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Review

COVID-19 and Myocarditis: Pathogenetic Mechanisms and Histological Features

by
Cecilia Salzillo
1,2,* and
Andrea Marzullo
1
1
Pathology Unit, Department of Precision and Regenerative Medicine and Ionian Area, University of Bari Aldo Moro, 70121 Bari, Italy
2
PhD Course in Public Health, Department of Experimental Medicine, University of Campania Luigi Vanvitelli, 80138 Naples, Italy
*
Author to whom correspondence should be addressed.
Acta Microbiol. Hell. 2025, 70(1), 3; https://doi.org/10.3390/amh70010003
Submission received: 19 November 2024 / Revised: 9 January 2025 / Accepted: 24 January 2025 / Published: 26 January 2025
(This article belongs to the Special Issue Research in the Mediterranean and Neighboring Regions for COVID-19: Facts Scenarios and Growing Awareness)
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Abstract

:
The COVID-19 pandemic has highlighted several cardiovascular complications, including myocarditis, which can be a significant cause of sudden cardiac death in young people. SARS-CoV-2 infection can cause cardiac muscle inflammation through direct mechanisms, such as viral invasion of myocardial cells, and indirect mechanisms, such as the systemic inflammatory response. Myocarditis can lead to life-threatening electrical dysfunctions and arrhythmias. Although post-infection myocarditis is more common, rare cases of post-vaccination myocarditis have also been reported, especially with mRNA vaccines. However, these post-vaccination cases tend to be mild and self-limiting, with a good response to treatment. Despite the associated risks, the benefits of vaccination far outweigh the risks, significantly reducing the incidence and severity of COVID-19 infections and related heart complications. It is crucial to continue surveillance and research to better understand the association between COVID-19, myocarditis and sudden cardiac death in the young and improve prevention and intervention strategies. In this literature review, we analyzed the pathogenetic mechanisms and histological features of myocarditis associated with COVID-19 and its vaccination, and focused on the correlation with sudden cardiac death.

1. Introduction

Over the past three years, the COVID-19 pandemic, caused by the SARS-CoV-2 virus, has posed an unprecedented challenge to global public health, raising concerns about its broad and complex clinical manifestations [1]. Although most patients present with respiratory symptoms such as cough, fever, and difficulty breathing, the infection has been shown to have systemic effects involving various organs, including the cardiovascular system [2]. Among the most significant complications emerging from the disease, myocarditis can seriously compromise cardiac function and, in extreme cases, lead to lethal outcomes [3].
Myocarditis associated with COVID-19 has aroused particular interest among both researchers and clinicians, not only due to its incidence, but also due to its multifactorial nature. Recent studies have shown that SARS-CoV-2 infection can trigger an excessive inflammatory response, known as cytokine storm, which plays a crucial role in damaging cardiac tissue [4,5,6]. Furthermore, the possibility of direct invasion of the virus into the myocardium, through binding to ACE2 receptors, represents another pathogenic mechanism that requires attention [7,8,9]. It is important to note that myocarditis is not exclusively due to COVID-19 infection, as it has also been associated with vaccination against the virus, particularly with mRNA vaccines, sparking heated debate about the benefits and risks of vaccination [10,11,12].
The incidence of myocarditis in COVID-19 patients has been the subject of numerous clinical and epidemiological studies, suggesting a variable prevalence that seems to correlate with the severity of the infection, age, and pre-existing comorbidities [13]. Furthermore, post-vaccination myocarditis has raised questions about the safety of vaccines, particularly in younger and more vulnerable population groups, leading to recommendations for post-vaccination monitoring and surveillance [14].
The diagnosis of myocarditis associated with COVID-19 is complicated by the overlap of symptoms with those of other respiratory and cardiovascular diseases, making it necessary to implement rigorous diagnostic protocols. Diagnostic tools, such as electrocardiogram, serum biomarkers, and cardiac magnetic resonance imaging, are essential for timely and accurate diagnosis [15,16].
The clinical management of myocarditis linked to COVID-19 varies depending on the severity and characteristics of the clinical setting, requiring a multidisciplinary approach that includes both symptomatic treatment and cardiac support in case of serious complications [17,18,19].
SARS-CoV-2 variants have emerged as a critical factor in the COVID-19 pandemic, significantly impacting transmissibility and management of the infection. As reported in the study conducted in the Nabatieh region of Lebanon, the spread of highly transmissible variants, identified by the lack of the S gene in PCR tests, coincided with a dramatic increase in the prevalence of positive cases. In fact, since January 2021, these variants have reached a prevalence of 96.5% in infections, suggesting their superior transmission capacity. Lockdowns have proven effective in reducing infection rates, but the easing of restrictions and indoor gatherings have contributed to a sharp increase in cases, highlighting the importance of rigorous preventive measures and continuous monitoring of variants to contain the pandemic [20].
In this context, the present review aims to examine in detail the current evidence regarding the relationship between COVID-19 and myocarditis, analyzing the pathogenetic mechanisms underlying this complication and the histological characteristics, and also focuses on the correlation with sudden cardiac death.

