Myocarditis

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Advanced Concepts in Cardiovascular Physiology and Rehabilitation
Course:	KIN 500C
Instructor:	Dr. Darren Warburton
Session	Winter, 2026
Email:	darren.warbuton@ubc.ca
Office:	Lower Mall Research Station

Background

What is Myocarditis

Myocarditis is a severe condition marked by inflammation of the heart muscle, the myocardium (Yamagata & Malholtra, 2024). It can result in angina pectoris, acute heart failure, cardiogenic shock, conduction problems, and ventricular arrhythmias (Kyaw et al., 2023). Myocarditis can be classified as acute, fulminant, subacute, or chronic, with each classification requiring different treatment approaches (Kyaw et al., 2023). However, treatment protocols remain limited or are not fully proven (Kyaw et al., 2023).

Athletes who perform high-intensity training may be at increased risk due to factors such as reduced immunity, exposure to pathogens, and increased mental and physical stress (Yamagata & Malholtra, 2024). Myocarditis is also one of the leading causes of sudden cardiac death in competitive athletes, accounting for approximately 12% of deaths in young people (Thiene, 2018).

Pathophysiology of Myocarditis

The understanding of the pathophysiology of myocarditis has come from murine models, and a triphasic model has been proposed to describe the pathophysiology of acute myocarditis (Figs. 1 and 2) (Shams et al., 2025; Kanuri et al., 2023; Putschoeegl & Auerbach, 2020).

Phase I

Phase I generally lasts 1-7 days and involves direct myocardial injury caused by infectious agents, such as: viruses (ex., Adenovirus and Coxsackie virus); toxins and drugs (ex., alcohol, illegal stimulants, chemotherapy drugs, and snake venom); or autoimmune mechanisms (ex., Chron’s disease, Lupus, Sarcoidosis or Rheumatoid arthritis) (Myocarditis foundation, 2024; Shams & Collier, 2025; Kanuri et al., 2023). For many viruses, the exact cardiac infection site and the underlying pathogenic mechanisms are not confirmed (Schultheiss et al., 2011). It is proposed that these infectious agents enter the body through processes such as endocytosis and rapid viral replication, myocellular necrosis and apoptosis, or an innate immune response (Kanuri et al., 2023; Putschoeegl & Auerbach, 2020). The result being the release of intracellular danger signals (ex., myocyte antigens) into the circulatory system triggering the activation of an innate immune response and ultimately leading to degradation of the myocardial tissue (Kanuri et al., 2023; Putschoeegl & Auerbach, 2020). Acute myocardial injury can result from either direct virus-mediated lytic processes, or may be caused by the emerging antiviral immune response (Schultheiss et al., 2011). This innate immune response can be considered to be a double-edged sword, as it serves a dual purpose by helping in the clearance of viral infected cardiomyocytes, as well as aggravating virus induced myocardial damage (Kanuri et al., 2023). If the immune response is not successful in curtailing, restricting, or healing of the viral myocarditis, progression to phase II will occur (Kanuri et al., 2023).

Phase II

The activation of antigen-specific immunity mediated by T-cells, B-cells, and antibody production (adaptive immune response) initiates the second phase, lasting 1-4 weeks (Schultheiss et al., 2011; Shams & Collier, 2025; Putschoeegl & Auerbach, 2020). The recruitment of leukocytes to sites of infection is crucial to the inflammatory clearance of pathogens, with various molecules controlling this inflammatory cell trafficking (ex., chemokines) (Schultheiss et al., 2011). Chemokines are important for the containment of the infectious agents but may extend injury to the tissue, and, if attracted, inflammatory cells produce pathological mediators that injure terminally differentiated cardiomyocytes or induce extensive fibrosis (ex., TGF-β) (Schultheiss et al., 2011).

