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 Table of Contents  
Year : 2021  |  Volume : 7  |  Issue : 1  |  Page : 69-75

Left ventricular thrombus in patients with COVID-19 – A case series

1 Department of Cardiology, Yashoda Hospitals, Somajiguda, Hyderabad, Telangana, India
2 Department of Internal Medicine, Yashoda Hospitals, Somajiguda, Hyderabad, Telangana, India

Date of Submission30-Aug-2020
Date of Decision25-Jan-2021
Date of Acceptance12-Mar-2021
Date of Web Publication24-Apr-2021

Correspondence Address:
Pankaj Jariwala
Consultant Interventional Cardiologist, MD, DNB, DNB, MNAMS, FACC, FSCAI, ICPS, Paris; Department of Cardiology, Yashoda Hospital, Somajiguda, Hyderabad - 500 082, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcs.jpcs_87_20

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Scarred culprit vessel territory secondary to nonreperfused myocardial infarctions (MIs), nonischemic cardiomyopathy, left ventricular (LV) noncompaction, endomyocardial fibrosis, and long-standing arrythmias are usually causes of LV thrombus (LVT) formation. However, in the setting of MI, large infarctions, apical akinesia or dyskinesia, LV aneurysms are often predisposed t'o the formation of LVT. The hypercoagulable or inflammatory disorder can rarely predispose to the formation of LVT. In early prethrombolytic and thrombolytic periods, LVT was present in 20%–50% of patients in the context of acute MI, more commonly in acute anterior or apical MI. While the incidence of LVT has dropped in recent times, its identification is expected to rise during the COVID-19 pandemic. Patients with chest pain are more likely to delay initial hospitalization because of a fear of contracting COVID-19. Infection with COVID-19 was associated with the remarkably hypercoagulable state which increased the risk of the early development of LVT in the setting of MI or underlying prethrombotic conditions. We present a series of four cases in which COVID-19 and cardiovascular disease were characterized by various configurations of large LVT.

Keywords: Arterial thrombosis, COVID-19 and left ventricular thrombus, COVID-19 and STEMI, COVID-19 and thrombogenesis, D-dimer

How to cite this article:
Jariwala P, Punjani A, Boorugu H, Reddy MA. Left ventricular thrombus in patients with COVID-19 – A case series. J Pract Cardiovasc Sci 2021;7:69-75

How to cite this URL:
Jariwala P, Punjani A, Boorugu H, Reddy MA. Left ventricular thrombus in patients with COVID-19 – A case series. J Pract Cardiovasc Sci [serial online] 2021 [cited 2021 Sep 23];7:69-75. Available from: https://www.j-pcs.org/text.asp?2021/7/1/69/314482

  Introduction Top

Its early identification and successful anticoagulation treatment are utterly crucial given the risk of thromboembolism associated with a left ventricular thrombus (LVT), particularly in the context of COVID-19. Patients with COVID-19 can develop a hypercoagulable state and consequently, LVT much sooner than anticipated.[1] In all COVID-19 would require easy, reproducible, bedside imaging such as echocardiography after acute myocardial infarction (AMI).[2],[3]

We describe a case series that has 4 patients with large LV thrombi including a case with thromboembolic complication. Our cases indicate the importance of early detection of LVT in COVID-19 patients with an underlying cardiac abnormality, as the early institution of medical therapy in the form of antithrombotic therapy and or surgical intervention can prevent systemic embolization or help with dissolution.

  Materials and Methods Top

For this case series, all echocardiography performed for COVID-19 patients admitted from March 2020 to our institute were retrospectively reviewed using electronic medical records (EMRs). From these EMRs, a total of 14 patients diagnosed with intracardiac thrombus were found, and digitally stored echocardiography images were reviewed by a team of qualified cardiologists and cardiac technicians. Clinical and echocardiographic data for 4 patients who had LVT were retrieved from EMRs. During the COVID-19 pandemic, we encountered 4 unusual cases of LV thrombi which were enumerated in brief as below. A summary of the cases presented in this report is given in [Table 1].
Table 1: Main characteristics of patients with Left ventricular thrombus in COVID-19 patients