2. Pathogenetic Mechanisms

2.1. COVID-19 Myocarditis

Myocarditis associated with SARS-CoV-2 infection is a complex phenomenon involving several pathogenic mechanisms. Understanding these mechanisms is crucial to develop effective diagnostic and therapeutic strategies. The main mechanisms through which COVID-19 can lead to myocarditis are reported below (Table 1) [21,22,23,24,25,26,27,28,29,30,31,32]:
  • Direct Invasion of the Myocardium [21,22]: one of the proposed mechanisms for myocarditis from COVID-19 is the direct invasion of the myocardium by the virus. SARS-CoV-2 binds to ACE2 (angiotensin-converting enzyme 2) receptors, which are present not only in lung cells, but also in other cells of the body, including cardiomyocytes. This interaction can lead to the following:
    • Direct Cellular Injury: The entrance of the virus into cardiac cells can result in cell death and impaired cardiac function.
    • Apoptosis and Necrosis: The virus can induce apoptosis (programmed cell death) and necrosis in cardiomyocytes, contributing to inflammation and cardiac dysfunction.
  • Inflammatory Response and Cytokine Storm [23,24,25]: one of the most serious complications of SARS-CoV-2 infection is the cytokine storm, an excessive immune reaction characterized by the massive production of inflammatory cytokines. This mechanism manifests itself in various ways:
    • Release of Pro-inflammatory Cytokines: Cytokines such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α) are released in high quantities. These molecules can damage cardiac cells and amplify inflammation.
    • Cellular Infiltration: The cytokine storm leads to an infiltration of immune cells (such as lymphocytes and macrophages) into the cardiac tissue, contributing to inflammation and myocardial damage.
  • Coagulopathy and Microthrombosis [26,27,28]: COVID-19 is associated with a predisposition to coagulation and thrombus formation. This mechanism can affect the myocardium in several ways:
    • Coronary Vessel Microthrombosis: The formation of microthrombi can compromise the blood supply to cardiac tissues, causing ischemia and myocardial damage.
    • Endothelial Damage: The infection can damage the vascular endothelium, contributing to a systemic inflammatory response and increasing the risk of thrombotic events.
  • Autoimmune Reactions [29,30]: another important aspect concerns the possible development of autoimmune reactions in response to SARS-CoV-2 infection:
    • Molecular Mimicry: Some studies suggest that viral proteins may present structural similarities with cardiac proteins, leading to an immune response that also attacks cardiac tissues.
    • T Lymphocyte Activation: The immune response can activate specific T lymphocytes against cardiac antigens, further contributing to inflammation and myocardial damage.
  • Autonomic Nervous System Dysregulation [31,32]: SARS-CoV-2 infection can affect the autonomic nervous system, which regulates several cardiac functions:
    • Cardiac Control Alterations: Dysregulation of the autonomic nervous system can lead to dysfunctions in heart rate and cardiac contractility.
    • Autonomic Stress: Acute stress situations can exacerbate inflammatory responses and myocardial damage.
The timing of the development of myocarditis in patients with SARS-CoV-2 infection may vary based on the complexity of the mechanisms of myocardial damage.
In the acute phase of the infection, myocarditis can occur within a few days of the onset of respiratory symptoms, suggesting direct myocardial damage induced by the virus. SARS-CoV-2 can directly infect cardiomyocytes through ACE2 cell entry receptors, causing myocyte necrosis and lymphocyte inflammatory infiltrates [21,22]. Furthermore, the systemic inflammatory response, known as a cytokine storm, may also contribute [23,24,25]; it is characterized by a massive release of pro-inflammatory cytokines, such as IL-6 and TNF-α, which can amplify systemic tissue damage, including at the cardiac level.
In some cases, myocarditis develops in the post-acute stage of the infection, probably due to autoimmune mechanisms triggered by the virus. In particular, the immune system may produce specific anti-heart antibodies due to molecular mimicry between viral antigens and myocardial proteins. Molecular mimicry between viral proteins, such as Spike, and myocardial antigens can trigger autoimmune responses, contributing to myocarditis and dilated cardiomyopathy. These autoantibodies have also been detected in post-COVID syndrome, highlighting persistent inflammation with potential for chronic heart damage [29,30].
Late manifestations may also be associated with chronic conditions such as long COVID, in which persistent alterations to the immune system continue to cause subclinical inflammation in the heart, a syndrome characterized by persistent multisystem symptoms, which may include fatigue, arrhythmias, and chest pain.
Delayed myocarditis can evolve towards a chronic course, with consequences such as subclinical myocardial dysfunction, fibrosis of the cardiac tissue, and in some cases, progression towards dilated cardiomyopathy. These outcomes may predispose individuals to complications such as cardiac failure or malignant arrhythmias, increasing the risk of fatal cardiovascular events [33].
Consequently, continuous surveillance is essential, both during the infection and in the recovery phase, to identify early signs of cardiac involvement and develop targeted therapeutic strategies.

