eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Myocarditis, Viral: Treatment & Medication

Author: Edwin Rodriguez-Cruz, MD, Assistant Professor, Department of Pediatrics, San Juan Bautista Medical School and Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Prediatrics, Hospital El Maestro and San Juan Bautista Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Cardiology, Cardiovascular Center of Puerto Rico and the Caribbean and Veterans Affairs Hospital and Medical Center of Puerto Rico
Coauthor(s): Robert D Ross, MD, Co-Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Division of Pediatric Cardiology, Professor, Children's Hospital of Michigan and Wayne State University
Contributor Information and Disclosures

Updated: Oct 9, 2008

Treatment

Medical Care

In the acute phase, the patient should be admitted to the hospital, even if only mild signs of respiratory distress or congestive heart failure are present. Rapid progression to overt heart failure, hemodynamic collapse, or both may occur.

Medical care is aimed at minimizing hemodynamic demands of the body. No specific proven therapy is available to prevent the myocardial damage, but maintenance of tissue perfusion is the goal to avoid further complications. Normal arterial blood oxygen levels should be maintained with supplemental oxygen as needed.

Surgical Care

Extracorporeal membrane oxygenation (ECMO) has been used as an interim treatment to provide rest to the heart and as a bridge for transplant in selected patients with good results.

Consultations

Consultation with a cardiologist is indicated.

Diet

A low-salt diet is recommended for patients with congestive heart failure.

Activity

Bed rest is necessary during the acute phase of the illness and may slow the intramyocardial replication of the virus. Activity is permitted as partial or complete recovery is achieved.

Medication

If congestive heart failure is present, digitalis may be useful in maintaining adequate function. Diuretics can be given concomitantly to remove excess extracellular fluid and to decrease preload. Caution should be exercised because removal of fluid may cause low cardiac output and shock. A higher venous-filling pressure may be necessary to maintain an adequate cardiac output. Intracardiac pressure monitoring can facilitate maintenance of adequate filling pressures.

Inotropic agents are used when cardiac output cannot be maintained by less invasive measures. Dopamine, dobutamine, inamrinone (formerly amrinone), and milrinone are the most commonly used vasopressors.

Afterload reduction is most important in treating acute myocarditis and is used when hypotension is not present. This decreases the workload for the compromised myocardium and can allow patients to recover from the acute phase of illness. Agents that reduce afterload improve cardiac output by decreasing systemic arterial resistance. Intravenous medications such as nitroprusside, inamrinone, and milrinone can be replaced with oral ACE inhibitors when the patient stabilizes.

The use of immunosuppressive agents for the treatment of viral myocarditis is still controversial. Some animal studies revealed an exacerbation of viral cytotoxicity when treated with immunosuppressive agents. Other small series in humans have shown that the conditions of patients improve when the patients are treated with these agents. The Multicenter Myocarditis Treatment Trial aimed to establish differences in outcome among 3 treatment modalities.8 A total of 111 patients were randomized into one of the 3 following groups:

  • Prednisone/azathioprine
  • Prednisone/cyclosporine
  • Conventional therapy without immunosuppression

Findings revealed left ventricular function and survival were not significantly different among the 3 groups.

Intravenous gamma globulin may be important in the treatment of acute myocarditis.9,10 It has been associated with improved left ventricular function and improved survival.

New therapeutic agents are being studied as candidates for the treatment of myocarditis. These include agents that inhibit the virus entrance to the cells; antiviral agents that inhibit translation, transcription, or both; and interferon, among others. However, these strategies are still in early stages and, although they have promising results, some time may go by before they are widely accepted. Pleconaril, an investigational agent that inhibits viral attachment to host cell receptors, has a broad antienteroviral activity and, in clinical trials, has demonstrated benefit in children with enteroviral meningitis. This medicine is being tested in children with myocarditis. Pleconaril is currently an investigational drug from Schering-Plough Corporation.

Conventional management includes digoxin, diuretics, and afterload reduction. Severe cases with hemodynamic compromise may require intravenous inotropic agents, afterload reduction, vasodilators, and anticoagulation.

Cardiac glycosides

These agents may improve left ventricular function by increasing myocardial contraction by inhibiting the sodium/potassium adenosine triphosphatase (ATPase) pump. This leads to sodium accumulation within the myocyte, which stimulates the sodium-calcium exchange. The increased intracellular calcium increases the force of contraction.


Digoxin (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.

