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Myopericarditis

Myopericarditis
Literature review current through: May 2024.
This topic last updated: Jan 11, 2024.

INTRODUCTION — Myopericarditis, a complication of acute pericarditis, is characterized by extension of pericardial inflammation to the myocardium, which can manifest as an elevated troponin level and electrocardiogram (ECG) changes (mainly ST-segment elevation). It is generally evaluated and treated as acute pericarditis. The key challenge in managing myopericarditis is excluding the presence of an acute coronary syndrome (algorithm 1).

Perimyocarditis also presents as acute pericarditis, but it is characterized by a decrease in left ventricular (LV) function; it should be evaluated as myocarditis and, if present, treated as myocarditis.

The clinical presentation, diagnostic evaluation, and treatment for myopericarditis will be reviewed here. The etiology, treatment, and prognosis of acute pericarditis, other pericardial diseases, and myocarditis are discussed separately. Myocardial injury related to coronavirus disease 2019 is also discussed separately.

(See "Etiology of pericardial disease".)

(See "Acute pericarditis: Clinical presentation and diagnosis".)

(See "Acute pericarditis: Treatment and prognosis".)

(See "Recurrent pericarditis".)

(See "Constrictive pericarditis: Diagnostic evaluation".)

(See "Myocarditis: Causes and pathogenesis".)

(See "Treatment and prognosis of myocarditis in adults".)

(See "COVID-19: Cardiac manifestations in adults", section on 'Myocardial injury'.)

TERMINOLOGY — While the terms myopericarditis and perimyocarditis are often used interchangeably, the terms represent two different disease processes, each with a distinct approach to diagnosis and treatment [1-4].

"Myopericarditis" refers to cases of confirmed acute pericarditis with elevated troponin but without LV systolic dysfunction. The focus of this topic is myopericarditis.

"Perimyocarditis" refers to cases presenting as acute pericarditis with elevated troponin and LV ejection fraction (LVEF) less than 55 percent. The diagnostic approach to perimyocarditis is the same as for myocarditis [4]. The approach to treatment depends on findings from the diagnostic evaluation but does not intrinsically include treatments common to acute pericarditis and myopericarditis. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Clinical manifestations' and "Treatment and prognosis of myocarditis in adults".)

ETIOLOGY — The causes of myopericarditis are similar to those of acute pericarditis (eg, viral, neoplastic, autoimmune, post-myocardial infarction, postsurgical) (table 1). (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Establishing a definite etiology'.)

Myopericarditis is a rare complication of smallpox vaccination (vaccinia virus inoculation), as discussed below. (See 'Vaccinia-associated myopericarditis' below.)

Coronavirus 2019 (COVID-19) vaccination is rarely associated with myopericarditis, myocarditis, or pericarditis, as discussed separately. (See "COVID-19: Vaccines", section on 'Myocarditis'.)

CLINICAL PRESENTATION — The clinical presentation of myopericarditis is similar to the presentation of acute pericarditis (eg, positional and pleuritic chest pain, ECG with new widespread ST elevation or PR depression) [2,5]. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Clinical features'.)

In a study of 254 patients presenting with acute pericarditis, the presence of a pericardial effusion decreased the likelihood of myopericarditis versus isolated acute pericarditis (38 versus 60 percent), while the following presenting features increased the likelihood of myopericarditis [2]:

Younger age (36 years versus 55 years)

Male sex (75 versus 46 percent)

Recent febrile illness (50 versus 22 percent)

ST elevation (90 versus 70 percent)

Cardiac arrhythmias (predominantly ventricular; 65 versus 17 percent)

DIAGNOSTIC EVALUATION

General approach — Myopericarditis should be suspected in a patient with confirmed acute pericarditis whose initial testing for chest discomfort reveals a troponin level above the upper reference limit (average troponin I in myopericarditis is 7.2 to 9.4 ng/dL) and normal LV function (eg, portable ultrasound, formal echocardiography) (algorithm 1) [3,6-9]. As noted above, patients with myopericarditis more commonly have ECG changes (mainly widespread or localized ST-segment elevation) compared with those with simple pericarditis. Patients with suspected myopericarditis warrant hospitalization for evaluation and management.

The diagnosis is confirmed by reasonably excluding other life-threatening causes of elevated troponin (eg, acute coronary syndromes [ACS], acute aortic syndromes, pulmonary embolism):

We use coronary angiography in patients at intermediate and high risk for ACS to assess for myocardial infarction. (See 'When to assess for coronary artery disease' below.)