2.2. COVID-19 Vaccine Myocarditis

Post-COVID-19 vaccination myocarditis, although rare, has attracted significant scientific interest and clinical concern, especially among young male adults. Studies indicate that most cases of myocarditis occur after administration of the second dose of mRNA vaccines. The pathogenetic mechanisms leading to post-vaccination myocarditis are still under investigation, but several factors and mechanisms have been proposed that may contribute to this condition (Table 2) [33,34,35,36,37,38,39].
  • Vaccine-Induced Immune Response [33,34]: the COVID-19 mRNA vaccine is designed to stimulate an immune response against the Spike protein of the SARS-CoV-2 virus. This immune response may, in rare cases, have adverse effects:
    • Activation of the Inflammatory Response: Administration of the vaccine causes the release of pro-inflammatory cytokines and chemokines, which may activate a systemic immune response. In some individuals, this response may be exaggerated, leading to myocardial inflammation.
    • Antibody Production: The vaccine induces the production of specific antibodies against the Spike protein. In rare cases, these antibodies may react with similar structures in cardiac tissue, contributing to autoimmune damage.
  • Molecular Mimicry [34,35]: another proposed mechanism for post-vaccination myocarditis is molecular mimicry:
    • Structural Similarity: Viral proteins, particularly the Spike protein, may have structures like cardiac proteins. This similarity may lead to an inappropriate immune response, in which the immune system attacks cardiac cells thinking it is fighting a viral infection.
    • Autoimmunity: Activation of an autoimmune response against the myocardium may occur, leading to inflammation and tissue damage.
  • Immune Regulatory Dysfunction [36,37]: after vaccination, the immune system is activated and must regulate the inflammatory response:
    • Dysregulation of the Inflammatory Response: In some individuals, the inflammatory response may not be adequately controlled, leading to a cytokine storm like that seen in severe cases of COVID-19. This can cause significant tissue damage in the heart.
    • T-Cell Activation: T-cells may be over-activated, contributing to the infiltration of immune cells into the myocardium and subsequent inflammation.
  • Vascular Response Side Effects [37,38]: vaccination may also affect the vascular system, contributing to potential cardiac complications:
    • Endothelial Activation: The response to the vaccine may lead to endothelial inflammation, which can damage the blood vessels that supply blood to the heart. This can lead to myocardial ischemia and inflammation.
    • Coagulopathy: Although less evident than what is observed in COVID-19 cases, mild coagulopathy may occur in some patients, which could contribute to the formation of microthrombi and cardiac ischemia.
  • Genetic Factors and Individual Predisposition [38,39]: not all subjects develop post-vaccination myocarditis, suggesting that genetic factors or personal predispositions may play a role:
    • Genetic Variability: Differences in individual immune response, potentially linked to genetic factors, may influence susceptibility to myocarditis.
    • Preexisting Comorbidities: Some individuals may have preexisting conditions—such as autoimmune diseases or other immunological abnormalities—that make them more vulnerable to developing cardiac inflammation.