Adult

Total digitalizing dose (TDD): 0.75-1.5 mg PO; 0.5-1 mg IV/IM
Divide TDD: Initially give 50% of TDD, and then give the remaining two 25% portions at 6- to 12-h intervals (1/2, 1/4, 1/4)
Maintenance dose: 0.125-0.5 mg PO; 0.1-0.4 mg IV/IM
Individualize dose based on levels

Pediatric

TDD PO:
Preterm infant: 20-30 mcg/kg
Term infant: 25-35 mcg/kg
1 month to 2 years: 35-60 mcg/kg
2-5 years: 30-40 mcg/kg
5-10 years: 20-35 mcg/kg
>10 years: 10-15 mcg/kg
TDD IV/IM:
Preterm infant: 15-25 mcg/kg
Term infant: 20-30 mcg/kg
1 month to 2 years: 30-50 mcg/kg
2-5 years: 25-35 mcg/kg
5-10 years: 15-30 mcg/kg
>10 years: 8-12 mcg/kg
Divide TDD: Initially give 50% of TDD, and then give the remaining two 25% portions at 6- to 12-h intervals (1/2, 1/4, 1/4)
Maintenance dose PO:
Preterm infant: 5-7.5 mcg/kg divided bid
Term infant: 6-10 mcg/kg divided bid
1 month to 2 years: 10-15 mcg/kg divided bid
2-5 years: 7.5-10 mcg/kg divided bid
5-10 years: 5-10 mcg/kg divided bid
>10 years: 2.5-5 mcg/kg qd
Maintenance dose IV/IM:
Preterm infant: 4-6 mcg/kg divided bid
Term infant: 5-8 mcg/kg divided bid
1 month to 2 years: 7.5-12 mcg/kg divided bid
2-5 years: 6-9 mcg/kg divided bid
5-10 years: 4-8 mcg/kg divided bid
>10 years: 2-3 mcg/kg qd

Neomycin and phenytoin decrease the effects/levels of digoxin; drugs that increase the effects/toxicity/levels of digoxin include amphotericin B, erythromycin, cyclosporin, verapamil, calcium preparations, and itraconazole

Documented hypersensitivity; constrictive pericarditis; outflow tract obstruction; idiopathic hypertrophic subaortic stenosis

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

During periods of inflammation, myocardium may be sensitive to digitalis; TDD may need to be lowered based on drug concentrations obtained; adjust dose for patients with decreased renal function; dosing must be individualized and titrated; serum levels should be followed; this drug is arrhythmogenic and interacts with several drugs used commonly to treat arrhythmias; patients with hypokalemia, hypomagnesemia, hypercalcemia, and hypermagnesemia are predisposed to digoxin toxicity; CNS effects, such as drowsiness, and GI effects, such as nausea and vomiting, are some of the more common adverse drug reactions

Diuretics

Hypoperfusion of the kidneys causes retention of sodium and water, which produces peripheral and pulmonary edema. Diuretics decrease the intravascular volume overload.


Furosemide (Lasix)

This loop diuretic is the diuretic of choice in pediatric patients. 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.

Adult

20-80 mg/d PO/IV/IM divided q6-12h

Pediatric

0.5-2 mg/kg/dose PO/IV/IM up to tid

Pay special attention if given with aminoglycosides, cephalosporins, lithium, salicylates, ethacrynic acid, or indomethacin as concomitant administration with these medications may produce or worsen renal insufficiency; ototoxicity may be increased with concomitant administration of aminoglycosides

Documented hypersensitivity; hypokalemia; renal failure

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

Potent diuretic that may cause profound diuresis and electrolyte loss; metabolic alkalosis is a common complication; should not be given in the same intravenous line with inamrinone since it may cause precipitation of the compounds; may cause renal stones, especially in premature newborns; concomitant administration of chlorothiazide may decrease the hypercalciuria; administer PO dose with food or milk to decrease stomach upset


Chlorothiazide (Diuril)

This is a thiazide diuretic. If given with furosemide, it may decrease hypercalciuria. Inhibits sodium reabsorption at the distal tubule in the kidney.

Adult

500 mg to 2 g/d PO qd or divided bid
100-500 mg/d IV qd or divided bid

Pediatric

<6 months: 20-40 mg/kg/d PO divided bid; 2-8 mg/kg/d IV divided bid
>6 months: 20 mg/kg/d PO divided bid; 4 mg/kg/d IV divided bid

Thiazide diuretics may decrease the effectiveness of anticoagulants, antigout agents, and sulfonylureas; effectiveness may be decreased by bile acid sequestrants, methenamine, and NSAIDs; thiazide diuretics may increase the toxicity of allopurinol, anesthetics, antineoplastics, calcium salts, diazoxide, digitalis, lithium, loop diuretics, methyldopa, muscle relaxants, and vitamin D; amphotericin B and anticholinergics may increase the toxicity of thiazide diuretics.

Documented hypersensitivity; anuria

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Safety of IV use in children has not been established; this drug can produce electrolyte imbalance; not to be given SC or IM


Spironolactone (Aldactone)

Potassium-sparing diuretic. Acts on the distal convoluted tubule of the kidney as an aldosterone antagonist.