Phase III

Phase III, commonly referred to as chronic myocarditis, can last months to years post-diagnosis (Kanuri et al., 2023; Putschoeegl & Auerbach, 2020). If viral infection and autoimmune processes have completely resolved, with the patient fully recovering, the magnitude of the remaining damage to the tissue will determine the further course of the disease (Schultheiss et al., 2011; Shams & Collier, 2025; Putschoeegl & Auerbach, 2020). Other outcomes may include cardiac remodelling, myocardial fibrosis,, or the progression to dilated cardiomyopathy (Schultheiss et al., 2011; Shams & Collier, 2025; Putschoeegl & Auerbach, 2020). Aetiology-specific treatment is probably not useful, with only standard heart failure medication and/or devices potentially proving to delay progression and improve prognosis (Schultheiss et al., 2011).

Populations at Risk for Myocarditis

As explained previously within the pathophysiology section, myocarditis is understood to have many aetiologies, including but not limited to viral infections, toxin/drug exposures, and autoimmunity; therefore, myocarditis has the potential to impact diverse populations. Diagnosis of myocarditis can be difficult due to the heterogeneity in presentation of non-specific symptoms and presence of a large range of severity from subclinical to sudden cardiac death (Caforio et al., 2013; Kwan et al., 2025). However, specific risk factors may increase one’s susceptibility or risk of the development of myocarditis.

People living with current illnesses or conditions can be predisposed to the development of myocarditis due to the interaction of the conditions with cardiac function and structure. Individuals experiencing acute respiratory illness such as COVID-19, autoimmune conditions, or cardiac conditions and abnormalities such as ventricular arrhythmias, atrial fibrillations, myocardial infarction, and heart failure have been found to possess increased rates of myocarditis diagnoses (Kwan et al., 2025).

Non-infectious myocarditis may result from drugs, toxins, or other physical agents. One drug highlighted to affect myocarditis is the use of chemotherapeutics and other immune checkpoint inhibitors, which act to fight many cancers (Moslehi et al., 2018). Lifestyle factors such as illicit drug and excessive alcohol use increase the risk of non-infectious myocarditis (National Heart, Lung, and Blood Institute, 2023). Within non-infectious myocarditis, immune-mediated myocarditis may result from a variety of exposures that induce an autoimmune response, such as allergens as well as preexisting autoimmune or chronic conditions (Moslehi et al., 2018).

Table 1. Causes of Myocarditis (Adapted from Caforio et al., 2013)
Infectious Myocarditis	Immune-Mediated Myocarditis	Toxic Myocarditis
Bacterial	Allergens	Drugs
Spirochaetal	Alloantigens	Heavy Metals
Fungal	Autoantigens	Animal bites and stings
Protozoal		Hormones
Parasitic		Physical Agents
Rickettsial
Viral

Demographic risk factors for the development of myocarditis include younger populations, specifically those 15-39, who are at a higher risk, with 30-34 being the age group with the highest incidence of myocarditis (Zhao et al., 2026). While 35-39 age range has the highest mortality rates due to myocarditis (Zhao et al., 2026). Individuals assigned male at birth also experience high incidence and mortality due to myocarditis (Fairweather et al., 2023b; Zhao et al., 2026). Family history and genetic components additionally influence the development of myocarditis due to the way in which an individual’s body responds to inflammation as well as inherited conditions such as familial Mediterranean fever (National Heart, Lung, and Blood Institute, 2023). Finally, athletes and individuals who experience heightened levels of physical stress during or after illness may be more at risk for the development of myocarditis due to the combination of various risk factors previously outlines. For example, athletes experience a combination of reduced immunity post physical activity, increased exposures infectious agents through competition, training, and travels, as well as heighten cardiac strain which may result in higher incidence of myocarditis (Yamagata & Malholtra, 2024).

Diagnosis

Signs and symptoms

Myocarditis can be difficult to diagnose because its symptoms can vary from mild and nonspecific complaints to severe cardiovascular problems. Common symptoms include chest pain, palpitations, shortness of breath, exercise intolerance, presyncope or syncope, and, in more serious cases, signs of heart failure (Drazner et al., 2025; Schulz-Menger et al., 2025). In athletes, diagnosis may be even more challenging because symptoms can be mistaken for normal fatigue, detraining, or incomplete recovery after illness. Recent research in collegiate athletes suggests that chest pain during return to exercise is especially important. In one study of collegiate athletes, 20.8% of those with chest pain who underwent cardiac magnetic resonance imaging (CMR) showed probable or definite cardiac involvement, whereas none of those with exertional symptoms without chest pain did (Petek et al., 2022).