3. Histological Features

The histological features of COVID-19 and its vaccination-associated myocarditis have similarities, but also distinctive features, as reported in Table 3. These findings suggest that myocardial damage is partly mediated by direct inflammation and partly by microvascular ischemia. In addition, some analyses have shown poor viral replication in myocardial tissue, suggesting a possible secondary role of immune-mediated damage compared to direct infection [21,40,41].
In the case of myocarditis associated with mRNA vaccination, histological analyses have shown predominantly lymphocytic inflammatory infiltrates, like those of viral myocarditis. However, post-vaccination cases tend to be less extensive and more localized, with necrotic myocardial damage generally less pronounced than in virally induced myocarditis. These findings are consistent with a hyperactive or autoimmune immune response, probably induced by molecular mimicry between vaccine antigens and myocardial tissue proteins [35,42]. Furthermore, recent studies have hypothesized that lipid messenger RNA may temporarily activate the innate immune response, contributing to a transient inflammatory picture [43].
Further insights into histopathological analysis and immunological studies could contribute to clarifying the specific mechanisms of pathogenesis and guiding targeted therapeutic strategies.
The histological differences between the myocarditis associated with COVID-19 infection and its vaccination (Figure 1) are significant and reflect the different etiology of these conditions.
The histological differences are due to the more systemic and severe nature of the inflammatory and vascular damage in COVID-19 myocarditis compared to the more localized and self-limiting inflammatory reaction in rare cases of vaccination-induced myocarditis.

4. Treatment of Myocarditis

Treatment of myocarditis varies based on severity and etiology, with symptomatic management and intensive support being needed in more severe cases.
In acute forms of myocarditis, treatment is based on cardiovascular stabilization, with inotropic drugs and diuretics for heart failure and antiarrhythmics.
In patients with autoimmune or prolonged inflammation-mediated myocarditis, such as in post-COVID-19 or chronic forms, corticosteroids and other immunosuppressants, such as azathioprine or cyclosporine, can be used to reduce myocardial inflammation [39].
Prolonged forms of myocarditis, often associated with fibrosis and myocardial dysfunction, require continued monitoring and targeted treatment to prevent pathological cardiac remodeling. ACE inhibitors and beta-blockers are commonly used to improve ventricular function and reduce cardiac burden, while aldosterone receptor antagonists may be indicated in the presence of advanced fibrosis [33].
In patients with a high risk of arrhythmic complications, such as sustained ventricular tachycardia, implantation of cardiac defibrillators may be necessary [38].
Future research is aimed at developing targeted therapies based on the pathogenetic mechanisms of myocarditis, such as cytokine inhibitors or next-generation immune modulators, which could offer more specific and less toxic options for patients with prolonged forms [36].

5. Sudden Cardiac Death

Sudden cardiac death (SCD) is a clinical event characterized by a sudden loss of cardiac function, often caused by fatal arrhythmias such as ventricular fibrillation or sustained ventricular tachycardia [44,45]. This phenomenon represents a major cause of mortality associated with both SARS-CoV-2 infection and, in rare cases, COVID-19 vaccination, although the underlying mechanisms are distinct [46,47].
In patients with COVID-19, the risk of SCD is significantly increased, especially in cases of severe disease. Several factors contribute to this condition: direct myocarditis induced by the virus, activation of the immune system with release of pro-inflammatory cytokines, and hypercoagulability associated with thromboembolism. Autopsies of patients who died from COVID-19 have shown widespread myocardial lesions, including interstitial inflammatory infiltrates and focal necrosis, confirming the direct impact of the infection on the myocardium. Furthermore, metabolic alterations and systemic hypoxia can aggravate the electrical instability of the heart, predisposing individuals to fatal arrhythmic events [48].
On the other hand, vaccination against COVID-19, which is essential to prevent severe disease and mortality, has been associated with rare cases of myocarditis and pericarditis, especially with mRNA vaccines. Such cases have been predominantly observed in young males, with an incidence of approximately 1–5 cases per 100,000 doses administered. Although post-vaccination myocarditis is generally self-limiting and mild, rare episodes of severe arrhythmias have been reported, with the theoretical possibility of SCD. The main pathogenic hypothesis involves an aberrant immune response, potentially mediated by a cross-autoimmune reaction or by an exaggerated activation of T and B cells [35,42].
The overall assessment of the risks and benefits of vaccination clearly indicates a positive balance: vaccines have drastically reduced the incidence of severe COVID-19, hospitalizations and deaths, including those linked to cardiovascular events. However, continued vigilance is needed to identify potential rare side effects and to further improve the safety of vaccination campaigns. Future studies are crucial to delve into the molecular mechanisms of cardiac complications of both infection and vaccination, to develop targeted therapeutic strategies and prevent fatal events [43,49].

