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Acute Myocarditis

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Description: Acute myocarditis is an inflammation of the heart muscle that can reduce the heart's ability to pump and cause rapid or irregular heart rhythms.
Type: Acute myocarditis is typically an inflammatory condition of the heart muscle, often caused by viral infections. It is not generally considered a genetic disorder, and thus does not have a type of genetic transmission associated with it.
Signs And Symptoms: The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium or to the weakness and dysfunction of the heart muscle that is secondary to the inflammation. While myocarditis may develop over periods ranging from hours to months, patients typically present with signs and symptoms that resemble heart failure, including the following:
Since myocarditis is often due to a viral illness, many patients experience symptoms consistent with a recent viral infection including a fever, rash, loss of appetite, abdominal pain, vomiting, diarrhea, joint pains, and easily becoming tired. Additionally, myocarditis is often associated with pericarditis, and many people with myocarditis present with signs and symptoms that suggest myocarditis and pericarditis at the same time.Children primarily present with the aforementioned symptoms associated with a viral infection. Later stages of the illness can involve the respiratory system and lead to increased work of breathing. These are often mistaken for asthma.Myocarditis can be distinguished as either fulminant or acute based on the severity of symptoms on presentation, as well as the time course over which symptoms develop and persist. This categorization can help predict the treatment, outcomes, and complications of myocarditis.
Fulminant myocarditis is defined as sudden and severe myocarditis that is associated with signs and symptoms of heart failure while at rest. More specifically, fulminant myocarditis is characterized by a distinct, rapid onset of severe heart failure symptoms, such as shortness of breath and chest pain, that develop over the course of hours to days. Additionally, treatment requires the use of medications or mechanical devices to improve heart function.Acute non-fulminant myocarditis has a less distinct onset in contrast to fulminant myocarditis, and evolves over days to months. While the symptoms of acute myocarditis overlap with those of fulminant myocarditis, they do not typically occur at rest, and treatment does not require the use of mechanical circulatory support.
Prognosis: The prognosis associated with myocarditis is stratified by the severity and time course along which symptoms develop. In addition to symptom severity, there are also several indicators of heart function that can be used to predict patient outcomes, many of which are part of the standard evaluation of patients presenting with cardiovascular dysfunction. Most people with myocarditis have an uncomplicated, self-limited and mild course while making a full recovery. However, those with myocarditis that present with a decreased ejection fraction, or those who present with heart failure, advanced atrioventricular block, with sustained ventricular arrhythmias or with hemodynamic instability have a worse prognosis with an increased risk of death or need for heart transplantation.An electrocardiogram is one of the most common screening tools used in cases of suspected cardiac pathology, such as myocarditis. The findings that correlate with poorer outcomes are non-specific and include widened QRS complexes and QT intervals, partial or complete atrial-ventricular heart block, and malignant ventricular arrhythmias like sustained ventricular tachycardia or ventricular fibrillation. Electrocardiogram findings of ST elevations with upward concavity and an early repolarization pattern, however, were associated with a better cardiovascular prognosis in general.In cases of acute myocarditis, cardiac magnetic resonance imaging can reveal several prognostic indicators that, similar to ECGs, are non-specific and reflect poorer cardiac physiology. Late gadolinium enhancement on cardiac MRI demonstrates perturbations in extracellular volume as a result of cell necrosis or edema, and is significantly associated with increases in all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events. The association was strongest with any late gadolinium enhancement, but remained true for findings of anterolateral-specific enhancement. A similar relationship was found between a left ventricular ejection fraction < 50%, increased mortality, and increased major adverse cardiovascular events.Myocarditis has been reported to be a major cause of sudden cardiac death (SCD) in infants, adolescents, and young adults, but the reported rates show wide variation (1 to 14 percent) among young people depending on differences in SCD definition and classification/ definition of myocarditis post-mortem as well as heterogeneity of study populations.In fulminant myocarditis, in which an inflammatory cytokine storm occurs, cardiac functions decline rapidly and the death rate is high.
