eMedicine Specialties > Emergency Medicine > Cardiovascular

Myocarditis

David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine, University of Chicago/Pritzker School of Medicine
Ethan A Booker, MD, Attending Physician, Department of Emergency Medicine, Washington Hospital Center

Updated: Aug 5, 2008

Introduction

Background

Myocarditis is collection of diseases of infectious, toxic, and autoimmune etiologies characterized by inflammation of the heart. Subsequent myocardial destruction can lead to dilated cardiomyopathy.

Myocarditis is an elusive illness to study, diagnose, and treat because the clinical presentation may range from nearly asymptomatic to overt heart failure requiring transplantation; a myriad of causes exist, and it is occasionally the unrecognized culprit in cases of sudden death.

Pathophysiology

Myocarditis is defined as inflammatory changes in the heart muscle and is characterized by myocyte necrosis.

Animal models of viral myocarditis have lead to a much greater understanding of the pathophysiology of acute, severe myocarditis and correlate with the findings in susceptible patients who apparently uptake viral RNA and develop a cytotoxic necrosis and rapid (1-2 d) cell death without the appearance of the interstitial infiltrate usually associated with myocarditis.

Over 4-14 days, those cells that survive the initial insult, in response to macrophage activation and cytokine expression, develop the classic, histologically apparent infiltration of mononuclear cells. In this subacute viral-clearing phase, natural killer cells target myocardium expressing viral RNA and continue myocyte necrosis. Tumor necrosis factor is also involved in rapidly clearing virus, but its involvement results in the further recruitment of inflammatory cells, activates endothelial cells, and has negative inotropic effects. In the latter stages of the subacute process, cytotoxic T lymphocytes infiltrate the myocardium and direct lysis of cardiocytes, which present virus fragments via the histocompatibility complex on the surface of myocyte membrane. Neutralizing antiviral antibodies also develop to assist in the clearing of virus.

In the chronic phases, the deleterious effects of either inadequate or inappropriately abundant immune response can lead to the unfortunate long-term sequelae of dilated cardiomyopathy and heart failure. In animal models of insufficient immune response, viral replication can continue and cause chronic destruction of myocytes. Biopsy results of patients with acute myocarditis who develop dilated cardiomyopathy demonstrate changes consistent with those seen in polymerase chain reaction (PCR) amplifying RNA from enteroviruses. On the opposite spectrum of immune activity, overabundant T cells may continue activity into the chronic phase and also may cause tissue destruction and heart failure.

Frequency

United States

The true incidence of myocarditis is unknown because many cases are asymptomatic, and some symptoms related to significant morbidity may not be appropriately credited. One major urban US medical examiners office attributed 1.3% of sudden and unexpected deaths to myocarditis¹ , consistent with other autopsy studies that demonstrate evidence of myocardial inflammation in 1-1.5% of deaths. In the United States, viral and medication-related cases are the most commonly identified causes.

International

Internationally other etiologies (ie, Chagas disease, diphtheria) play a greater role than in the United States, and true frequency of disease is even more difficult to appreciate.

Mortality/Morbidity

Because of its difficulty in diagnosis, the large number of cases that likely never come to medical attention, and its previously underappreciated role in sudden dysrhythmic death, morbidity and mortality data are difficult to construct.

• Rarely, acute myocarditis is fulminant and leads rapidly to death. 
• Mortality for clinically significant and biopsy proven myocarditis varies widely. Recent studies have demonstrated death to be as low as 4% of cases for patients without heart failure and with no persistent viral genome expression. On the opposite end of the spectrum, in patients with persistent viral genome expression, myocarditis related mortality may be as high as 25%.
• The appropriate delicate balance of the immune response to viral invasion of myocytes indicates that a certain number of individuals, perhaps with genetic predispositions, will advance to dilated cardiomyopathy and heart failure, the most common long-term sequelae in those patients who do not recover completely.

Sex

The male-to-female ratio is 1.5:1.

Age

The average age of patients with myocarditis is 42 years. It is a prominent cause of sudden cardiac death in young adults, accounting for 8-12% of such deaths.