6. Variations in Global Reporting and Long-Term Outcomes

A more balanced perspective on COVID-19- and vaccination-associated myocarditis could emerge from more uniform global reporting and thorough assessment of long-term outcomes.
Currently, differences in reporting systems between countries and variability in diagnostic resources significantly impact understanding of incidence and severity. Indeed, differences in diagnostic protocols and access to advanced tools, such as cardiac magnetic resonance imaging, can lead to an underestimation of less severe cases [33].
Furthermore, the paucity of long-term studies limits understanding of the clinical evolution of both forms of myocarditis. COVID-19 myocarditis can lead to chronic complications such as subclinical cardiac dysfunction or increased susceptibility to arrhythmias, even months after the initial infection [12,46]. In the rare cases of post-vaccination myocarditis, studies indicate a benign course, but prolonged monitoring is necessary to assess the possible onset of late effects [38].
Greater standardization in epidemiological and clinical data collection, together with long-term monitoring of patients, could better balance the risks and benefits of prevention strategies, such as vaccination.
Furthermore, the development of international registries could help improve the transparency and comparability of data, providing crucial information to optimize preventive and therapeutic interventions [36].

7. Future Directions

Future directions of COVID-19 myocarditis research and vaccination should focus on the in-depth exploration of molecular mechanisms and development of targeted therapeutic strategies.
A more detailed understanding of immune and cellular interactions, such as molecular mimicry between viral or vaccine proteins and cardiac antigens, could elucidate the role of autoimmune responses in myocardial damage [39].
Genetic studies could identify predisposing variants that make certain individuals more susceptible to myocarditis, contributing to a more personalized approach to prevention and treatment [37].
New advanced biomarkers, such as specific molecular signals of myocardial damage or subclinical inflammation, could improve early detection and monitoring of disease progression [38].
Therapeutically, there is a need to test more specific strategies such as cytokine inhibitors or immune response modulators, which could reduce myocardial inflammation without compromising the effectiveness of the immune system [36].
Finally, the implementation of international registries for longitudinal data collection could allow for a more accurate comparison of long-term outcomes and facilitate the definition of optimized clinical guidelines [33].

8. Conclusions

Myocarditis associated with COVID-19 and its vaccination is a multifactorial condition involving mechanisms such as direct viral invasion, inflammatory responses, coagulopathy, and autoimmunity. Although rare, post-vaccination myocarditis requires attention to improve the safety of vaccination campaigns, while highlighting a largely positive benefit-risk balance.
In-depth understanding of the pathogenetic mechanisms is crucial for developing targeted diagnoses and therapies and reducing serious complications such as sudden cardiac death. Continued monitoring and further studies remain essential to optimize management and build confidence in prevention and treatment strategies.

