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A Case of Multiple Large Left Ventricular Clots in a Patient with COVID-19


avatar Azin Alizadehasl ORCID 1 , avatar Soudeh Roudbari 2 , avatar Pegah Salehi ORCID 2 , * , avatar Alireza Sistani 3 , avatar Atousa Mostafavi 4 , avatar Hossein Kamranzadeh Fumani 5 , avatar Alireza Yaghoubi 6 , avatar Faranak Karegar 6 , avatar Sara Adimi 7

1 Cardio-Oncology Department and Research Center, Rajaie Cardiovascular Medical and Research Center, Tehran, IR Iran

2 Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, IR Iran

3 Emergency Department, Arak University of Medical Sciences, Arak, IR Iran

4 Department of Cardiology, Tehran University of Medical Sciences, Shariati Hospital, Tehran, IR Iran

5 Hematology-Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, IR Iran

6 Heart Valve Disease Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, IR Iran

7 Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, IR Iran

How to Cite: Alizadehasl A, Roudbari S, Salehi P, Sistani A, Mostafavi A, et al. A Case of Multiple Large Left Ventricular Clots in a Patient with COVID-19. Int Cardio Res J. 2030;15(1):e107642.


International Cardiovascular Research Journal: 15 (1); e107642
Published Online: March 15, 2021
Article Type: Case Report
Received: July 17, 2020
Accepted: October 06, 2020


Introduction: In January 2020, a new coronavirus was identified as the source of a
newly developing type of pneumonia (COVID-19) in China. The number of infected
people has been rising swiftly throughout the world since then and it has been reported
to affect multiple systems apart from causing usual atypical pneumonia, one of which
being the cardiovascular system. The underlying mechanism leading to cardiac injury
has been hypothesized to be linked to a cytokine storm with unbalanced response to
T-cell subtypes or secondary hemophagocytic lympho-histiocytosis, direct cardiac
injury through viral myocarditis or cardiomyopathy through the ACE2 receptor, oxygen
supply/demand imbalance with or without coronary artery disease, hypoxemia, and
positive pressure ventilation leading to increased right ventricular afterload due to
respiratory acidosis.
Case Presentation: A 49-year-old female with a non-notable medical history presented
to the emergency department with the chief complaint of dyspnea, fever and chills, severe
dry coughs, and diarrhea. COVID-19 was confirmed by chest Computed Tomography
(CT) scan and Real-Time Polymerase Chain Reaction (RT-PCR). Due to high troponin
levels, echocardiography was done, indicating that the patient had a reduced left
ventricular ejection fraction with multiple large Left Ventricular (LV) clots, but she had
no lesions in coronary angiography.
Conclusions: The pathological mechanism by which SARS-COV-2 causes viral
myocarditis is still uncertain. However, it may result in cardiac injury via multiple
mechanisms. COVID-19 may also predispose the body to thromboembolism in different
ways. The current data suggested the existence of a hyper-coagulability state in patients
with COVID-19 and endotheliitis could explain the reason why these patients seem
more prone to venous and arterial thrombosis. However, further studies are needed to
determine the other causes of the cardiovascular complications of COVID19.


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