Clinical

History

• Many patients present with a nonspecific illness characterized by fatigue, mild dyspnea, and myalgias. A few patients present acutely with fulminant congestive heart failure (CHF) secondary to widespread myocardial involvement. Small and focal areas of inflammation in electrically sensitive areas may be the etiology in patients whose initial presentation is sudden death.
• Most cases of myocarditis are subclinical; therefore, the patient rarely seeks medical attention during acute illness. These subclinical cases may have transient ECG abnormalities.
• An antecedent viral syndrome is present in more than one half of patients with myocarditis. The appearance of cardiac-specific symptoms occurs primarily in the subacute virus-clearing phase; therefore, patients commonly present 2 weeks after the acute viremia.
• Fever is present in 20% of patients.
• Other symptoms include fatigue, myalgias and arthralgias, and malaise.
• Chest pain
  • Chest discomfort is reported in 35% of patients.
  • The pain is most commonly described as a pleuritic, sharp, stabbing precordial pain.
  • It may be substernal and squeezing and, therefore, difficult to distinguish from that typical of ischemic pain.
• Dyspnea on exertion is common.
• Orthopnea and shortness of breath at rest may be noted if CHF is present.
• Palpitations are common. Syncope in a patient with a presentation consistent with myocarditis should be carefully approached because it may signal high-grade atrioventricular (AV) block or risk for sudden death.
• Pediatric patients, particularly infants, present with nonspecific symptoms, including the following:
  • Fever
  • Respiratory distress
  • Poor feeding or, in cases with CHF, sweating while feeding
  • Cyanosis in severe cases

Physical

Physical findings can range from nearly normal examination findings to signs of fulminant CHF.

• Patients with mild cases of myocarditis have a nontoxic appearance and simply may appear to have a viral syndrome.
• Tachypnea and tachycardia are common. Tachycardia is often out of proportion to fever.
• More acutely ill patients have signs of circulatory impairment due to left ventricular failure.
• A widely inflamed heart shows the classic signs of ventricular dysfunction including the following:
  • Jugular venous distention
  • Bibasilar crackles
  • Ascites
  • Peripheral edema
• S₃ or a summation gallop may be noted with significant biventricular involvement.
• Intensity of S₁ may be diminished.
• Cyanosis may occur.
• Hypotension caused by left ventricular dysfunction is uncommon in the acute setting and indicates a poor prognosis when present.
• Murmurs of mitral or tricuspid regurgitation may be present due to ventricular dilation.
• In cases where a dilated cardiomyopathy has developed, signs of peripheral or pulmonary thromboembolism may be found.
• Diffuse inflammation may develop leading to pericardial effusion, without tamponade, and pericardial and pleural friction rub as the inflammatory process involves surrounding structures.

Causes

The causes of myocarditis are numerous and can be roughly divided into infectious, toxic, and immunologic etiologies, with viral etiologies most common in North America.