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  Case Reports Top

Case 1

A 67-year-old male diabetic, a reformed smoker, presented with retrosternal chest pain for 2 days. Vital parameters were pulse rate of 98/min, blood pressure of 112/68 mmHg, respiratory rate of 22/min and room air saturation of 94%. Electrocardiogram (ECG) revealed acute ST-segment elevation MI (STEMI) with persistent ST-segment elevation and deep T-wave inversions of chest leads [Figure 1]a. Echocardiography demonstrated severe left ventricular (LV) dysfunction with regional wall motion abnormality (RWMA). The most conspicuous finding was a large, oval-shaped LVT attached to apical segments [Figure 1]b and [Figure 1d]. Computed tomography (CT) of the chest revealed bilateral peripheral ground-glass opacities (CO-RADS 4) [Figure 1]c. High sensitivity (HS)-troponin I, d-dimer levels elevated. COVID-19 severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection was strongly speculated, and this finding was verified by a nasopharyngeal real-time reverse transcriptase-polymerase chain reaction assay (RT-PCR). Hence, the patient was stabilized medically in the form of aspirin, clopidogrel, furosemide, eplerenone, perindopril, carvedilol, dexamethasone, doxycycline, ivermectin, Vitamin C, and zinc. Initially, parenteral anticoagulation in the form of enoxaparin (1 mg/kg, twice daily) for 7 days followed by direct oral anticoagulant (DOAC), dabigatran 150 mg twice daily was administered. 2 weeks later, he underwent coronary angiography (CAG) which revealed 30% lesion of the left anterior descending artery (LAD) with thrombolysis in MI 3 flow. Furthermore, repeat echocardiography demonstrated resolution of LVT hence, guideline-based therapy continued with the advice of close follow-up. In particular, DOAC was prescribed for 6-month, followed by long-term single antiplatelet therapy, clopidogrel was scheduled.
Figure 1: Electrocardiogram showed persistence of ST-segment elevation in chest leads (V1-6) with sinus tachycardia (a); Echocardiography in four-chamber view demonstrated a large left ventricular (LV) apical thrombus (black arrow, (b). Computed tomography of the chest demonstrated CO-RADS 4 changes consistent with COVID-19 and cardiomegaly (c). Cardiac magnetic resonance of the LV apex delineated LV thrombus attached to apical segments of LV (black arrow, (d). RV: Right ventricle.

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Case 2

A 45-year-old male, smoker, De novo diabetic, presented with a history of chest pain for 2 days. There were no risk factors or any significant past medical history. ECG demonstrated symmetrical T-wave inversions in chest leads, V1-6 (Wellen's sign) [Figure 2]a but echocardiography and cardiac magnetic resonance imaging would reveal a large, adherent crescent-shaped LVT attached to LV apex with moderate LV dysfunction [Figure 2]b and [Figure 1]d. CT chest revealed peripheral ground-glass opacity (CO-RADS 4) [Figure 2]c which suggestive of COVID-19 SARS-CoV-2 infection and naso/oropharyngeal swab RT-PCR confirmed it further. Laboratory investigations showed elevated d-dimer, ferritin, HS-troponin I levels, and also, hyperhomocysteinemia. The medical management in the form of dual antiplatelet therapy (DAPT), statins, DOAC (apixaban 2.5 mg twice daily), and other guideline-based therapy was started. A triple anti-thrombotic regime in the form of DAPT and DOAC was recommended for 6 months, followed by guideline-based DAPT. CAG documented thrombotic occlusion of the proximal segment of the LAD. The patient was subjected to percutaneous coronary transluminal angioplasty using a drug-eluting stent. The patient did well during follow-up with the complete resolution of LVT and the disappearance of his symptoms.
Figure 2: Electrocardiogram showed symmetrical T-wave inversion in chest leads (V1-6, I aVL) suggestive of non-ST-segment elevation myocardial infarction (a). Echocardiography in a two-chamber view revealed a crescent-shaped fixed left ventricular (LV) thrombus (white arrow, (b). Computed tomography of the chest demonstrated CO-RADS 4 changes consistent with COVID-19 (c) Cardiac magnetic resonance of the LV apex delineated crescent-shaped LV thrombus attached to apical segments of LV (white arrow, (d). LA: Left atrium.

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Case 3

A 83-year-old male, hypertensive, presented with a history of angioplasty to the LAD and the left circumflex artery, 1 year back, presented with the progressive weakness of the right side along with dysarthria and facial weakness for 8 h. The patient received anabolic steroids to improve his appetite from a local medical physician. Vital parameters recorded in the emergency room revealed that he was febrile, pulse rate of 136/min, blood pressure of 104/66 mm Hg, and besides, he was tachypnoeic with room air saturation of 76%. Arterial blood analysis demonstrated type I respiratory failure. Laboratory parameters revealed acute kidney injury and marked elevation of liver enzymes.