We routinely obtain cardiovascular magnetic resonance (CMR) imaging (if available) during the initial presentation or within two weeks of presentation to support the diagnosis of myopericarditis. If CMR imaging is not available, we perform serial echocardiograms to detect further decreases in LV function, which may signal myocarditis. (See 'Role of magnetic resonance imaging' below.)

If LV systolic function is abnormal (ie, less than 55 percent), the patient is provisionally diagnosed with perimyocarditis, which requires an evaluation for myocarditis [4]. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Approach to diagnosis of myocarditis'.)

Role of magnetic resonance imaging — We obtain CMR imaging with late gadolinium enhancement (LGE) in all patients with suspected myopericarditis to support the diagnosis. CMR imaging is not used to "rule out" ACS [8].

Timing of CMR imaging CMR imaging is most useful when performed at the initial presentation or within two weeks of symptom onset. CMR imaging should be obtained prior to hospital discharge if perimyocarditis or myocarditis are strongly suspected. If CMR imaging is not immediately available and suspicion for myocarditis is high, additional imaging (eg, repeat echocardiography) may be necessary to manage the patient until CMR imaging is available. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Clinical manifestations'.)

Diagnostic CMR image findings CMR imaging can detect evidence of pericardial and myocardial inflammation and is most specific for myopericarditis in the presence of both edema and inflammation. Myocardial edema is suggested by the presence of global or regional increases in myocardial T2 relaxation time or an increase in mycardial signal intensity in T2-weighted images. Myocardial inflammation is suggested by global or regional increases in myocardial T1, extracellular volume, or LGE. The presence of edema and inflammation increase the specificity for myopericarditis, though a single marker (eg, edema or inflammation) is sufficient to support the diagnosis of myopericarditis. CMR imaging can also detect other features of acute pericarditis (eg, pericardial thickening, pericardial edema, pericardial LGE, and pericardial effusion) that support the diagnosis of myopericarditis [10,11]. (See "Clinical utility of cardiovascular magnetic resonance imaging", section on 'Pericardial disease'.)

When to assess for coronary artery disease — Coronary angiography should be performed in selected patients with myopericarditis to rule out ACS. We perform coronary angiography (or coronary computed tomography angiography [CCTA], where available) in the presence of one or more of the of the following clinical features:

History of prior coronary artery disease.

ECG with possible ischemia (eg, "nonclassical" ECG findings consistent with ischemia).

Unstable arrhythmias.

Markedly elevated troponin (eg, troponin I >10 ng/dL) or an acute rise and/or fall pattern.

Intermediate to high-risk Global Registry of Acute Coronary Events (GRACE) (table 2) or Thrombolysis in Myocardial Infarction (TIMI) (table 3) score for coronary artery disease.

Persistent symptoms despite treatment for myopericarditis.

Patients with perimyocarditis (rather than myopericarditis) are evaluated similarly to myocarditis (algorithm 1) [4]; indications for coronary angiography in patients with myopericarditis are reviewed separately. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Cardiac catheterization'.)

The timing of invasive coronary angiography or CCTA depends entirely on the clinician’s clinical suspicion for an ACS. If the suspicion for an ACS is intermediate or high, we recommend urgent coronary angiography (invasive angiography or CCTA). CCTA may have a role in intermediate-risk patients when CCTA can be rapidly obtained and interpreted. CMR imaging is not a substitute for timely coronary artery evaluation in intermediate- to high-risk patients. (See "Overview of the acute management of non-ST-elevation acute coronary syndromes", section on 'Early risk stratification' and "Clinical use of coronary computed tomographic angiography".)

Studies of myopericarditis note a high use of coronary angiography for evaluation of myopericarditis, though coronary angiography is often negative. As an example, in one retrospective study of 486 patients ultimately diagnosed with either myopericarditis, perimyocarditis, or acute pericarditis, coronary angiography was performed in 76 percent, 76 percent, and 2 percent, respectively [9].

Indications for endomyocardial biopsy — We rarely perform an endomyocardial biopsy (EMB) in patients with suspected myopericarditis and reserve EMB for complicated cases in which symptoms or signs of heart failure or major arrhythmias develop despite appropriate therapy (eg, suspected complicated perimyocarditis, myocarditis) [4]. Indications for EMB are discussed in detail separately [12,13]. (See "Endomyocardial biopsy".)