Onset: The onset of acute myocarditis can vary widely among individuals. It may begin suddenly with severe symptoms or develop gradually. Common initial symptoms include chest pain, fatigue, shortness of breath, and palpitations. In some cases, symptoms may mimic those of a viral infection, such as fever, body aches, and sore throat.
Prevalence: The prevalence of acute myocarditis can vary depending on demographics and diagnostic methods, but it is estimated to be approximately 10 to 20 cases per 100,000 people annually. This rate may be underreported due to the often asymptomatic nature or misdiagnosis of the condition.
Epidemiology: The prevalence of myocarditis is estimated to be about 1-10 cases per 100,000 persons per year, with higher estimates at 22 cases per 100,000 persons annually. The highest incidence of myocarditis is seen in men between the ages of 20 and 40. Fulminant myocarditis, the most severe subtype, has been shown to occur in up to 2.5% of known myocarditis presentations. When looking at different causes of myocarditis, viral infection is the most prevalent, especially in children; however, the prevalence rate of myocarditis is often underestimated as the condition is easily overlooked and is sometimes asymptomatic. Viral myocarditis being an outcome of viral infection depends heavily on genetic host factors and the pathogenicity unique to the virus. If one tests positive for an acute viral infection, clinical developments have discovered that 1-5% of said population may show some form of myocarditis.In regard to the population affected, myocarditis is more common in pregnant women, children, and those who are immunocompromised. Myocarditis, however, has shown to be more common in the male population than in the female. Multiple studies report a 1:1.3-1.7 female-male ratio of prevalence of myocarditis. In young adults, up to 20% of all cases of sudden death are due to myocarditis. Young males specifically have a higher incidence rate than any other population due to their testosterone levels creating a greater inflammatory response that increases the chance of cardiac pathologies. While males tend to have a higher risk of developing myocarditis, females tend to display more severe signs and symptoms, such as ventricular tachycardia and ventricular fibrillation, but do so at an older age. Among patients with HIV, myocarditis is the most common cardiac pathological finding at autopsy, with a prevalence of 50% or more.Myocarditis is the third most common cause of death among young adults with a cumulative incidence rate globally of 1.5 cases per 100,000 persons annually. Myocarditis accounts for approximately 20% of sudden cardiac death in a variety of populations, including adults under the age of 40, young athletes, United States Air Force recruits, and elite Swedish orienteers. With individuals who develop myocarditis, the first year is difficult as a collection of cases have shown there is a 20% mortality rate.
Intractability: Acute myocarditis is not inherently intractable. The course and prognosis depend significantly on the underlying cause, severity, and response to treatment. While some cases resolve with appropriate medical management, others may lead to chronic conditions or severe complications such as heart failure, necessitating more intensive interventions like medications, mechanical support, or even heart transplantation. Early diagnosis and appropriate treatment are crucial for better outcomes.
Disease Severity: Acute myocarditis can range from mild to severe. In mild cases, symptoms may be minimal and resolve with little intervention. Severe cases can lead to significant cardiac dysfunction, heart failure, or life-threatening arrhythmias, requiring intensive medical treatment or even heart transplantation.
Healthcare Professionals: Disease Ontology ID - DOID:3951
Pathophysiology: Acute myocarditis is the inflammation of the heart muscle (myocardium) often caused by a viral infection. The pathophysiology involves direct viral invasion and subsequent immune-mediated injury. The initial phase includes viral replication causing myocyte necrosis. The second phase is characterized by the activation of the immune system, releasing cytokines and immune cells that attack the infected cardiac tissue, potentially causing further myocardial damage. This leads to impaired cardiac function, potentially resulting in heart failure, arrhythmias, or sudden cardiac death.
Carrier Status: Acute myocarditis does not have a carrier status as it is not an inherited or genetically-transmitted condition. It typically occurs due to infections, autoimmune diseases, toxins, or other external factors.
