AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Although most myocarditis (ie, inflammation of heart muscles) cases have a viral etiology, many nonviral causes also exist. Many common infectious illnesses of childhood may be associated with myocarditis. In addition, myocarditis can be a manifestation of hypersensitivity or can be secondary to a drug reaction. The severity of myocarditis varies from relatively asymptomatic disease to fulminant severe disease with a rapid, progressive, downhill course.

Epidemiologically, myocarditis appears to be sporadic. The most common cause is thought to be coxsackievirus B. Bacterial, parasitic, fungal, toxic, and drug-related causes are examples of other causes.

Pathophysiology

With clinically significant myocarditis present (regardless of cause), myocardial function is reduced in the presence of and as a result of extensive interstitial inflammation and/or injury. Systolic function of the left ventricle with concomitant dilatation of the heart and cardiac enlargement occurs. The overall result is an attendant reduction in cardiac output.

In addition, the progressive congestive heart failure (CHF) with increased left ventricular end-diastolic volume and pressure results in an increase in left atrial pressure, which is transmitted into the pulmonary venous system. This may also result in pulmonary edema secondary to increased pulmonary arterial hydrostatic forces. Finally, during the healing stages of myocarditis, fibroblasts may replace existing myocytes with resultant scar formation. Chronic CHF may result.

Frequency

United States

Myocarditis is not common in children. In a study at Texas Children's Hospital conducted from 1954-1977, myocarditis was diagnosed in only 0.3% of 14,322 patients observed in the cardiology service. Actual frequency may be higher because clinicians do not recognize all cases of myocarditis. A much higher incidence of myocarditis is noted in several autopsy series than in clinical practice, though the clinical relevance of this is not clear.

Recent evidence suggests that a percentage of patients undergoing endomyocardial biopsy for unexplained ventricular arrhythmias or ventricular dysfunction have findings suggestive of myocarditis.

Mortality/Morbidity

Myocarditis can result in significant mortality and morbidity. Acute myocarditis can result in death in up to 20-30% of cases. In addition, a variable, but not small, percentage of children who survive myocarditis are left with a chronic dilated cardiomyopathy that may require chronic medications and eventual cardiac transplantation.

• Just as in viral myocarditis, nonviral myocarditis has variable presentations. Myocarditis may be associated with symptoms of both acute and chronic CHF requiring both immediate as well as long-term medical therapies.
• Some patients who recover from myocarditis may require cardiac transplantation because of severe, chronic CHF symptoms.
• Some patients with myocarditis may die either during the acute presentation or when symptoms of chronic CHF manifest. The actual frequency of these events is uncertain because the denominator and specific etiologies of myocarditis may not easily be determined.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Clinical presentation of nonviral myocarditis varies considerably; factors that influence the clinical presentation include etiologic agent, age, sex, and immunocompetence. Many patients with myocarditis are asymptomatic, while others may present with a fulminant, rapidly progressive, fatal illness.

• Clinical manifestations of myocarditis, regardless of etiology, tend to be more severe in newborns than in older infants and children.
• Symptoms in newborns are nonspecific and include the following:
• • Lethargy
  • Poor feeding
  • Cyanosis
  • Respiratory distress
  • Tachypnea
  • Tachycardia
  • Vomiting
• In older infants and children, the symptoms often encountered include the following:
• • Low-grade fever
  • Irritability
  • Mild respiratory symptoms
  • Abdominal pain

Physical

The physical examination may include verification of the above symptoms in the History section. The nonspecific signs and symptoms noted in infants with myocarditis may be evidenced on physical examination but may be documented in patient history. Fever, irritability, respiratory signs, and abdominal pain may be noted on physical examination of children and adults with myocarditis. If the disease has progressed, physical examination usually reveals the following:

• Decreased cardiac output
• Pallor and cool skin in distal extremities
• Rapid respirations
• Possible thready pulse
• Tachycardia usually present (gallop rhythm may be heard)
• If CHF has progressed, the following signs may be noted:
• • A mitral regurgitant murmur, a blowing holosystolic murmur heard best at the apex of the heart, may be present.
  • Lung examination may show scattered rhonchi and rales.
  • Full cardiovascular collapse is possible.

Causes

The following is a relatively comprehensive list of causes of myocarditis, including nonviral causes. Though rare, as mentioned, a few of the more common causes of nonviral myocarditis are then discussed in greater detail.