TREATMENT — Our approach to the treatment of myopericarditis assumes that perimyocarditis, myocarditis, and acute coronary syndrome have been reasonably excluded. Most patients are treated with nonsteroidal antiinflammatory drugs (NSAIDs) and colchicine. Inflammatory markers (eg, C-reactive protein) may be more commonly elevated in patients with pericarditis than those with myopericarditis [9]. Patients who do not respond to initial therapy should be reevaluated and the therapeutic regimen should be reconsidered. (See 'Diagnostic evaluation' above and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'When to suspect myocarditis'.)

Initial pharmacologic treatment — For most patients with acute myopericarditis, we suggest initial therapy with colchicine combined with NSAIDs (aspirin or other NSAIDs) rather than NSAIDs alone. In clinical practice, the efficacy of colchicine to prevent additional events is similar to that reported in simple pericarditis.

We treat myopericarditis with doses typically recommended for acute pericarditis (table 4):

Aspirin 650 to 1000 mg three times daily.

OR

Ibuprofen 600 to 800 mg three times daily.

OR

Indomethacin 25 to 50 mg three times daily is an alternative for those not responding to aspirin or ibuprofen.

PLUS

Colchicine 0.5 to 0.6 mg once daily for patients weighing <70 kg.

OR

Colchicine 0.5 to 0.6 mg twice daily for patients weighing ≥70 kg.

In most patients, symptoms resolve within 72 hours, at which time NSAIDS are tapered weekly over two to four weeks. Colchicine is typically continued for three months and then discontinued without tapering the dose. (See "Acute pericarditis: Treatment and prognosis", section on 'NSAID dosing' and "Acute pericarditis: Treatment and prognosis", section on 'Colchicine dosing'.)

Our approach to initial treatment is based on clinical experience and limited observational data in myopericarditis and on the safety and efficacy of colchicine reported in randomized trials of patients with acute or recurrent pericarditis [2,14,15]. While NSAID therapy is associated with higher mortality in animal models of myocarditis, we do not believe this evidence applies to patients with myopericarditis [16]. (See "Acute pericarditis: Treatment and prognosis", section on 'Colchicine' and "Recurrent pericarditis", section on 'Colchicine'.)

A preliminary study in an experimental model of viral myocarditis found that colchicine reduced markers of myocardial injury (eg, troponin), improved LVEF, and reduced apoptosis and inflammatory markers without impairing the clearance of the viral agent [17].

Patients with refractory symptoms and signs — If chest symptoms persist beyond 72 hours, cardiac biomarkers remain elevated, and/or LV function decreases, we reevaluate the diagnosis of myopericarditis. (See 'Diagnostic evaluation' above.)

If myopericarditis remains the leading diagnosis, patients with intolerance to NSAIDS or colchicine, or with symptoms refractory to NSAIDs and colchicine, may be treated with a short course of glucocorticoids (after a discussion of the risks and benefits). Beta blockers may be used to treat residual symptoms (eg, palpitations, chest pain). The evidence for the use of glucocorticoids, beta blockers, and other treatments (eg, anakinra, rilonacept) for treatment of myopericarditis is inferred from observational studies showing a possible benefit in acute or recurrent pericarditis. (See "Recurrent pericarditis", section on 'Treatment'.)

Exercise restriction — We counsel complete cessation of competitive sports and limitation of fitness activity to walking and light weight training (not more than 5 kg) for at least three months and until complete clinical remission. For competitive sport activity, a longer restriction time of three to six months may be considered according to individual remission times [18]. (See "Treatment and prognosis of myocarditis in adults" and "Athletes: Overview of sudden cardiac death risk and sport participation", section on 'Myocarditis'.)

FOLLOW-UP AND PROGNOSIS — Given the presence of myocardial injury characteristic of myopericarditis, we routinely perform the following tests within two weeks of discharge:

Cardiac troponin

C-reactive protein (CRP)

Echocardiography to assess ventricular function

Elevated troponin levels usually resolve within days [9]. CRP may rise after the initial presentation, but should decline in response to NSAID therapy [19]. Repeat CMR imaging may be indicated to assess residual myocardial fibrosis in those with initial evidence of myocardial late gadolinium enhancement (LGE). Follow-up CMR should be planned at three to six months. In the acute phase, myocardial LGE may reflect myocardial edema instead of fibrosis as at a later stage (>1 month) when inflammation is relieved and expansion of extracellular space is due to myocardial fibrosis.