Mechanism: Most forms of myocarditis involve the infiltration of heart tissues by one or two types of pro-inflammatory blood cells, lymphocytes and macrophages plus two respective descendants of these cells, NK cells and macrophages. Eosinophilic myocarditis is a subtype of myocarditis in which cardiac tissue is infiltrated by another type of pro-inflammatory blood cell, the eosinophil. Eosinophilic myocarditis is further distinguished from non-eosinophilic myocarditis by having a different set of causes and recommended treatments.The pathophysiology of viral myocarditis is not well understood, but it is believed to involve cardiotropic viruses (viruses with a high affinity for the heart muscle) gaining entry to cardiac muscle cells, usually via binding to a transmembrane receptor. Over approximately the next 1–7 days the virus replicates and causes inflammation leadings to necrosis and apoptosis of cardiac muscle cells (myocytes) and activation of the innate immune system. Over the next 1–4 weeks, viral replication continues with subsequent activation of the acquired immune system leading to T cell infiltration and the formation of antibodies, including possibly auto-antibodies. Over the next few months to years, this process either resolves and concludes with viral clearance or it may progress to cause permanent heart damage such as dilated cardiomyopathy, ventricular dysfunction or other cardiomyopathies. Coxsackie B, specifically B3 and B5, has been found to interact with coxsackievirus-adenovirus receptor (CAR) and decay-accelerating factor (DAF). However, other proteins have also been identified that allow Coxsackieviruses to bind to cardiac cells. The natural function of CAR and mechanism that the Coxsackievirus uses to infect the cardiac muscle is still unknown. The mechanism by which coxsackie B viruses (CBVs) trigger inflammation is believed to be through the recognition of CBV virions by Toll-like receptors.The binding of many types of coronaviruses, including the SARS-CoV-2 virus, through ACE2 receptors present in heart muscle may be responsible for direct viral injury leading to myocarditis. In a study done during the 2002-2004 SARS outbreak, SARS viral RNA was detected in the autopsy of heart specimens in 35% of the patients in the Toronto, Canada area who had died due to SARS. It was also observed that an already diseased heart has increased expression of ACE2 receptor contrasted to healthy individuals which may lead to greater viral infiltration in the heart muscle. Hyperactive immune responses in COVID-19 patients may lead to the initiation of the cytokine storm. This excess release of cytokines may lead to myocardial injury. In addition to direct cardiac myocyte (heart muscle cell) damage due to SARS-CoV-2 viral infiltration and inflammation, there are other suspected mechanisms that Covid-19 may indirectly cause myocarditis. During COVID-19, the other indirect mechanisms thought to contribute to myocarditis include: oxygen supply-demand mismatch to the heart muscle leading to myocardial (heart muscle) injury; microvascular thrombi, or blood clots in the small blood vessels of the heart causing injury; the systemic hyperinflammatory state in Covid-19 leading to heart muscle injury; or the virus causing indirect damage to the heart by inducing auto-immune mediated damage to the heart muscle (and frequently other organs).
Treatment: While myocarditis has many etiologies and a variable constellation of signs and symptoms, many causes do not have a specific treatment thus the primary focus is on supportive care and symptom management. In some cases of biopsy-proven myocarditis, the causative cell type may indicate condition specific treatments that are beneficial. These treatments typically consist of corticosteroids, or immunosuppressants. Eosinophilic myocarditis, giant cell myocarditis and cardiac sarcoidosis are usually responsive to immunosuppressive treatments; in the form of glucocorticoids with or without azathioprine and cyclosporine. Some of these immune mediated forms of myocarditis require an extended course (maintenance course) of immunosuppressive therapy. It is recommended to rule out drugs and parasites as potential causes of eosinophilic myocarditis as these common causes of the variant can be effectively treated with discontinuation of the offending drug or specific anti-parasitic treatment respectively. Empiric IV glucocorticoids are indicated in acute myocarditis with cardiogenic shock, heart failure, ventricular arrhythmias or high degree AV block that is suspected due to auto-immune disease; but the European Society of Cardiology also recommends subsequent viral genome testing of endomyocardial biopsy specimens due to risk of viral activation, which may necessitate discontinuation of immunosuppression therapy.In a majority of cases, the main therapies are used to support patients and are dependent on the severity of symptoms and the time course across which myocarditis develops. Supportive therapies can be divided into two broad categories, medications and mechanical support.
Compassionate Use Treatment: Acute myocarditis is an inflammatory condition of the heart muscle that can lead to severe complications, including heart failure and arrhythmias. While standard treatments focus on managing symptoms and complications, several compassionate use, off-label, and experimental treatments are sometimes considered:

1. **Intravenous Immunoglobulin (IVIG)**: Used off-label to modulate the immune response in severe cases of acute myocarditis, particularly when the condition is believed to be immune-mediated.

2. **Immunosuppressive Therapy**: Drugs such as corticosteroids, azathioprine, and cyclosporine are occasionally used off-label, particularly in cases where autoimmune processes are suspected to play a significant role in pathogenesis.

3. **Antiviral Agents**: In cases where viral infections, such as those caused by enteroviruses or adenoviruses, are identified as the underlying cause, antiviral medications are sometimes used, though this is largely experimental.

4. **Mechanical Circulatory Support**: While not a pharmacological treatment, devices like ventricular assist devices (VADs) and extracorporeal membrane oxygenation (ECMO) are used in severe cases to stabilize patients until recovery or heart transplantation.

5. **Interferon Therapy**: Experimental use of interferons has been investigated to treat viral myocarditis, although this is not yet standard practice.

Clinical trials and individual case assessments often guide the consideration of these therapies, and their efficacy varies based on the underlying cause and severity of the myocarditis.
Lifestyle Recommendations: For acute myocarditis, lifestyle recommendations typically include:

1. **Rest**: Adequate rest is essential to reduce the strain on the heart.
2. **Avoid strenuous activities**: Limit physical exertion to prevent exacerbating the heart's condition.
3. **Healthy diet**: Focus on a balanced diet rich in fruits, vegetables, whole grains, lean proteins, and healthy fats. Reduce salt intake to manage blood pressure.
4. **Hydration**: Drink plenty of fluids but monitor intake if there are any fluid retention issues.
5. **Alcohol and tobacco**: Avoid alcohol and tobacco, as both can negatively impact heart health.
6. **Follow medical advice**: Adhere to any prescribed medications and follow-up appointments with healthcare providers.
7. **Monitor symptoms**: Keep track of any worsening symptoms and seek immediate medical attention if they occur.

These recommendations aim to support heart health and aid in recovery, but individual advice should be tailored by a healthcare professional.
Medication: The specific medications that are used to support patients are directly related to the cause of the symptom or sign. Just as the symptoms of myocarditis mirror those of congestive heart failure, so too do the therapies. Additionally, the order in which therapies are used depends on the degree of heart dysfunction, with stabilization of patient blood pressure and breathing taking highest priority when present. This can involve the use of inotropes, or medications that make the heart contract with greater force, as well as antiarrhythmic drugs such as adenosine or carvedilol. In patients that have stable and adequate heart function, further treatments are based on heart failure guidelines. ACE inhibitors or Angiotensin Receptor Blockers (ARBs) can have a protective benefit to the heart, so either are typically used in any patient with symptomatic myocarditis. Simultaneously, beta blockers are used in patients that can tolerate their heart beating at a slower rate. Shortness of breath at rest and swelling can be relieved with diuretics such as furosemide, and the addition of aldosterone receptor blockers can augment the diuresis while preventing the excess loss of potassium. In patients with symptoms while resting, additional medications can be added such as digoxin.
Repurposable Drugs: Acute myocarditis is an inflammatory condition of the heart muscle. Here are some drugs that have potential for repurposing in its treatment:

1. **Colchicine:** Typically used for gout, this anti-inflammatory drug has shown promise in reducing inflammation in myocarditis.
2. **Immunosuppressive agents:** Medications like intravenous immunoglobulins (IVIG) and corticosteroids might be repurposed to reduce immune-mediated damage in certain types of myocarditis.
3. **Beta-blockers:** These drugs, like carvedilol or metoprolol, primarily used for heart failure and hypertension, can help manage symptoms by reducing heart workload.
4. **Angiotensin-converting enzyme (ACE) inhibitors:** Drugs such as enalapril or lisinopril, commonly used for heart failure and hypertension, can help improve cardiac function in myocarditis patients.

Always consult a healthcare provider for personalized medical advice.
Metabolites: In acute myocarditis, certain metabolites can be indicators of inflammation and myocardial injury. Some key metabolites include:

1. **Troponins (cTnI, cTnT):** Elevated levels indicate myocardial injury.
2. **Creatine Kinase-MB (CK-MB):** Elevated levels can be a sign of cardiac muscle damage.
3. **B-type Natriuretic Peptide (BNP) and NT-proBNP:** Elevated levels suggest heart failure and are often used as biomarkers.
4. **Lactate Dehydrogenase (LDH):** Elevated levels can indicate tissue damage, including cardiac tissue.

These biomarkers are critical for diagnosing and assessing the severity of acute myocarditis.
Nutraceuticals: Nutraceuticals, such as omega-3 fatty acids, antioxidants like Coenzyme Q10, and certain vitamins (e.g., vitamin D), have been suggested to potentially support heart health and reduce inflammation. However, their specific efficacy in acute myocarditis isn't well-established and should be considered as complementary to conventional medical treatments. Always consult a healthcare provider before starting any supplement regimen.
Peptides: For acute myocarditis, the role of peptides in its diagnosis or treatment is an evolving area of research. Certain peptide biomarkers, like cardiac troponins (troponin I and T), are currently used for detecting myocardial injury, which can occur in myocarditis. Researchers are also exploring therapeutic peptides that may have anti-inflammatory or cardioprotective effects. However, Nanotechnology (nan) is not yet widely applied in standard clinical practice for acute myocarditis but holds future potential for targeted drug delivery, improved imaging, and novel treatment approaches.