• Viral (see Myocarditis, Viral)
• Rickettsial - Rickettsia rickettsii, Rickettsia tsutsugamushi
• Bacterial organisms/infections
• • Klebsiella species
  • Leptospira species
  • Salmonella species
  • Brucella species
  • Legionella pneumophila
  • Meningococci
  • Clostridia
  • Streptococci (scarlet fever)
  • Staphylococci
  • Pneumococci
  • Tuberculosis
  • Syphilis
  • Tetanus
• Protozoa and protozoal infections
• • Trypanosoma cruzi (Chagas disease)
  • Toxoplasmosis
  • Amebiasis
• Other parasites and parasitic infections
• • Toxocara canis
  • Schistosomiasis
  • Heterophyiasis
  • Cysticercosis
  • Echinococci
  • Visceral larva migrans
• Fungal infections
• • Actinomycosis
  • Coccidioidomycosis
  • Histoplasmosis
  • Candidiasis
• Toxic etiology - Scorpion envenomations and diphtheria
• Drugs
• • Cyclophosphamide
  • Phenylbutazone
  • Acetazolamide
  • Amphotericin B
  • Indomethacin
  • Tetracycline
  • Isoniazid
  • Methyldopa
  • Phenytoin
  • Penicillin
  • Sulfonamides
• Hypersensitivity/autoimmune
  • Rheumatoid arthritis
  • Rheumatic fever
  • Ulcerative colitis
  • Systemic lupus erythematosus
  • Kawasaki syndrome
  • Dermatomyositis
• Other
  • Sarcoidosis
  • Scleroderma
  • Idiopathic
  • Giant cell
  • Peripartum myocarditis
• More common causes of nonviral myocarditis
  • Chagas disease is caused by a protozoal infestation with Trypanosoma cruzi. It is very uncommon in North America but can affect up to half the population in endemic areas such as South America.
    • Acute infection can cause protracted heart failure and death.
    • Endomyocardial biopsy and microscopic examination typically demonstrate both organisms, neutrophils, lymphocytes, macrophages, and eosinophils.
• • In giant cell myocarditis, giant cells are present in the myocardium with or without granulomas. This type may be evidenced by tuberculosis, syphilis, rheumatoid arthritis, rheumatic heart disease, or with fungal or parasitic infections.
    • The characteristic cell probably is histiocytic in origin and usually is found in nonviral myocarditis.
    • Similar cells have been noted in patients with myocarditis associated with drugs such as phenylbutazone.
    • This type of myocarditis may not be specific but, rather, may represent a final common pathologic pathway.
  • Systemic lupus erythematosus (SLE) may demonstrate myocardial fibrinoid lesions found in the connective tissue with an accompanying cellular reaction. This reaction also may affect the valves, most notably, the mitral and aortic valves. Libman and Sacks describe this latter type of endocarditis.
    • Although the predominant cardiac manifestation of SLE is pericarditis, myocardial involvement with CHF can occur (see Systemic Lupus Erythematosus).
    • The treatment of choice is corticosteroids.
  • Kawasaki disease may reveal myocardial involvement that usually occurs in the acute phase; it can occur independent of any coronary artery involvement and usually resolves completely. However, in some cases, the diffuse myocarditis may be severe and may lead to heart failure and death. Although the pathophysiologic mechanisms that occur in Kawasaki disease are not known, it is suspected that a generalized autoimmune disorder may be involved (see Kawasaki Disease).
  • Dermatomyositis, a multisystem disease (most likely autoimmune), is characterized by diffuse, nonsuppurative inflammation of skeletal muscle and skin. However, cardiac involvement, including a loss of striations, fragmentation, and vascularization of muscle fibers, has been reported. Interstitium may also show a variable amount of edema.
    • Tachycardia and conduction abnormalities are described. Heart failure is uncommon.
    • Long-term therapy with prednisone is beneficial in the majority of cases.
    • Children have good long-term prognosis, as most recover, and medication may be discontinued in 1-2 years.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Imaging Studies

• Echocardiography
• • Echocardiography (ECHO) is critical in diagnosing myocarditis.
  • Typically, the presence of diminished ventricular function with dilation of one or several chambers of the heart becomes obvious.
  • ECHO also rules out pericardial effusion or structural congenital heart disease as the etiology of the symptoms.

