Myocarditis

Myocarditis is inflammation of the cardiac muscle. Myocarditis can progress to inflammatory cardiomyopathy when there is associated ventricular remodeling and cardiac dysfunction due to chronic inflammation. Symptoms can include shortness of breath, chest pain, decreased ability to exercise, and an irregular heartbeat.

Myocarditis is most often due to a viral infection. An ultrasound of the heart is important to rule out other potential causes, such as heart valve problems. While people of all ages are affected, the young are most often affected. It is slightly more common in males than females.

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:

{| class="wikitable"

!Symptoms

!Notes

!Signs

!Notes

|Chest pain

|Often described as sharp or stabbing in nature

|Fever

|Especially when infectious, e.g., from parvovirus B19

|Shortness of breath

|Worse when lying down or in a prone position

|Dull heart sounds

|Muffling occurs with inflammation, especially with pericarditis

|Palpitations

|Feeling like one's heart is beating forcefully

|Abnormal heart rhythm

|Determined using an electrocardiogram

|Dizziness or fainting

|Can reflect inadequate blood flow to the brain

|Damage to heart cells

|Seen as elevated troponin and inflammation on imaging

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. 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. Worldwide, however, the most common cause is Chagas disease, an illness endemic to Central and South America that results from infection with the protozoan Trypanosoma cruzi. Globally, Chagas disease is the leading cause of myocarditis, which results from infection with the protozoan Trypanosoma cruzi. A list of the most relevant infectious organisms is below.

Viral: adenovirus, parvovirus B19, coxsackie virus, rubella virus, polio virus, Epstein–Barr virus, hepatitis C virus, influenza virus and severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2, causing COVID-19)
Protozoan: Trypanosoma cruzi and Toxoplasma gondii (causing Chagas disease and toxoplasmosis, respectively)
Bacterial: Brucella, Corynebacterium diphtheriae, Neisseria gonorrhoeae, Haemophilus influenzae, Actinomyces, Tropheryma whipplei, Vibrio cholerae, Borrelia burgdorferi, Leptospira, Rickettsia, Mycoplasma pneumoniae
Fungal: Aspergillus
Parasitic: Ascaris, Echinococcus granulosus, Paragonimus westermani, Schistosoma, Taenia solium, Trichinella spiralis, visceral larva migrans, Wuchereria bancrofti

Immune conditions

Allergic reaction (e.g., to acetazolamide or amitriptyline)
Kawasaki disease
Autoimmunity (scleroderma, lupus, sarcoidosis, and systemic vasculitides)
Toxic shock syndrome

Drug reactions and toxins

Anthracyclines and other forms of chemotherapy
Antipsychotics including clozapine
Alcohol
Stimulants such as mephedrone and cocaine
Arsenic
Carbon monoxide
Snake venom
Heavy metals (copper or iron)

Vaccination

Myocarditis and pericarditis can be a side effect of some vaccines like the smallpox vaccine.
Myocarditis can be a side-effect of the Covid-19 mRNA vaccines. The FDA and European Medicines Agency estimates the risk of myocarditis after the Covid-19 vaccine as 1 case per 100,000 of those who are vaccinated. The risk of myocarditis after Covid-19 vaccination was observed to be highest in males between 16–29 years of age, and after receiving the second dose of the mRNA Covid-19 vaccine. For this group, incidence of myocarditis has been reported to be between 1 case in 2500 to 1 case per 10,000.

Physical injuries

Electric shock
Hyperpyrexia, and radiation

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. 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.

Myocardial inflammation can be suspected on the basis of elevated inflammatory markers including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), or an increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated. The ECG finding most commonly seen in myocarditis is sinus tachycardia with non-specific ST or T wave changes. Cardiac MRI is most sensitive when performed 2–3 weeks after the initial clinical presentation of myocarditis and may be repeated 6–12 months after onset to monitor the evolution of disease or response to treatment. The Lake Louise Criteria include increased signal intensity after gadolinium contrast enhancement (a sign of hyperemia, or increased blood flow to damaged tissue), increased myocardial T2 relaxation time or an increased T2 signal intensity (which are signs of tissue edema or swelling), and late gadolinium contrast enhancement (which is a sign of tissue necrosis (tissue damage) or fibrosis (scarring)). Cardiac MRI, if available, is recommended in all cases of suspected myocarditis.

File:UOTW 7 - Ultrasound of the Week 2.webm|Ultrasound showing cardiogenic shock due to myocarditis 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.

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.

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.

Mechanical support

Mechanical support is used in cases of myocarditis in which medications alone do not lead to adequate heart function and the body requires additional support to achieve organ perfusion. An implantable cardioverter-defibrillator (ICD) is sometimes required in those with cardiomyopathy or heart failure caused by myocarditis due to the risk of fatal ventricular arrhythmias. Electrocardiogram findings of ST elevations with upward concavity and an early repolarization pattern, however, were associated with a better cardiovascular prognosis in general. 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. The highest incidence of myocarditis is seen in men between the ages of 20 and 40. 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. Myocarditis, however, has shown to be more common in the male population than in the female. In young adults, up to 20% of all cases of sudden death are due to myocarditis.

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. with the myocarditis being associated with a spectrum of severities from asymptomatic to fulminant. The symptoms for myocarditis following a COVID-19 infection can present as chest pain, shortness of breath, fatigue, and irregular heartbeats which can make the accurate diagnosis of myocarditis challenging. In one cohort study, comparing the autopsy reports of 277 hearts of people who died from COVID-19, clinically significant myocarditis was seen in approximately 2% of hearts. Other estimates of the incidence of myocarditis in those with COVID-19 range from 2.4 cases of definite/probable myocarditis (based on clinical criteria) per 1,000 people with COVID-19 to 4.1 cases per 1,000 persons in those who are hospitalized with COVID-19.

Although myocarditis is relatively rare in those with COVID-19, when it is present it is likely to follow a severe and fulminant course for those previously hospitalized with COVID-19. Of those with COVID-19 and myocarditis, 39% presented with severe myocarditis associated with hemodynamic instability, needing mechanical circulation support or other major interventions.

History

Cases of myocarditis have been documented as early as the 1600s, but the term "myocarditis", implying an inflammatory process of the myocardium, was introduced by German physician Joseph Friedrich Sobernheim in 1837. However, the term has been confused with other cardiovascular conditions, such as hypertension and ischemic heart disease. Following admonition regarding the indiscriminate use of myocarditis as a diagnosis from authorities such as British cardiologist Sir Thomas Lewis and American cardiologist and co-founder of the American Heart Association Paul White, myocarditis was under-diagnosed.