Medical testing

The initial evaluation of suspected myocarditis usually includes a clinical history, physical examination, electrocardiogram (ECG), blood tests, and echocardiography (Schulz-Menger et al., 2025). Common laboratory tests include high-sensitivity troponin, NT-proBNP, C-reactive protein, and a differential blood count (Schulz-Menger et al., 2025). Current guidance describes three classic clinical presentations of myocarditis: chest pain, heart failure or cardiogenic shock, and arrhythmia-related symptoms, such as presyncope or syncope (Drazner et al., 2025). Endomyocardial biopsy (EMB) remains the gold standard for confirming myocarditis, but it is generally reserved for higher-risk cases, such as rapidly progressive heart failure, hemodynamic instability, electrical instability, or suspicion of specific histological forms, including giant cell or eosinophilic myocarditis (Drazner et al., 2025; Lewis et al., 2020).

Imaging

Echocardiography is often the first imaging test used in suspected myocarditis because it is widely available and can detect abnormalities such as reduced systolic function, regional wall motion abnormalities, increased wall thickness, or pericardial effusion (Schulz-Menger et al., 2025). Cardiac magnetic resonance (CMR) has become one of the most important non-invasive tools for diagnosing myocarditis because it can detect myocardial edema, necrosis, fibrosis, and non-ischaemic injury patterns (Lewis et al., 2020). Both ACC and ESC guidance highlight CMR as central to modern diagnostic work-up, with interpretation based on abnormalities in T1- and T2-based imaging markers, consistent with the updated Lake Louise Criteria (Drazner et al., 2025; Schulz-Menger et al., 2025). CMR is valuable in practice because it is non-invasive and allows assessment of the myocardium as a whole. (Lewis et al., 2020).

Myocarditis in Various Populations

Myocarditis in Athletes and Return to Play

Current Return-to-Play (RTP) guidelines in Western Medicine, recommended by the European Society of Cardiology and American Heart Association, emphasize a structured, physiologically focused approach to return to sport. (Yamagata & Malholtra, 2024).

The RTP process begins with a three-to-six month period of restricted exercise following myocarditis diagnosis. The duration depends on the severity of illness, left ventricular (LV) systolic function, and the extent of late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMRI) (Yamagata & Malholtra, 2024).

Following this period, the patient undergoes reassessment, including 24-hour Holter monitoring, echocardiogram, exercise electrocardiogram, and CMRI. Recovery is then marked by normalized LV ejection fraction, resolution of serum markers of myocardial injury and inflammation, and absence of arrhythmias on the Holter monitoring and exercise stress tests (Yamagata & Malholtra, 2024).

If the athlete is asymptomatic and free of risk factors after four weeks, they may be considered for early RTP. Gradual increases in exercise intensity and ongoing clinical surveillance for new symptoms are recommended before full return to sport. Routine re-evaluation over the first two years following diagnosis is also strongly recommended (Yamagata & Malholtra, 2024).

Pellicia et al. (2019) emphasize the importance of shared decision-making and individualization when determining RTP. Decisions should consider symptoms, risk factors, medical history, and age. This is important, as removal from sport can have significant personal and financial consequences. Shared decision-making allows athletes to receive detailed information about their diagnosis and to discuss the risks associated with returning to sport.

Two Eyed Seeing and Indigenous Ways of Knowing

Current RTP protocols largely omit psychological, social, and cultural considerations. Indigenous frameworks emphasize a wholistic approach that includes physical, spiritual, emotional, and mental well-being (Reading & Wien, 2009). Additionally, healthcare practitioners are encouraged to practice cultural safety by reflecting on their own perspectives and addressing systemic barriers to reduce inequities in care (Curtis et al., 2019).