• Amongst the infectious causes, viral acute myocarditis is by far the most common.
  • Identification of the coxsackie-adenovirus receptor protein explains the prevalence of these viruses as a frequent cause. The receptor is the common target of coxsackievirus B of the enterovirus family and serotypes 2 and 5 of the adenovirus family.
  • Other viruses implicated in myocarditis include influenza virus, echovirus, herpes simplex virus, varicella-zoster virus, hepatitis, Epstein-Barr virus, and cytomegalovirus. Hepatitis C, in particular, is becoming a major focus of research.
  • Human immunodeficiency virus (HIV) deserves special mention because it seems to function differently than other viruses. Although some evidence indicates that HIV directly invades myocytes, HIV genomes can be amplified from patients without histologic signs of inflammation. In addition, in patients who are infected with HIV, T-cell mediated immune suppression increases the risk of contracting myocarditis due to other infectious causes.
  • Nonviral infectious causes are numerous and varied. Worldwide the most common bacterial cause is diphtheria, and, in South America, the protozoal Chagas disease is a common entity. Streptococcal and staphylococcal species and Bartonella, Brucella, Leptospira, and Salmonella species can spread to the myocardium as a consequence of severe cases of endocarditis. Borrelia burgdorferi, the spirochete agent in Lyme disease, is also a known cause of myocarditis. Parasitic myocarditis from trypanosomiasis; trichinosis; and, in the immunocompromised host, toxoplasmosis have been identified.
• Toxic myocarditis has a number of etiologies including both medical agents and environmental agents.
  • Among the most common drugs that cause hypersensitivity reactions are clozapine, penicillin, ampicillin, hydrochlorothiazide, methyldopa, and sulfonamide drugs. This syndrome is associated with peripheral eosinophilia, fever, and rash in patients who have biopsy findings of an eosinophilic infiltrate of the myocardium.
  • Numerous medications (eg, lithium, doxorubicin, cocaine, numerous catecholamines, acetaminophen) may exert a direct cytotoxic effect on the heart. Zidovudine (AZT) has been associated with myocarditis.
  • Environmental toxins include lead, arsenic, and carbon monoxide. Cases have been attributed to Chinese sumac.
  • Wasp, scorpion, and spider stings
  • Radiation therapy may cause a myocarditis with the development of a dilated cardiomyopathy.
• Immunologic etiologies of myocarditis encompass a number of clinical syndromes and include the following:
  • Connective tissue disorders such as systemic lupus erythematosus (SLE), rheumatoid arthritis, scleroderma, and dermatomyositis that can often result in a dismal prognosis
  • Idiopathic inflammatory and infiltrative disorders such as Kawasaki disease, sarcoidosis, and giant cell arteritis
• Rejection of the post transplant heart may present as inflammatory myocarditis.

Differential Diagnoses

Workup

Laboratory Studies

• Cardiac enzyme levels
  • These levels are only elevated in a minority of patients.
  • Normally, a characteristic pattern of slow elevation and fall over a period of days occurs; however, a more abrupt rise is observed in patients with acute myocardial infarction.
• Cardiac troponin I may be more sensitive because it is present for longer periods after myocardial damage from any cause.²
• Erythrocyte sedimentation rate (ESR) is elevated in 60% of patients with acute myocarditis.
• Leukocytosis is present in 25% of cases.

Imaging Studies

• Chest radiography
  • A chest radiograph often reveals a normal cardiac silhouette, but pericarditis or overt clinical CHF is associated with cardiomegaly.
  • Vascular redistribution
  • Interstitial and alveolar edema
  • Pleural effusion
• Echocardiography
  • Impairment of left ventricular systolic and diastolic function
  • Segmental wall motion abnormalities
  • Impaired ejection fraction
  • A pericardial effusion may be present, although findings of tamponade are rare.
  • Ventricular thrombus has been identified in 15% of patients studied with echocardiography.
• MRI is capable of showing abnormal signal intensity in the affected myocardium.
  • Cardiac MRI is an emerging field in general, and contrast-enhanced T1- weighted MRI has been shown to have sensitivities and specificities approaching 100% for diagnosis.³
  • MRI can demonstrate nodular and patchy areas of inflammation, often seen first in the lateral and inferior wall and can be used to guide later biopsy.
  • MRI is also one of the modalities used in the evaluation of young patients with apparently idiopathic dysrhythmias, and this imaging study can differentiate focal and diffuse inflammation from the rare electrically significant myocardial tumor.

Other Tests

• Electrocardiography 
  • Sinus tachycardia is the most frequent finding.
  • ST-segment elevation without reciprocal depression, particularly when diffuse, is helpful in differentiating myocarditis from acute myocardial infarction.
  • Decreased QRS amplitude and transitory Q-wave development is very suggestive of myocarditis.
  • As many as 20% of patients will have a conduction delay, including Mobitz I, Mobitz II, or complete heart block.
  • Left or right bundle-branch block is observed in approximately 20% of abnormal ECG findings and may persist for months.
• Viral isolation from other body sites may be supportive of the diagnosis.
• Polymerase chain reaction (PCR) identification of a viral infection from myocardial tissue, pericardial fluid, or other body fluid sites can be helpful. Persistent viral genome, as detected by PCR, has been identified as one marker of increased incidence of dilated cardiomyopathy and mortality.
• If a systemic disorder (eg, SLE) is suspected, antinuclear antibody (ANA) and other collagen vascular disorder laboratory investigations may be useful.