ECG showed q-waves in inferior leads with the poor progression of the “R” wave [Figure 3]a. CT brain showed a large infarct in the middle cerebral artery territory. Bedside echocardiography demonstrated a long in-transit thrombus extending into the LV outflow tract, protruding across the aortic valve in systole with RWMAs of basal and mid-lateral segments with mild LV dysfunction [Figure 3]b and [Figure 3]d. CT chest revealed bilateral extensive ground-glass appearance (CO-RADS 5) [Figure 3]c. His d-dimer levels were markedly elevated. At the bifurcation of the carotid artery, bilateral carotid Doppler showed nonobstructive plaques.
Figure 3: Electrocardiogram documented deep q-waves in inferior leads (III, aVF) with the poor progression of the “R” wave in the chest leads (V1-4) with sinus tachycardia. (a) Echocardiography in four-chamber (b) and parasternal views (d) demonstrated long, tubular-shaped “in-transit thrombus” in the left ventricular outflow tract. Computed tomography of the chest demonstrated CO-RADS 5 changes consistent with COVID-19 and cardiomegaly (c).

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A nasopharyngeal swab was positive for SARS-CoV-2 on real-time RT-PCR assay. Considering the high risk for any cardiac surgery, he was managed medically using low molecular weight heparin, enoxaparin (0.75 mg/kg once a day) for 7 days. The condition of the patient worsened further requiring endotracheal intubation and despite specific COVID-19 medication including remdesivir, dexamethasone and other supportive therapy could not save him. Renal and liver parameters deranged further leading to metabolic encephalopathy and he died secondary to multi-organ failure.

Case 4

A 54-year-old male, smoker, diabetic, presented with breathlessness at rest, New York Heart Association class IV for 2 days. Vital parameters recorded sinus tachycardia with borderline blood pressure with mild tachypnea. Arterial blood gas analysis revealed a pH of 7.48, partial oxygen pressure of 60 mmHg, and partial carbon dioxide pressure of 35.5 mm Hg, indicating type I respiratory failure with compensatory respiratory alkalosis. O2 therapy commenced but necessitated continuous positive airway pressure. ECG revealed ST-segment elevation in the chest leads with deep T-wave inversions [Figure 4]a. Laboratory parameters showed elevated HS-troponin I levels, d-dimer, and other inflammatory indices. Echocardiography revealed a dumbbell-shaped LV apical thrombus [Figure 4]b with RWMAs in the form of akinetic anterior, inferoposterior walls, and severe LV dysfunction (ejection fraction-28%). CT chest demonstrated increased bronchovascular markings, bilateral ground-glass appearance (CO-RADS 5) [Figure 4]c. Given the COVID-19 pandemic, RT-PCR was done which came positive. Myocardial viability analysis using cardiac MRI demonstrated delayed enhancement of the contrast of apical segments of the LV indicative of transmural infarct with apical aneurysm formation and a large apical thrombus. After medical stabilization, he was subjected to CAG that showed triple vessel disease, hence underwent coronary artery bypass surgery, LV thrombectomy, and surgical ventricular restoration [Figure 4]d. He did well at a 1-month follow-up with medical management.
Figure 4: Electrocardiogram demonstrated ST-segment elevation with T-wave inversions in chest leads (V1-6). The persistencePersistence of ST-segment elevation was suggestive of LV apical aneurysm (a). Echocardiography in zoomed-modified, three-chambered view recorded a mobile dumbbell-shaped left ventricular (LV) thrombus with aneurysm of LV apical segments (white arrow, (b). Computed tomography of the chest demonstrated CO-RADS 5 changes consistent with COVID-19 (c). Intra-operative photo showing “surgical ventricular restoration” using a technique of “endo-aneurysmorraphy” (d).

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  Discussion Top

Before an early revascularization strategy was established in the setting of the acute coronary syndrome, the incidence of LVT was very high as reported in various case series of 20%–50%, but in recent times it has dropped to <1.8%–2.5%.[4],[5] In a meta-analysis, Chi et al. observed an incidence of 23.9% of hospitalized patients with COVID-19 who developed venous thromboembolism even after receiving anticoagulation.[6] In conversely, the occurrence of arterial thrombosis is much lower than that of venous thromboembolism. As only a few cases of LVT associated with COVID-19 have been identified in the literature, the true incidence of LVT is not known, most of which had MI.[7],[8]

COVID-19 can be associated with the excessive inflammatory response with impaired coagulation system activation and manifestations of vasculitis in small vessels and severe microvascular thrombosis.[9],[10] COVID-19 can be associated with the excessive inflammatory response with impaired coagulation system activation and manifestations of vasculitis in small vessels and severe microvascular thrombosis. There is insufficient evidence of cardiac complications, such as intracardiac thrombosis and large vessel thromboembolism.[11],[12] We tried to collect the data of LVT cases in our institute to know the pattern of involvement and potential effects on patient outcomes.