Other Tests

• Electrocardiography
• • Sinus tachycardia out of proportion to the degree of fever may be noticeable in patients with myocarditis.
  • Arrhythmias, including ST-T wave changes in up to 80% of patients, may be associated with myocarditis.
  • These changes may be both sensitive indicators of myocardial ischemia as well as nonspecific findings.

Procedures

• Endomyocardial biopsy
• • The role of biopsy in the diagnosis of myocarditis remains controversial.
  • Biopsy may present somewhat of a risk in the acutely ill and unstable patient.
  • Histologic diagnosis may not be easy.
  • Typical sampling usually includes small areas of the right ventricle. Because myocarditis may be focal and may primarily involve the left ventricle, results of the sampling techniques used may not fully represent the true incidence of myocarditis. In other words, a negative biopsy result does not rule out myocarditis.
  • A major problem with endomyocardial biopsy is the possibility of overinterpretation or misinterpretation of the biopsy specimen.
  • Clinicians argue that results of endomyocardial biopsy may not change the treatment. This may be true, at least until a clearer role emerges of what immunosuppression therapy should be used in patients with myocarditis.
  • Little work with pediatric patients has been done in this area.
  • There has certainly been some rationale for immunosuppressive therapy since it appears that the pathophysiology of myocarditis involves the immune system's "reaction" against the myocardium.
• Adult studies have failed to clearly determine the role of immunosuppressive therapy.
• • Some preliminary data suggest certain combinations of these agents may be beneficial in patients with acute myocarditis.
  • There may be some rationale in performing a biopsy to establish a subset of pediatric patients with active myocarditis in order to study different therapies in a controlled, prospective manner.

Histologic Findings

The major purposes of a tissue biopsy are to establish a diagnosis of myocarditis and to classify the stage of disease as acute, healed, or chronic. The specific histologic findings differ based on the particular etiologic agent associated with myocarditis.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Medical therapy for CHF is fairly standard. The general principles of therapy for CHF are also applicable for this group of patients. These general principles include manipulation of preload, afterload, and contractility. Therefore, fluid restriction and diuretics, inotropic support to optimize contractility with continuous intravenous inotropic agents, as well as intravenous vasodilator agents are all important potential interventions for CHF caused by myocarditis of a nonviral origin. Additional general maneuvers to reduce the workload of the heart, thereby improving symptoms of CHF, are outlined below.
  • Inotropes via continuous drip
  • Afterload reducing agents
  • Diuretics
  • Digitalis
  • Beta-blockers
  • Mechanical ventilation
  • Arrhythmia therapy
  • Anticoagulation
  • Metabolic demand reduction
  • Bed rest
• Treatment of the specific causes of the myocarditis (ie, bacterial sepsis, rickettsial disease)
• Therapy to treat or reverse the presumed underlying pathophysiologic process (immunosuppressive therapy)
• Surgical therapy for chronic CHF
• • See Heart Transplantation
  • Left ventricular volume reduction surgery (Battista operation)

Surgical Care

Surgical care for this group of patients is recommended primarily if medical treatment fails and if the patient is symptomatic. Surgical treatment may include cardiac transplantation for patients that develop a chronic, symptomatic dilated cardiomyopathy. An exhaustive discussion of indications and issues related to cardiac transplantation can be found elsewhere in this journal (see Heart Transplantation). Additionally, other surgical therapies for dilated cardiomyopathy, such as left ventricular volume reduction surgery (Battista operation) or latissimus dorsi augmentation wrap, also can be found elsewhere in this journal.

Diet

Advise patients with moderate-to-severe chronic CHF a "no-added-salt" diet is probably beneficial. Otherwise, ensure adequate calories and nutrition for growth.

Activity

During the acute phase of myocarditis, most agree that bed rest should be recommended. Several animal studies have suggested that exercise during the acute viremia can potentiate the disease. However, after recovery and during the healing and/or chronic phases of myocarditis, it is believed that activity as tolerated is acceptable.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical therapy for CHF includes the use of inotropic agents, afterload reducing agents, diuretics, beta-blockers, and anticoagulants. Antiarrhythmic agents may also be required if secondary rhythm disturbances erupt. For more details on these maneuvers, see Congestive Heart Failure.