Procedures

• Cardiac catheterization usually reveals normal coronary vessels and regional wall motion abnormalities with diminished ejection fraction. It has no benefit over noninvasive echocardiography.
• Endomyocardial biopsy continues to be of use in diagnosing myocarditis  
• The Dallas criteria, the classic histological criteria required for diagnosis of myocarditis, are no longer broadly accepted due to stated biopsy sample errors, problems with inter-rater reliability, and the identification of alternate patterns of inflammation besides the previously defined lymphocytic infiltrate with myocyte necrosis.⁴
• The use of MRI to target biopsy, immunohistochemical staining, and the ability to identify viral genome by PCR has allowed endomyocardial biopsy to remain a powerful tool. In one study of nearly 900 patients, biopsy altered diagnosis in 21% of patients.

Treatment

Emergency Department Care

Because many cases of myocarditis are not clinically obvious, a high degree of suspicion is required to identify acute myocarditis.

Fortunately, most patients have mild symptoms consistent with viral syndromes, and they recover with simple supportive care on an outpatient basis.

• Standard treatment of clinically significant disease includes the detection of dysrhythmia with cardiac monitoring, supplemental oxygen, and managing fluid status.
• Left ventricular dysfunction developing from myocarditis should be approached in much the same manner as other causes of CHF with some exceptions (see Medication).
• In general, sympathomimetic drugs should be avoided because they increase the extent of myocardial necrosis and mortality.
• Beta-blockers should be avoided in the acutely decompensating phase of illness, but studies that have used carvedilol have shown decreases in the expression of several different histochemicals, subsequent inflammatory myocyte infiltrate, and mortality.
• Patients who present with Mobitz II or complete heart block require pacemaker placement. Some authors also suggest the placement of automatic implantable cardioverter-defibrillators (AICDs) in patients with significant, persistent decreases in left ventricular (LV) function.

Consultations

Patients who require emergency room treatment for new-onset CHF, dysrhythmia, or cardiogenic shock should be admitted to the hospital with continuous cardiac monitoring and cardiology consultation.

Medication

Medical therapy for myocarditis is an area of avid research interest but with little success in human trials. Treatment primarily involves managing the complications of myocarditis, chiefly thromboembolism, dysrhythmia, and CHF, and is addressed in detail in the corresponding eMedicine Journal articles; little is specific to myocarditis except for a few specific aspects of the treatment of myocarditis-related CHF.

Despite continued research interest in immunosuppressives for treatment of myocarditis, no randomized controlled trial, of which there have been several, has shown any short- or long-term benefit to all patients. However, in the subset of patients with cardiac sarcoid, hypersensitivity myocarditis, and giant cell myocarditis, general immunosuppression likely can play a significant role in preventing progression and reversing inflammation.

A great amount of research is currently focussed on immune modulators that target particular steps in the immune cascade without eliminating the ability of the body's defenses to shed virus. Immunomodulating therapy, such as IV-IG and interferon alfa and beta, show great promise in animal models, research trials, and limited clinical experience. In research trials, of interferon beta, patients have had elimination of viral genome and have gained and maintained improved LV function after treatment. These therapies are not yet used outside of research protocols.

Medication treatment specific for myocarditis is an area of avid research, mostly focussing on immunomodulators as discussed below, but many areas are being explored. An interesting Chinese study demonstrated a potent antiviral effect against coxsackievirus replication from a polyphenol extracted from the spice tumeric.

Angiotensin converting enzyme inhibitors

These agents are beneficial in the management of blood pressure and LV function in heart failure. Captopril, in particular, has been shown to be beneficial in the treatment of significant LV dysfunction. Other ACE inhibitors have not shown the same effect in animal trials, indicating captopril's oxygen radical scavenging properties in the morbidity effect.

Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Dosing

Adult

6.25-12.5 mg PO tid; not to exceed 150 mg tid

Pediatric

0.15-0.3 mg/kg PO bid/tid

Interactions

NSAIDs may reduce hypotensive effects of captopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

Contraindications

Documented hypersensitivity; renal impairment

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment, valvular stenosis, or severe CHF

Calcium channel blockers

Although they have limited use in ischemic causes of CHF, calcium channel blockers may prove to be useful in myocarditis-related myopathies. Amlodipine, in particular, perhaps due to its effect on nitric oxide, showed benefit in animal models and in a placebo controlled trial.

Amlodipine (Norvasc)

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias.

Dosing

Adult

2.5-5 mg PO qd
10 mg PO qd maximum

Pediatric

Not established

Interactions

Fentanyl and alcohol may increase hypotensive effects; calcium channel blocker may increase cyclosporine levels; H2 blockers (cimetidine), erythromycin, nafcillin, and azole antifungals may increase toxicity (avoid combination or monitor closely); carbamazepine may reduce bioavailability (avoid this combination); rifampin may decrease levels (monitor and adjust dose of calcium channel blocker)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose in renal or hepatic impairment; may cause lower extremity edema; allergic hepatitis has occurred but is rare

Loop diuretics

These agents are used for management of fluid overload.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Dosing

Adult

20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states

Pediatric

1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Interactions

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication

Contraindications

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, CO₂, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Cardiac glycosides

These agents decrease AV nodal conduction primarily by increasing vagal tone. They may aid in the dysrhythmia and CHF aspects of myocarditis.

Digoxin (Digitek, Lanoxicaps, Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Dosing

Adult

0.125-0.375 mg PO qd

Pediatric

<5 years: Not established
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
Maintenance dose: Use 25-35% of PO loading dose

Interactions

Many medications can alter levels of digoxin, which has a fairly narrow therapeutic window

Contraindications

Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients with myocarditis seem to be particularly sensitive to digoxin toxicity

Beta-adrenergic blockers

Beta-blockers should be avoided in the acutely decompensated phase of CHF and fulminant case of myocarditis but show long-term improvements in mortality.

Carvedilol (Coreg)

Nonselective beta- and alpha-adrenergic blocker. Also has antioxidant properties. Does not appear to have intrinsic sympathomimetic activity. May reduce cardiac output and decrease peripheral vascular resistance. Shown to be of benefit in patients with heart failure. Some evidence suggests it is even more beneficial than metoprolol.

Dosing

Adult

6.25-50 mg PO bid as tolerated (maximum of 75 mg/d if <85 kg, 100 mg/d if >85 kg)

Pediatric

Not established

Interactions

Rifampin, barbiturates, cholestyramine, colestipol, NSAIDs, salicylates, and penicillins may decrease effects; carvedilol may increase effects of antidiabetic agents, digoxin, and calcium channel blockers; concurrent administration with clonidine may increase blood pressure and decrease heart rate; carvedilol may decrease effect of sulfonylureas; cimetidine, fluoxetine, paroxetine, and propafenone may increase carvedilol levels

Contraindications

Documented hypersensitivity; hypotension; bradycardia; AV/SA node disease; cardiogenic shock; overt cardiac failure

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure being treated with digitalis, diuretics, or ACE inhibitors (AV conduction may be slowed); discontinue if liver impairment occurs; caution in peripheral vascular disease, hyperthyroidism, and diabetes mellitus

Follow-up

Further Inpatient Care

• Patients admitted to the hospital are treated for the complications of myocarditis.
• The increased use of MRI for targeting biopsy, novel immunohistochemical staining, and PCR for viral genome detection have lead to improved accuracy of the technique of endomyocardial biopsy and have secured its continued place in the evaluation and treatment of patients with suspected myocarditis.
• Although temporary pacemaker placement for advanced degrees of heart block is indicated, in the setting of myocarditis, these conduction disturbances are usually transitory. Therefore, permanent pacemaker placement usually is not necessary.
• Bedrest with restriction of activity and sodium intake is beneficial.
• Mechanical assist devices and extracorporeal membrane oxygenation are growing in use as bridges to recovery or heart transplant.
• Patients with fulminant heart failure may require transplantation, which can be life saving. Unfortunately, these patients have a higher rate of rejection than patients whose underlying cause of heart failure is not myocarditis.