The recurrence of pericardial effusion, pericarditis, and myopericarditis are less frequent than simple pericarditis, and usually occur in 10 to 15 percent of cases [2,9]. In a prospective study that compared 234 patients with presumed viral or idiopathic acute pericarditis with 40 patients with myopericarditis, complication rates (including recurrent myopericarditis and acute pericarditis, cardiac tamponade, and constriction) were similar [2]. At 12 months, echocardiography, ECG, and treadmill testing were normal in 39 of the 40 myopericarditis cases. Similar findings were reported in a larger study that also noted no deaths [9].

VACCINIA-ASSOCIATED MYOPERICARDITIS — Smallpox vaccine (vaccinia virus inoculation) is associated with acute pericarditis, myopericarditis, and, rarely, myocarditis [4,12,13]. Vaccinia-associated inflammatory disease is defined as any cardiac inflammatory syndrome occurring within 30 days of vaccination without another identifiable cause [20]. The clinical presentation is similar to that seen with myopericarditis of any etiology, though the intensity of symptoms and severity of disease may be less in vaccinia-associated cases. The incidence and etiology of vaccinia-associated myopericarditis are discussed separately. (See "Vaccines to prevent smallpox, mpox (monkeypox), and other orthopoxviruses", section on 'Complications'.)

Treatment – In general, the treatment of vaccinia-associated myopericarditis is similar to that used for myopericarditis of any etiology. (See 'Treatment' above.)

Specific guidelines for the management of vaccinia-associated myopericarditis have been outlined by the Department of Defense Vaccine Healthcare Center [21]. According to this algorithm, most symptomatic patients should receive treatment with analgesics and/or NSAIDs, activity restriction for at least four to six weeks, and follow-up assessment in 6 to 12 weeks and again in 6 to 12 months. In vaccinia-associated myopericarditis not responding to NSAID and colchicine, low to moderate doses of glucocorticoids are efficacious.

In patients with progressive symptoms, reduced LVEF, sustained ventricular arrhythmias, or recurrent or persistent troponin release, endomyocardial biopsy should be considered as a guide to therapy [4,12,13] (see "Endomyocardial biopsy"). Fortunately, this rarely occurs in patients with myopericarditis. If biopsy reveals no active viral infection, the process is likely to be autoimmune; glucocorticoids alone or in association with other immunosuppressive drugs may be beneficial [2,4,12,13]. Active viral infection with vaccinia (as documented by polymerase chain reaction) is a very rare finding on endomyocardial biopsy [21]. If vaccinia infection is present, vaccinia immune globulin (VIG) may be effective given its efficacy in treating noncardiac complications of smallpox vaccine (see "Vaccines to prevent smallpox, mpox (monkeypox), and other orthopoxviruses", section on 'Vaccinia immune globulin'). VIG is available from the United States Centers for Disease Control and Prevention on a compassionate use basis (404-639-3670) [22].

Prognosis – Most patients with vaccinia-associated myopericarditis have mild disease and recover with few short-term effects. On follow-up, functional status, ECG, and echocardiogram normalize in almost all patients [23]. However, up to 13 percent describe atypical, nonlimiting chest discomfort, and fatalities have rarely been reported [21,23].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pericardial disease".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Pericarditis in adults (The Basics)")

SUMMARY AND RECOMMENDATIONS

Terminology – "Myopericarditis" refers to cases of confirmed acute pericarditis with elevated troponin but without left ventricular (LV) systolic dysfunction. "Perimyocarditis" refers to cases presenting as acute pericarditis with elevated troponin and LV ejection fraction (LVEF) less than 55 percent. Myopericarditis is generally evaluated and treated as acute pericarditis, whereas perimyocarditis is evaluated and treated as for myocarditis. (See 'Terminology' above.)

Etiology – The causes of myopericarditis are similar to those of acute pericarditis (eg, viral, autoimmune, post-myocardial infarction, postsurgical) (table 1). (See 'Etiology' above.)

Clinical presentation – The clinical presentation of myopericarditis is similar to the presentation of acute pericarditis (eg, positional and pleuritic chest pain, ECG with new widespread ST elevation or PR depression), but ECG changes are more common than in cases with simple pericarditis. (See 'Clinical presentation' above.)