Drug Category: Inotropic agents

These agents are used to increase cardiac contractility. Positive inotropic agents increase the force of contraction of the myocardium and are used to treat acute and chronic CHF. Some may also increase or decrease the heart rate (ie, positive or negative chronotropic agents), provide vasodilatation, or improve myocardial relaxation. These additional properties influence the choice of drug for specific circumstances.

Drug Name	Dobutamine (Dobutrex)
Description	Produces vasodilation (decreasing afterload) and increases inotropic state; at higher dosages, may cause increased heart rate, exacerbating myocardial ischemia.
Adult Dose	5-10 mcg/kg/min IV
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis and atrial fibrillation or flutter
Interactions	Beta-adrenergic blockers antagonize effects of dobutamine; general anesthetics may increase toxicity
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Following MI, use with extreme caution; hypovolemic state should be corrected before using this drug

Drug Name	Epinephrine (Adrenaline)
Description	Has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
Adult Dose	0.1 mcg/kg/min IV; titrate to desired effect
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; cardiac arrhythmias or angle-closure glaucoma; do not use during labor (may delay second stage of labor)
Interactions	Increases toxicity of beta- and alpha-blocking agents, and that of halogenated inhalational anesthetics
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in elderly patients, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias

Drug Name	Milrinone (Primacor)
Description	Bipyridine-positive inotrope and vasodilator (afterload reducer) with little chronotropic activity. Different in mode of action from both digitalis glycosides and catecholamines.
Adult Dose	25-50 mcg/kg IV loading dose infused over 10 min followed by continuous IV infusion at 0.5-1 mcg/kg/min
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Precipitates in presence of furosemide
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Monitor fluids, electrolyte changes, and renal function during therapy; excessive diuresis may increase potassium loss and predispose digitalized patients to arrhythmias; important to correct hypokalemia with potassium supplementation prior to treatment; patients showing excessive decreases in BP should have infusion rates slowed or stopped; previous vigorous diuretic therapy has caused significant decreases in cardiac filling pressure, cautiously administer milrinone and monitor blood pressure, heart rate, and clinical symptomatology

Drug Name	Digoxin (Lanoxin, Lanoxicaps)
Description	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.
Adult Dose	0.125-0.375 mg PO qd
Pediatric Dose	Total digitalizing dose (TDD): Note: Administer TDD within 24 h Premature infants: 20 mcg/kg PO divided q8h Full-term infants: 30 mcg/kg PO divided q8h 1-24 months: 40-50 mcg/kg PO divided q8h >2 years: 30-40 mcg/kg PO divided q8h Maintenance dose: Infants: 6-8 mcg/kg/d PO 2-5 years: 10-15 mcg/kg/d PO 5-10 years: 7 to 10 mcg/kg/d PO >10 years: 3-5 mcg/kg/d PO <10 years: Administer daily dose divided bid
Contraindications	Documented hypersensitivity; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome
Interactions	Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil; medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Hypokalemia may reduce positive inotropic effect; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent toxicity; patients diagnosed with incomplete AV block may progress to complete block; caution in hypothyroidism, hypoxia, and acute myocarditis

Drug Category: Diuretics

These agents promote excretion of water and electrolytes by the kidneys. They are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention has resulted in edema or ascites. These agents cause preload reduction through diuresis.

Drug Category: Afterload-reducing agents

These agents reduce systemic vascular resistance and increase systemic blood flow resulting from CHF. They cause vasodilation resulting in afterload reduction.

Drug Name	Captopril (Capoten)
Description	Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. Useful in chronic CHF and in transition to oral agents from IV agents. The dosage range is wide and can be titrated to effect.
Adult Dose	6.25-12.5 mg PO tid; not to exceed 150 mg tid
Pediatric Dose	0.1-0.5 mg/kg/dose PO tid
Contraindications	Documented hypersensitivity; renal impairment
Interactions	NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases; probenecid may increase captopril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Pregnancy category D in second and third trimester; caution in renal impairment, valvular stenosis, or severe CHF; adverse effects include headache and cough

Drug Category: Anticoagulants

These agents are used to prevent recurrent or ongoing thromboembolic occlusion. They are recommended in patients with severe left ventricular dysfunction and/or in the patient with documented left heart thrombus.

