COVID-19 News: Study Finds That SARS-CoV-2 Can Lead To Fluid Build-Up In the Heart - Myocardial Oedema!

COVID-19 News: In the ongoing COVID-19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a collaborative study between the Medical University of Vienna in Austria and the Medical University of Lodz in Poland has unearthed a concerning revelation. The study delves into the impact of SARS-CoV-2 on the cardiovascular system, specifically highlighting the development of myocardial oedema (MO). This COVID-19 News report aims to provide an in-depth exploration of the intricate details unveiled by this research, shedding light on the pathophysiological processes that contribute to myocardial oedema (MO).


 Myocardial Oedema Detected Via MRI In A COVID-19 Patient

It should also be noted that many are unaware that they are having this condition in them till it gets to a serious stage! Often it can lead to heart failure and also fatal outcomes!
 
Microvascular Integrity and Myocardial Fluid Homeostasis
Maintaining microvascular integrity is crucial for myocardial fluid homeostasis, a delicate balance involving capillary filtration, lymphatic fluid removal, interstitial hydration, water uptake by cardiomyocytes, and lymphatic removal. Pathological conditions, such as inflammation, hypoxia, alterations in vascular perfusion, and coagulability, can disrupt this equilibrium, leading to myocardial oedema. The study underscores the pivotal role of glycocalyx, a major component of the endothelial filtration barrier, and pericyte disintegration in the accumulation of interstitial and intracellular water. Furthermore, lymphatic dysfunction contributes to MO by increasing metabolic waste products, cytokines, and inflammatory cells in the interstitial space, ultimately leading to myocardial stiffness and impaired contractility.
 
Pathophysiological Processes Leading to Myocardial Oedema
The article provides an extensive review of various inflammatory processes contributing to MO, emphasizing their impact on the cardiovascular system. Myocarditis, ischaemia-reperfusion injury, and viral infections are explored, with specific attention given to the pathomechanisms triggered by SARS-CoV-2 infection. Notably, the interaction of pathological processes initiated or exacerbated by MO, including inflammation, endothelial cell dysfunction, and prothrombotic states, creates a vicious circle that can result in tissue necrosis, fibrosis, and organ failure. The study posits that SARS-CoV-2 infection significantly amplifies these processes, contributing to the severity of cardiovascular complications in COVID-19 patients.
 
Physiological Background of Myocardial Fluid Filtration
To provide a comprehensive understanding, the study delves into the physiological background of myocardial fluid filtration, elucidating the Starling forces and microvascular fluid filtration. The Starling principle and the revised Starling equation are discussed in detail, emphasizing the role of capillary hydraulic conductivity, differences in hydrostatic and osmotic pressure, and the permeability of the endothelial barrier. The article explains how alterations in these factors can lead to enhanced fluid filtration, resulting in MO. The intricate dynamics of myocardial fluid exchange, particularly during diastole, are highlighted, emphasizing the importance of maintaining microvascular homeostasis for preventing MO.
 
The Glycocalyx as a Key Regulator
A substantial portion of the article is dedicated to unraveling the intricacies of the glycocalyx, a critical regulator of the endothelial barrier. Composed of proteoglycans, glycoproteins, and glycosaminoglycans, the glycocalyx plays a vital role in preventing MO formation. The article explores glycocalyx disintegration, often associated with inflammation, and its impact on endothelial barrier function, microvascular flow regulation, and protection against oxidative stress and thrombus formation. The glycocalyx's negative charge and its role in regulating plasma flow and the passage of differently charged molecules are detailed, providing insights into its multifaceted functions.
 
Intercellular Junctions and Key Signaling Processes:
Continuing the exploration of microvascular homeostasis, the study emphasizes the role of intercellular junctions, specifically tight and adherens junctions, in maintaining the endothelial barrier. The intricate signaling processes involving Rac1, a molecule coordinating actin-binding proteins to stabilize intercellular junctions, are discussed. The study also delves into the role of actin filaments, attached to tight and adherens junction proteins, in opening intercellular gaps via contraction after a rise in cytosolic Ca2+. Inflammatory conditions disrupt these junctions, leading to increased permeability and fluid movement into the interstitium. The study underscores how understanding these signaling processes is crucial for developing targeted interventions to mitigate MO.
 
Inflammation and Myocardial Oedema
The profound impact of inflammation on the endothelial barrier and fluid filtration is further explored in this section. Pro-inflammatory cytokines, systemic capillary leak syndrome, and the role of SARS-CoV-2 in disrupting microvascular homeostasis are discussed in greater detail. The article highlights how inflammation, coupled with MO, can lead to impaired myocardial contraction, ventricular dysfunction, and adverse effects on various myocardial disease entities. Special attention is given to the pro-inflammatory cytokines associated with AJ and TJ internalization and increased permeability, such as TNF-α, lipopolysaccharide (LPS), and thrombin.
 
Detection of Myocardial Oedema and Myocarditis
The study elaborates on the non-invasive evaluation of myocarditis, utilizing the updated Lake Louise Criteria and cardiac magnetic resonance imaging (CMR) sequences. The challenges in applying these criteria to COVID-19 cases are acknowledged, and the importance of endomyocardial biopsy (EMB) for definitive diagnosis is emphasized. Various CMR sequences are employed to evaluate MO, hyperaemia, capillary congestion or leakage, necrosis, and fibrosis. The study recognizes the limitations in applying these diagnostic criteria to COVID-19 cases, given the unique challenges presented by the virus.
 
SARS-CoV-2's Impact on Microvascular Homeostasis
The study expands on the impact of SARS-CoV-2 on microvascular homeostasis, providing insights from a hamster model of COVID-19. Associations between fibrin-rich microthrombi, pericyte loss, and oedematous cardiomyocyte swelling are explored. The disruption of human cardiac pericytes by the SARS-CoV-2 spike protein and its involvement with the CD147 receptor are detailed. The study speculates on local hypoxia as a contributing factor to cardiomyocyte oedema formation, conferred by prothrombotic and inflammatory stimuli with impaired hypoxia resolvability.
 
Conclusion
As the world grapples with the ongoing COVID-19 pandemic, understanding the intricate interplay between SARS-CoV-2 infection and myocardial oedema is of paramount importance. This expanded review has provided a comprehensive exploration of the pathophysiological processes, physiological background, and detection methods associated with myocardial oedema. Further research is warranted to unravel unique signaling pathways and explore potential therapeutic opportunities for acute and chronic SARS-CoV-2 infections. The medical community must sustain collaborative efforts to mitigate the impact of COVID-19 on cardiovascular health and develop effective treatment strategies for those affected by myocardial oedema. By delving into the complexities of this cardiac complication, researchers and healthcare professionals can advance our understanding and enhance clinical approaches to manage the cardiovascular consequences of SARS-CoV-2 infection.
 
The study findings were published on a preprint server and are currently being peer reviewed.
https://www.preprints.org/manuscript/202312.1526/v1
 
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