokinetic segment seen [Figure 3]a,[Figure 3]b,[Figure 3]c,[Figure 3]d and [Video 3]. After 12 weeks of medical therapy, there was dissolution of the LV thrombus as evident on transthoracic echocardiogram. The LVEF was 56% with no evidence of regional wall motion abnormality [Figure 4]a,[Figure 4]b,[Figure 4]c,[Figure 4]d and [Video 4]. On 6 months' follow-up, he was doing well.{Figure 1}{Figure 2}{Figure 3}{Figure 4}


Video 1: Transthoracic echocardiogram showing left ventricular thrombus at apical region in (a) apical four-chamber view, (b) modified long-axis view, (c) short-axis view with colour Doppler and in (d) apical short-axis view.


Video 2: Left coronary artery angiogram in (a) left antero-posterior and cranial, (b) left anterior oblique and caudal, (c) caudal spin views showing mild disease in the proximal left anterior descending artery and no significant disease in the left circumflex artery. Right coronary artery angiogram in left anterior oblique cranial view showing (d) large thrombus in proximal and mid right coronary artery and (e) spasm of the proximal vessel. Post thrombosuction angiogram (f) showing resolution of the thrombus with good flow till distal right coronary artery.


Video 3: Cardiac Magnetic resonance imaging showing the left ventricular thrombus as a hypointense lesion in T2 image in (c) axial and (d) sagittal planes respectively.


Video 4: Echocardiogram after 12 weeks of therapy showing complete resolution of the left ventricular thrombus in (a) apical four-chamber view, (b) parasternal short-axis view and (d) parasternal long-axis view. (c) Good blood flow in the apical region seen in colour Doppler at low scale.


LVT is a known complication of acute MI. The incidence of LVT varied in different case series depending on the modality of the imaging. The CMR imaging reported incidence of 6.3%–20% with higher incidence in patients having associated LV dysfunction. Anterior wall MI is the dominant reason contributing up to 96% of cases of LVT in patients with MI in majority of the published studies.[1.2] The occurrence of LVT in acute inferior wall MI is very rare.[3],[4] One study reported inferior wall MI as the cause of LV thrombus in 4% of the cases.[5] Acute myocardial ischemia leads to sub endocardial tissue injury with inflammatory changes. A combination of endothelial injury, sluggish blood flow, and hypercoagulability also known as Virchow's triad forms the basis of LVT secondary to acute MI. Acute MI induces a hypercoagulability environment in the heart and causes LV wall motion abnormalities and dyskinesia which causes stasis of blood in the ventricles. These factors together lead to LV clot formation.[6] Large infarct size, extensive anterior wall ischemia, LV regional wall motion abnormality, LV aneurysm, and reduced LV function (LVEF <50%) are all considered risk factors for the development of LVT. Low LVEF is one of the most important causes of development of LVT.[1] The low ventricular function associated with cardiomyopathy or nonobstructive acute coronary artery syndrome like takotsubo cardiomyopathy can also lead to LV thrombus formation.[7]

In most cases, LV thrombus formation occurs at the site of wall motion abnormality due to sluggish flow. In our case, the thrombus formed at LV apex even though the wall motion abnormality was confined to the mid and basal inferior septum. It may be because apex is the portion of the heart which has least mechanical movement making it most prone for development of thrombus during the periods of sluggish blood flow and hypercoagulability. It is also possible that the patient had initially developed more extensive wall motion abnormality due to stunning and by the time he presented to us, apical contractile dysfunction had already recovered. Since the LV apex in our patient had dual blood supply, as evident from the angiography images, it recovered early and the wall motion abnormality was not evident but the inferior wall movement was still hypokinetic. Dual arterial supply in the apical region of LV is seen in 12.1% of cases.[8] Another less likely possibility would be that he had thrombotic occlusion of LAD artery also, with subsequent spontaneous recanalization. Such spontaneous reperfusion in coronary circulation is observed in 26%–30% of acute MI cases in the literature.[9] Finally, it may also be possible that the patient already had an LV clot and developed embolic occlusion of the RCA. However, it seems highly unlikely as there was no evidence of any procoagulant physiology in the index patient.

The coronary artery angiogram showed type III LAD with mild plaque and evidence of thrombus in RCA in the right dominant system. These features were suggestive of atherosclerosis as a possible cause of RCA obstruction and LVT occurrence. The LV clot in our case completely disappeared with 3-months' therapy as reported in the literature with 88% dissolution seen in 3–6 months of duration.[2]

Transthoracic echocardiogram is the first line imaging modality to diagnose LVT. It has the sensitivity of 24%–33% and specificity 90%–95%. The sensitivity of echocardiogram increases with transesophageal echocardiogram to 70% in patients with acute anterior wall MI with reduced LV systolic function. CMR imaging has higher sensitivity and better delineation of the LV clot when compared with echocardiogram. The sensitivity and specificity of CMR imaging for detection of LVT is reported as 88% and 99%, respectively.[10],[11],[12] Good imaging study tailored to the history of a patient with MI enhances the initial diagnosis and helps in monitoring the treatment.


LVT is a known complication of acute MI seen most commonly in acute anterior wall MI. Inferior wall MI less commonly causes LVT. Timely and accurate detection of this complication with appropriate imaging modalities such as echocardiogram and CMR is essential for optimum management and good outcome.


The authors would like to sincerely thank the all staff of the medical team involved in care of acute coronary syndrome.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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