The median age of patients was 60.5 years with male predominance. The risk factors in the form of diabetes and history of smoking were more prevalent in our cases. Among the 4 cases, moderate-to-severe LV systolic dysfunction had followed the development of LVT in 3 cases. In all of these cases, delayed presentation of anterior wall STEMI in those who did not receive thrombolytic therapy preceded LVT development secondary to apical LV aneurysms. In the remaining 2 cases, exaggerated response to the hypercoagulation state in COVID-19 may have induced LVT to occur along with LV dysfunction. Patient 2 has hyperhomocysteinemia, while the patient 3 got anabolic steroid as an appetizer as reported by earlier by Sabzi and Faraji.[13],[14]

In a recently published series, 18 patients with STEMI and COVID-19 infection were identified 18 patients with STEMI and COVID-19 infection were identified in a recently published series. As in our case series, there was a substantially elevated D-dimer in all these cases, which is an uncommon finding in AMI.[15] Notably, after the development of confirmed COVID-19 infection, eight out of 18 patients in this series suffered a STEMI. In another case series of 184 COVID-19 patients on intensive care units, 27% had a venous thromboembolic event, and following normal prophylaxis 3.7% had an arterial thrombotic event.[16] Besides, microvascular thrombotic lesion and post mortem tests in serious COVID-19 patients have indicated endothelial cell disruption. Another latest case series identified five large vessel ischemic strokes in patients with an age span of 33–49, all of whom were also detected on admission with COVID-19. There were already three of these people who had a substantial increase in D-Dimer levels increased.[17]

The “MI trigger theory” entails a cytochrome storm that contributes to an atheroma plaque disruption predisposing to acute coronary syndrome.[18] All the cases of LV thrombosis were preceded by AWMI with severe LV systolic dysfunction. In conjunction with LV dysfunction, the hypercoagulation in COVID-19 may have induced the development of LVT. In the literature, there are three case reports of LVT, all of which were preceded by AWSTEMI and one of which had a systemic embolization like in one of our cases.[19] The mortality and morbidity increases due to systemic embolization, particularly located in the LV outflow tract as in our case.[20]

Lattuca et al. examined 159 documented cases of LVT. Cases who were administered with vitamin K antagonists (48.4%), parenteral heparins (27.7%), and DOAC (22.6%) were included in the study. In 67.9%, antiplatelet therapy was used along with anticoagulation of which 35.2% had DAPT with anticoagulation. Major adverse cardiac events including mortality were linked with the development of LVT in the setting of AMI. Lowered mortality was consistent with complete LVT regression, achieved with multiple anticoagulant regimens.[21]

Given that, in the absence of associated atherosclerotic cardiovascular diseases such as coronary artery disease or cerebrovascular stroke, there is no hard proof for the prescription of antiplatelets.[22] No studies have documented the implications about the use of antiplatelet agents in the prevention of arterial thrombotic events in COVID-19 patients. Until then, antiplatelet therapy can be given carefully to critically ill COVID-19 patients who are at significant risk of thrombo-inflammation but at reduced risk of bleeding. With further research available in the future, the subset of patients with COVID-19 that are most likely to benefit from the use of antiplatelet therapy to avoid arteriovenous thrombotic incidents will then be identified.[23]

The Cardiological Society of India, Society for Cardiovascular Angiography and Interventions, the American College of Cardiology, and the American College of Emergency Physicians recommend that primary PCI continue to be the preferred therapy for STEMI patients in PCI-capable hospitals during the COVID-19 pandemic, where it can be delivered within a fair amount of time performed by equipped specialist team.[24],[25] A fibrinolysis-based treatment may be considered in non-PCI-capable referral hospitals or in special situations where primary PCI may not be done or is not considered the best option. Besides, anticoagulation therapy for LVT is recommended in accordance with the ESC 2017 guidelines for ACS management.[26] There was a slightly lower risk for the need of mechanical ventilation in people using oral anticoagulants. Similarly, some studies have indicated that therapeutic instead of prophylactic anticoagulation could be required during COVID-19, possibly to minimize microvascular thrombosis. It probably did not, however, transform into improvements in the rates of adverse outcomes, i.e., death.[27]

  Conclusion Top

COVID-19 patients are prone to intra-cardiac thrombosis due to a hypercoagulable state. Echocardiography is the most important, easy to use, imaging test for quick diagnosis and to assess the prognosis of the patient. Although the presence of LVT in patients with COVID-19, it represents unique features, as well as challenging situations for the cardiologists. Our case series is the largest one in the literature with 4 cases of LVT in the setting of COVID-19.

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.

  References Top

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[PUBMED]  [Full text]  
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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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