Integrating Indigenous ways of knowing can support a more wholistic RTP process following myocarditis. While Western RTP protocols are essential for reducing cardiac risk, they often do not address psychological, cultural and social aspects of health. Two-Eyed Seeing (Etuaptmumk) provides a framework for combining Western medicine and Indigenous perspectives (Bartlett et al., 2012), allowing RTP to incorporate both physiological measures and broader indicators of well-being.

Psychological readiness is an important factor that has been studied in RTP following ACL injuries (Adern et al., 2016). Research has shown that psychological readiness is strongly associated with successful return to sport following ACL reconstruction. Based on this, interventions targeting psychological readiness may be considered within myocarditis RTP protocols.

Building on the work of Pellicia et al. (2019), RTP following myocarditis could also involve family members, community leaders, and Elders in the decision-making process. This may strengthen social support systems and improve trust in the recovery process. This approach aligns with the literature suggesting that a lack of trust and limited shared decision-making are barriers to equitable care (Curtis et al., 2019).

To implement these strategies effectively, healthcare providers must also address historical and ongoing mistrust in health care systems (Wylie & McConkey, 2018). This mistrust has contributed to challenges in building positive relationships between indigenous patients and healthcare providers. Clinicians should provide respectful, patient-centred care that is tailored to individual needs, including creating a supportive environment that prioritizes cultural safety and inclusivity in RTP for all athletes (Curtis et al., 2019).

Myocarditis in Children

The incidence and prevalence of myocarditis in children is likely underestimated as many may only have mild symptoms that do not require medical attention (Putschoeegl & Auerbach, 2020). The annual incidence in children ranges from 1-2 per 100,000 children, with multiple studies showing a bimodal peak in incidence, with most cases occurring in infancy and adolescence (Goldberg et al., 2024; Putschoeegl & Auerbach, 2020). Children diagnosed in infancy tend to have worse outcomes compared to adolescents and adults (Putschoeegl & Auerbach, 2020). Viral myocarditis is more often seen in children compared to adults, with children also being more likely to present with acute, sudden-onset myocarditis (41-69% of cases) rather than chronic myocarditis, which is more typically seen in adults (Ricci et al., 2025). In research involving adult patients, a male dominance of diagnoses tends to be present and this sex ratio does not appear to be present in children (Ricci et al., 2025).

Diagnosis in children will involve taking a full clinical history, typically consisting of what symptoms the patient is presenting with (i.e., sudden onset of chest pain, dyspnea, fever) and laboratory findings, including elevated levels of troponin and inflammatory markers such as as C-reactive protein (Ammirati & Moslehi, 2023). Multiple studies of myocarditis in children have shown that ECG abnormalities are detected in nearly all patients (Law et al., 2021). The most common ECG abnormalities in a study of 24 pediatric myocarditis cases were abnormal Q-waves (67%), negative T-waves (63%), wide QRS complexes (58%), and abnormalities of ST segments (46%) (Matsuura et al., 2016; Ghelani et al., 2012; Butts et al., 2017). Given the increased awareness of myocarditis post-COVID-19 pandemic era, troponin evaluation is frequently obtained in children with chest pain or other cardiac symptoms, which has resulted in hospitalization of many children with mild elevation in their troponin levels that may not have previously been diagnosed with myocarditis (Goldberg et al., 2024). Real-time imaging and portability are key strengths for quickly assessing the severity of cardiovascular compromise, especially in children who may have limited cooperatively or hemodynamic instability (Law et al., 2021). The differential diagnoses of acute myocarditis in children will include Kawasaki disease, severe sepsis, idiopathic cardiomyopathy, primary ventricular arrhythmias, and COVID-19-related multisystem inflammatory syndrome (Ammirati & Moslehi, 2023). In low- and middle-income countries, differential diagnosis will also include rheumatic carditis (Ammirati & Moslehi, 2023).