Diagnostic evaluation – Myopericarditis should be suspected in a patient with confirmed acute pericarditis whose initial testing for chest discomfort reveals a troponin level above the upper reference limit and normal LV function (eg, portable ultrasound, formal echocardiography). The diagnosis is confirmed by reasonably excluding other potentially life-threatening causes of elevated troponin (eg, perimyocarditis, acute coronary syndromes [ACS], myocarditis, pulmonary embolism) (algorithm 1). (See 'General approach' above.)

We routinely obtain cardiovascular magnetic resonance (CMR) imaging to support the diagnosis of myopericarditis and to exclude myocarditis (ie, perimyocarditis). If CMR imaging to exclude LV systolic dysfunction is not readily available, we obtain serial echocardiography. (See 'Role of magnetic resonance imaging' above.)

We obtain coronary angiography in intermediate and high-risk patients to assess for myocardial infarction. (See 'When to assess for coronary artery disease' above.)

Treatment – Our approach to the treatment of myopericarditis assumes that perimyocarditis, myocarditis, and ACS have been reasonably excluded. (See 'Initial pharmacologic treatment' above and 'Diagnostic evaluation' above.)

For most patients with acute myopericarditis, we suggest initial therapy with colchicine combined with nonsteroidal antiinflammatory drugs (NSAIDs) rather than NSAIDs alone (Grade 2C). (See 'Initial pharmacologic treatment' above.)

Patients with intolerance to NSAIDS or colchicine, or with symptoms refractory to NSAIDs and colchicine, may be treated with a short course of glucocorticoids (after a discussion of the risks and benefits). (See 'Patients with refractory symptoms and signs' above.)

We counsel complete cessation of competitive sports and limitation of fitness activity to walking and light weight training (not more than 5 kg) for at least three to six months. (See 'Exercise restriction' above.)

Elevated troponin levels should resolve in days and months, respectively. C-reactive protein (CRP) may rise after presentation but should decline in response to NSAID therapy. Repeat CMR imaging is not indicated if the patient is recovering clinically, LV morphologic function has improved by echocardiography, and the patient has no myocardial late gadolinium enhancement (LGE) in the first CMR examination. (See 'Follow-up and prognosis' above.)

Vaccinia-associated myopericarditis – Vaccinia-associated myopericarditis has been defined as myocarditis and/or pericarditis occurring within 30 days after vaccination in the absence of another cause; it is treated the same as myopericarditis unless the disease is severe or refractory, in which case steroids or vaccinia immune globulin may be effective. (See 'Vaccinia-associated myopericarditis' above.)

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  2. Imazio M, Cecchi E, Demichelis B, et al. Myopericarditis versus viral or idiopathic acute pericarditis. Heart 2008; 94:498.
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  9. Imazio M, Brucato A, Barbieri A, et al. Good prognosis for pericarditis with and without myocardial involvement: results from a multicenter, prospective cohort study. Circulation 2013; 128:42.
  10. Ferreira VM, Schulz-Menger J, Holmvang G, et al. Cardiovascular Magnetic Resonance in Nonischemic Myocardial Inflammation: Expert Recommendations. J Am Coll Cardiol 2018; 72:3158.
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  12. Seferović PM, Tsutsui H, McNamara DM, et al. Heart Failure Association of the ESC, Heart Failure Society of America and Japanese Heart Failure Society Position statement on endomyocardial biopsy. Eur J Heart Fail 2021; 23:854.
  13. Tschöpe C, Ammirati E, Bozkurt B, et al. Myocarditis and inflammatory cardiomyopathy: current evidence and future directions. Nat Rev Cardiol 2021; 18:169.
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  16. Rezkalla S, Khatib G, Khatib R. Coxsackievirus B3 murine myocarditis: deleterious effects of nonsteroidal anti-inflammatory agents. J Lab Clin Med 1986; 107:393.
  17. Pappritz K, Lin J, El-Shafeey M, et al. Colchicine prevents disease progression in viral myocarditis via modulating the NLRP3 inflammasome in the cardiosplenic axis. ESC Heart Fail 2022; 9:925.
  18. Pelliccia A, Solberg EE, Papadakis M, et al. Recommendations for participation in competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and pericarditis: position statement of the Sport Cardiology Section of the European Association of Preventive Cardiology (EAPC). Eur Heart J 2019; 40:19.
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  20. Halsell JS, Riddle JR, Atwood JE, et al. Myopericarditis following smallpox vaccination among vaccinia-naive US military personnel. JAMA 2003; 289:3283.
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