Drug Name	Enoxaparin (Lovenox)
Description	Low molecular weight derivative of heparin. Used to prevent deep venous thrombosis (DVT), which may lead to pulmonary embolism in patients undergoing surgery who are at risk for thromboembolic complications. Enhances inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, preferentially increases inhibition of factor Xa.
Adult Dose	30 mg SC q12h
Pediatric Dose	<2 months: Prophylaxis: 0.75 mg/kg SC q12h Treatment: 1.5 mg/kg SC q12h >2 months: Prophylaxis: 0.5 mg/kg SC q12h Treatment: 1 mg/kg SC q12h
Contraindications	Documented hypersensitivity; subacute bacterial endocarditis, active bleeding, history of heparin-induced thrombocytopenia
Interactions	Dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine may increase risk of bleeding
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Elevation of hepatic transaminases may occur but is reversible; heparin-associated thrombocytopenia may occur with fractionated low-molecular-weight heparins; 1 mg of protamine sulfate reverses effect of approximately 1 mg of enoxaparin if significant bleeding complications develop

Drug Name	Aspirin (Bayer, Excedrin)
Description	Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2. In the absence of thrombus in the heart, and with moderate left ventricular dysfunction, aspirin may be indicated at an antiplatelet dosage.
Adult Dose	1-5 mg/kg/d PO
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; due to association of aspirin with Reye syndrome, do not use in children ( <16 y) with flu
Interactions	Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose lowering effect of sulfonylurea drugs
Pregnancy	D - Unsafe in pregnancy
Precautions	May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Need for and length of inpatient care varies with severity of the illness.
• Prolonged supportive therapy may be required until the patient can resume spontaneous ventilation and be adequately maintained on oral anticongestive therapy.

Further Outpatient Care

• Patients require close outpatient follow-up care, especially if significant residual CHF is present.
• Some patients may continue to have symptoms of moderate-to-severe CHF that may require eventual cardiac transplantation.

Prognosis

• Prognosis is variable and again depends on age, etiology, and severity at the time of presentation.
• Mortality rate in newborn infants is high (75%) in some reports.
• Older infants and children have a better prognosis, with mortality rates ranging from 10-25% in clinically recognizable cases.
• Some studies have suggested complete recovery in up to 50% of the cases.
• Perhaps as many as 25-35% of patients who present with clinical myocarditis may be left with a significant chronic dilated cardiomyopathy and may require cardiac transplantation.
• Cause of myocarditis certainly may affect prognosis. For example, patients with conduction abnormalities or arrhythmias secondary to diphtheric myocarditis tend to have a poor prognosis.
• Long-term prognosis in children is good since most recover, and medications can be discontinued in 1-2 years.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Medical/legal pitfalls primarily are related to determining the specific etiology of nonviral myocarditis, especially if it is a rare treatable cause of CHF. Since the specific etiology often is never determined or is untreatable other than with supportive care, there seems to be no specific common medical/legal issues.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Anderson R, Maccartney F, Shinebourne E, eds. Paediatric Cardiology. 1987:1165-1171.
• Billingham M. Acute myocarditis: a diagnostic dilemma. Br Heart J. Jul 1987;58(1):6-8. [Medline].
• Emmanoulides G, Allen H, Riemenschneider T. In: Moss, Adams, eds. Heart Disease in Infants, Children and Adolescents. 1995:1381-1390.
• Frustaci A, Pieroni M, Chimenti C. Immunosuppressive treatment of chronic non-viral myocarditis. Ernst Schering Res Found Workshop. 2006;343-51. [Medline].
• Garson A, Bricker T, McNamara D. The Science and Practice of Pediatric Cardiology. 1990:1577-1589.
• Hejtamanick R. The cardiovascular manifestations of SLE. Am Heart J. 1964;68:119-130.
• Libman E, Sacks B. A hitherto undescribed form of valvular and mural endocarditis. Archives of Internal Medicine. 1974;33:701-737.
• Maisch B, Lamparter S, Ristic A, Pankuweit S. [Pregnancy and cardiomyopathies]. Herz. May 2003;28(3):196-208. [Medline].
• Sugrue DD, Holmes DR Jr, Gersh BJ, et al. Cardiac histologic findings in patients with life-threatening ventricular arrhythmias of unknown origin. J Am Coll Cardiol. Nov 1984;4(5):952-7. [Medline].

Article Last Updated: Jun 15, 2006