Author Contributions

Conceptualization, C.S. and A.M.; methodology, C.S.; investigation, A.M.; resources, C.S.; writing—original draft preparation, C.S.; writing—review and editing, A.M.; supervision, A.M. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. Histological differences between the myocarditis associated with COVID-19 and its vaccination.
Figure 1. Histological differences between the myocarditis associated with COVID-19 and its vaccination.
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Table 1. Pathogenetic mechanisms of COVID-19 myocarditis.
Table 1. Pathogenetic mechanisms of COVID-19 myocarditis.
Pathogenetic
Mechanisms		DescriptionDetails
Direct Invasion of the Myocardium
[21,22]		The SARS-CoV-2 virus invades cardiomyocytes directly.Direct cell injury: cell death and cardiac dysfunction.
Apoptosis and necrosis: programmed and unprogrammed cell death.
Inflammatory Response and Cytokine Storm [23,24,25]Excessive immune reaction with massive production of inflammatory cytokines.Release of pro-inflammatory cytokines: high amounts of IL-6, IL-1β, and TNF-α.
Cellular infiltration: lymphocytes and macrophages in cardiac tissues.
Coagulopathy and
Microthrombosis
[26,27,28]		Predisposition to thrombotic and coagulation phenomena.Coronary vessel microthrombosis: ischemia and myocardial damage.
Endothelial damage: systemic inflammatory response and risk of thrombotic events.
Autoimmune
Reactions
[29,30]		Possible development of autoimmune responses against heart tissue.Molecular mimicry: similarity between viral and cardiac proteins.
T-cell activation: immune response against cardiac antigens.
Autonomic Nervous System Dysregulation [31,32]Alterations in the autonomic system that regulates cardiac functions.Cardiac control alterations: rate and contractility dysfunctions.
Autonomic stress: acute stress that aggravates myocardial damage.
Table 2. Pathogenetic mechanisms COVID-19 vaccine myocarditis.
Table 2. Pathogenetic mechanisms COVID-19 vaccine myocarditis.
Pathogenetic
Mechanisms		DescriptionDetails
Vaccine-Induced Immune Response
[33,34]		Immune reaction against the Spike protein of SARS-CoV-2.Activation of the inflammatory response: release of pro-inflammatory cytokines and chemokines.
Antibody production: possible cross-reaction with cardiac tissue.
Molecular Mimicry
[34,35]		Structural similarity between viral and cardiac proteins.Structural similarity: Spike proteins may resemble those of the myocardium.
Autoimmunity: activation of autoimmune responses against myocardium.
Immune Regulatory Dysfunction
[36,37]		Ineffective regulation of the post-vaccination inflammatory response.Cytokine storm: excessive inflammatory response.
T cell activation: infiltration of immune cells into the myocardium and subsequent inflammation.
Vascular Response Side Effects
[37,38]		Post-vaccination vascular system response.Endothelial activation: inflammation of the vessels that can cause ischemia and myocardial inflammation.
Coagulopathy: mild microthrombus formation and cardiac ischemia.
Genetic Factors and Individual Predisposition
[38,39]		Genetic variability and pre-existing comorbidities.Genetic variability: Individual immune response may influence susceptibility.
Preexisting comorbidities: Autoimmune conditions or immunological abnormalities may increase the risk of myocarditis.
Table 3. Histological features of myocarditis associated with COVID-19 and its vaccination.
Table 3. Histological features of myocarditis associated with COVID-19 and its vaccination.
Histological FeaturesCOVID-19 MyocarditisPost-Vaccination Myocarditis
Inflammatory infiltratePerivascular lymphocytic infiltrates, mainly CD4+ and CD8+ T cells.Lymphocytic infiltrates like viral myocarditis, but less extensive and more localized.
Myocyte necrosisFrequently observed focal myocardial necrosis.Necrotic myocardial damage is generally less pronounced than in viral myocarditis.
Interstitial edemaPresent, often associated with inflammation.Possible transient edema related to inflammation.
Intravascular microthrombiFrequent microthrombi formation, often linked to endothelial damage.Rare presence of microthrombi; less frequent than COVID-19 myocarditis.
Endothelial damageSignificant damage, associated with cytokine storm and microvascular ischemia.Less endothelial involvement compared to COVID-19 myocarditis.
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Salzillo, C.; Marzullo, A. COVID-19 and Myocarditis: Pathogenetic Mechanisms and Histological Features. Acta Microbiol. Hell. 2025, 70, 3. https://doi.org/10.3390/amh70010003

AMA Style

Salzillo C, Marzullo A. COVID-19 and Myocarditis: Pathogenetic Mechanisms and Histological Features. Acta Microbiologica Hellenica. 2025; 70(1):3. https://doi.org/10.3390/amh70010003

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Salzillo, Cecilia, and Andrea Marzullo. 2025. "COVID-19 and Myocarditis: Pathogenetic Mechanisms and Histological Features" Acta Microbiologica Hellenica 70, no. 1: 3. https://doi.org/10.3390/amh70010003

APA Style

Salzillo, C., & Marzullo, A. (2025). COVID-19 and Myocarditis: Pathogenetic Mechanisms and Histological Features. Acta Microbiologica Hellenica, 70(1), 3. https://doi.org/10.3390/amh70010003

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