Treatment efficacy continues to be controversial and there is no high-quality evidence to guide the treatment of acute myocarditis in children (Ammirati & Moslehi, 2023; Putshoeegl & Auerbach, 2020). Assessing treatment options will depend on what symptoms the patient is presenting with, how clinically stable they are, what phase of the disease they are in, and what their long-term prognosis is (Putschoeegl & Auerbach, 2020; Law et al., 2021). Intravenous (IV) immunoglobulines are frequently used in pediatric patients with acute myocarditis accompanied by cardiac dysfunction or ventricular arrhythmia (Ammirati & Moslehi, 2023). Empirical corticosteroids are used in approximately 25% of children with myocarditis, but no clinical trial evidence supports this practice (Ammirati & Moslehi, 2023). If the patient presents with fulminant myocarditis and hemodynamic instability, initial treatment may require the use of inotropes or mechanical circulatory support (MCS) (Law et al., 2021; Putschoeegl & Auerbach, 2020). For patients presenting with minimal symptoms and normal hemodynamics, they may require more acute treatment without the need for long-term therapy (Putschoeegl & Auerbach, 2020). In a national registry of 898 children with myocarditis, approximately 2-13% died or required a heart transplant. For children presenting with mRNA COVID-19-associated myocarditis and enterovirus myocarditis, mortality rates were vastly greater, with upwards of 31% of patients diagnosed in the United States, Australia, Israel, Hong Kong, and Europe (Ammirati & Moslehi, 2023).

Myocarditis and COVID-19

As mentioned previously, viral infections are one of the most common causes of myocarditis within Western countries (Sozzi et al., 2022). A salient example of this is the surge in cases of myocarditis witnessed throughout the COVID-19 pandemic (Fairweather et al., 2023a). Within the context of COVID-19 infections, there were also associations with COVID-19 vaccination and myocarditis cases. However, an improved benefit-to-risk ratio exists across all age and sex groups (Gluckman et al., 2022). Treatment of vaccine-associated myocarditis is identical to infection-induced myocarditis (Gluckman et al., 2022).

The mechanism by which COVID-19 promotes myocardial inflammation is understood through direct and indirect damage to the heart muscle. Direct damages are a result of SARS-CoV-2 entering cardiac muscle, immune, and blood flow related cells (cardiomyocytes, pericytes, mast cells and macrophages) resulting in cellular damage, toxin release, and death (cytotoxic effects, apoptosis, and necrosis) within the heart muscle which drives cardiac injury and thus induces autoimmune responses (Fairweather et al., 2023a). Indirect damages result from overactive immune responses known as cytokine storm due to high levels of virus replication in the lungs during infection, which can result in damage to the heart (Fairweather et al., 2023a).

Return to physical activity after viral myocarditis due to severe COVID-19 infection features a period of recovery with exercise cessation for 3-6 months (Gluckman et al., 2022). Individuals with severe cases are recommended to undergo triad testing of electrocardiogram, cardiac troponin, and echocardiogram to confirm structural clearance before commencing graded return to exercise (Gluckman et al., 2022; Schulz-Menger et al., 2025). Though not contained in official guidelines, it is recommended that exercise prescription consider the use of baseline symptom-limiting cardiopulmonary testing, supervised programming, and the integration of flexible exercise modality (Tur et al., 2022).

Conclusions

Myocarditis is a complex and serious condition that is characterized by inflammation of the heart muscle. It has a wide range of causes, clinical presentations, and potential outcomes. Its pathophysiology involves a multi-phase inflammatory process that can range from acute injury to long-term structural and functional changes. Myocarditis often has non-specific symptoms, making diagnosis challenging and highlighting the importance of careful evaluation through imaging and biomarkers.

Certain populations may be at an increased risk of myocarditis due to factors such as exposure to pathogens, underlying medical conditions, immune system responses, and varying levels of physical or psychological stress. Current RTP protocols following diagnosis emphasize a physiologically driven approach to ensure safe return to activity. These guidelines are effective for reducing medical risk, but often overlook psychological, social, and cultural factors of care. Incorporating approaches such as Two-Eyed Seeing and Indigenous ways of knowing, including individualized and wholistic recovery, may help improve health outcomes for individuals affected by myocarditis.

References

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