Further Outpatient Care

• The clinician may consider the placement of a Holter monitor to recognize dysrhythmias on an outpatient basis.
  • This may be undertaken after the initial ED evaluation of a patient who shows no sign of acute dysrhythmia, CHF, or other complication.
  • A Holter monitor may also be placed after the initial inpatient treatment.
• Upon discharge from the hospital, all patients with myocarditis should have follow-up visits with a cardiologist.
• Recovered patients should have restricted activity for 6 months because rapid return to activity has provoked recurrent inflammation in animal models.

Inpatient & Outpatient Medications

• Treatment of pain with a narcotic analgesic (eg, acetaminophen with codeine) is appropriate.
• Avoid nonsteroidal anti-inflammatory drugs (NSAIDs), which are relatively contraindicated in this condition.
• Other outpatient medications are associated with managing the resultant CHF and are discussed in Medication.

Complications

• Congestive heart failure
  • Pulmonary edema
  • Cardiogenic shock
  • Cardiac failure
• Dilated cardiomyopathy
• Dysrhythmias
• Recurrent myositis

Prognosis

• Most cases are believed to be clinically silent and resolve spontaneously without sequelae; therefore, making accurate statements concerning the prognosis of myocarditis is difficult.
• Patients who present with CHF experience morbidity and mortality based on the degree of left ventricular dysfunction.
• Of patients who present with cardiogenic shock, elderly patients and patients with giant cell arteritis have a poor prognosis.
• Patients with HIV and persistent viral genome expression from myocytes have dismal outcomes.
• One half of patients who present with new-onset CHF experience considerable improvement of cardiac function with treatment. One fourth of patients who present with CHF stabilize with compromised cardiac function. The conditions of the remaining one fourth of patients continue to deteriorate.
• Patients who require transplantation have an increased risk of recurrent myocarditis and graft rejection.

Patient Education

• Patients are advised to restrict activity since studies have shown that increased activity promotes progression of inflammation.

Miscellaneous

Medicolegal Pitfalls

• Myocarditis may present subtly, but it should be considered in the patient who presents with dyspnea and chest discomfort, particularly if the history includes a recent viral illness.
  • Careful physical examination looking for signs of CHF and pericarditis is helpful. Electrocardiography, ESR, and cardiac enzyme levels are useful screening tools.
  • Patients with evidence of dysrhythmia, CHF, or thromboembolism must be admitted.

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Keywords

myocarditis, heart inflammation, dilated cardiomyopathy, inflammatory changes in the heart muscle, myocyte necrosis, viral myocarditis, acute myocarditis, inflammatory myocarditis, Chagas disease, coxsackievirus B, influenza virus, echovirus, herpes simplex virus, varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, hepatitis C, HIV, diphtheria, Bartonella species, Brucella species, Leptospira species, Salmonella species, endocarditis, Borrelia burgdorferi, toxic myocarditis, parasitic myocarditis

Contributor Information and Disclosures

Author

David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine, University of Chicago/Pritzker School of Medicine
David S Howes, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Ethan A Booker, MD, Attending Physician, Department of Emergency Medicine, Washington Hospital Center
Ethan A Booker, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Eric M Kardon, MD, FACEP, Attending Emergency Physician, Georgia Emergency Medicine Specialists and Emergency Physicians of Tidewater; Division of Emergency Medicine, Athens Regional Medical Center
Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Paul Blackburn, DO, FACOEP, FACEP, Program Director, Department of Emergency Medicine, Maricopa Medical Center; Assistant Professor, Department of Surgery, University of Arizona
Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Harvard Medical School; Associate-Chief, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Schering  Honoraria Speaking and teaching

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