All authors read and approved the manuscript before submission. Funding Not applicable. Availability of data and materials Not applicable. Declarations Ethics approval and consent to participateNot applicable. Consent for publicationNot applicable. Competing interestsThe authors declare that Pramiracetam they have no competing interests. Footnotes Publisher’s Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.. however, the use of intravenous immunoglobulins and corticosteroids in combination may be effective, particularly in cases of fulminant myocarditis. Overall, the incidence of COVID-19 myocarditis requires further research, while the use of intravenous immunoglobulins and corticosteroids in conjunction requires large randomized controlled trials to determine their efficacy. Keywords: COVID-19, SARS-CoV-2, Myocarditis, Vaccine, Intravenous immunoglobulins Background An outbreak of pneumonia infections originating in December 2019, Wuhan, China, was given the name coronavirus disease 2019 (COVID-19) [1]. The cause was discovered to be a novel virus, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1]. The virus rapidly spread across the globe and on March 11, 2020, the World Health Organization declared COVID-19 a global pandemic [2]. As of August 31, 2021, there have been over 200 million confirmed cases of COVID-19 worldwide with over 4.5 million deaths [3]. The spike (S) protein of the SARS-CoV-2 virus is pivotal for its ability to bind and enter host cells [4]. The Pramiracetam S protein has two subunits, namely S1 and S2, with S1 allowing for binding Pramiracetam to host cells, while S2 carries out the process of fusion between the membranes of the virus and host cell [4]. Angiotensin-converting enzyme (ACE)-2 is the receptor to which the S protein binds [5]. Once binding has occurred, the SARS-CoV-2 virus is able to fuse its membrane with the host cell, allowing it to enter the host cell [6]. The fusion of membranes is mediated by type 2 transmembrane serine protease (TMPRSS2), a cell surface protein which cleaves ACE-2 [7]. Entry into host cells is followed by viral replication and an immune response, causing tissue damage and the clinical manifestations of COVID-19 [4]. COVID-19 typically manifests as pneumonia resulting in symptoms of cough, dyspnea and fever [8]. However, it has since been realized that COVID-19 can cause cardiovascular Pramiracetam complications, among these is myocarditis. The disease course of COVID-19 myocarditis can range from mild to severe. If not treated, the myocarditis may progress to life-threatening heart failure and arrythmias; therefore, it is imperative for clinicians to recognize possible cases of COVID-19 myocarditis and treat them accordingly [9C11]. Moreover, it may lead to an increase in ward admissions in a time where hospitals can already be overwhelmed. This literature review aims to discuss the pathophysiology and incidence of COVID-19 myocarditis, along with its presentation, diagnosis Pramiracetam and treatment. Pathophysiology of viral myocarditis Myocarditis is described as inflammation of the heart muscle, leading to damage in the absence of ischemia [12, 13]. Viruses have been suggested to be a significant etiology for myocarditis with a wide variety of causative agents including, but not limited to, adenovirus, parvovirus B19, Epstein Barr virus and cytomegalovirus [13C16]. Now, recent evidence suggests the SARS-CoV-2 virus may also be a significant infectious agent for myocarditis. The proposed pathophysiology of viral myocarditis is a combination of direct cell injury and immune-mediated cell death [12]. Early in the development of viral myocarditis high rates of Rabbit Polyclonal to BAGE3 viral replication leads to direct cardiomyocyte injury [17]. The damaged cells, and proteins released from them (such as cardiac myosin), activate toll-like receptors and inflammasomes, leading to the release of pro-inflammatory cytokines [18, 19]. As time progresses, these pro-inflammatory cytokines recruit immune cells, including natural killer cells, macrophages and T-lymphocytes, to the myocardium. These cells are involved in immune-mediated myocyte injury [17]. Moreover, interleukin (IL)-1 and IL-17 cause cardiac remodeling and fibrosis, which eventually leads to dilated cardiomyopathy and heart failure [20, 21]. Myocardial fibrosis leads to a disruption in the conduction system, leading to an increased risk of developing arrythmias [22]. Proposed mechanisms for COVID-19 myocarditis As mentioned previously, the SARS-CoV-2 virus enters human cells by binding to the ACE2 protein. While the.
All authors read and approved the manuscript before submission