Adult

100-200 mg/d PO qd or divided bid

Pediatric

2-3 mg/kg/d PO divided bid/tid

ACE inhibitors, cyclosporine, or potassium supplements increase risk of hyperkalemia; may increase the risk of digoxin toxicity; avoid salt substitutes or natural licorice

Documented hypersensitivity; hyperkalemia; hyponatremia; severe renal impairment; Addison disease

Pregnancy

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

Precautions

May cause electrolyte imbalance, especially hyperkalemia; concomitant use with indomethacin or ACE inhibitors may cause hyperkalemia; main adverse effects are GI upset, hyponatremia, hyperkalemia, hepatotoxicity, lethargy, confusion, impotence and gynecomastia; spironolactone is carcinogenic in rodents

Angiotensin-converting enzyme (ACE) inhibitors

Cardiac output and systemic resistance determine blood pressure. When systemic resistance is decreased with afterload reduction, myocardial shortening and stroke volume improve. Therefore, cardiac output can be maintained at a lower heart rate with lower myocardial oxygen demand. ACE inhibitors decrease production of angiotensin II, a potent vasoconstrictor. High levels of angiotensin II have also been associated with cellular damage in patients with myocarditis.


Captopril (Capoten)

Reduces afterload and myocyte necrosis. Beneficial in all stages of chronic heart failure. Pharmacologic effects result in a decrease in systemic vascular resistance, reducing blood pressure, preload, and afterload. Dyspnea and exercise tolerance are improved.

Adult

12.5-25 mg PO q8-12h; increase dose by 25 mg prn; not to exceed 450 mg/d divided tid

Pediatric

<6 months: 0.05-0.5 mg/kg/dose PO up to tid
>6 months: 0.5-2 mg/kg/dose PO up to tid
Test dose: 0.1 mg/kg/dose

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

Documented hypersensitivity; pregnancy; unilateral renal artery stenosis is a relative contraindication

Pregnancy

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

Precautions

Titrate to patient's tolerance and to effectiveness; decrease dose in renally impaired or volume depleted patients; may cause idiosyncratic hypotension after the first dose in children; test dose should be given and blood pressure monitored frequently after administration

Adrenergic agonist agents (inotropic agents)

Dopamine is a precursor to epinephrine, thus augmenting endogenous release of catecholamines. It also stimulates specific dopamine receptors. Dobutamine does not promote release of endogenous epinephrine. Dobutamine predominantly augments myocardial contractility via beta1 stimulation.


Dopamine (Intropin)

At lower doses, this drug stimulates beta1-adrenergic and dopaminergic receptors (renal vasodilation, positive inotropism); at higher doses, it stimulates alpha-adrenergic receptors (renal vasoconstriction).

Adult

2-20 mcg/kg/min continuous IV infusion

Pediatric

Administer as in adults

Effects are prolonged and intensified by MAOIs, alpha-blockers and beta-blockers, general anesthetics, and phenytoin

Documented hypersensitivity; outflow tract obstructions, such as subaortic stenosis

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

Hypovolemia should be treated before infusion of this drug; extravasation should be treated promptly with SC administration of phentolamine (Regitine); administration through a central vein is recommended; do not use umbilical artery for infusion; if dosages >20 mcg/kg/min are required, a different agent should be considered (eg, epinephrine, dobutamine)


Dobutamine (Dobutrex)

Stimulates beta1-adrenergic receptors. It has less alpha1 stimulation than dopamine; therefore, it produces less increase in systemic vascular resistance.

Adult

2-15 mcg/kg/min continuous IV infusion

Pediatric

Administer as in adults

Beta-adrenergic blockers antagonize effects of dobutamine; general anesthetics may increase toxicity

Documented hypersensitivity; subaortic stenosis

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Treat hypovolemia before infusion; treat extravasation promptly with SC administration of phentolamine (Regitine); administration through a central vein is recommended; do not use umbilical artery for infusion; may decrease central venous pressure (CVP) and wedge pressure

Cyclic adenosine monophosphate (c-AMP) phosphodiesterase inhibitors

Inotropic effects occur by inhibiting c-AMP phosphodiesterase, which increases the cellular levels of c-AMP. The sodium-potassium pump is not affected, as with digitalis. Vasodilatory activity is related to the direct relaxation effect on vascular smooth muscle.


Inamrinone - formerly amrinone (Inocor)

Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine; may exacerbate myocardial ischemia.

Adult

Loading dose: 0.75 mg/kg (undiluted) IV over 2-3 min
Maintenance dose: 5-10 mcg/kg/min IV; titrate to effect

Pediatric

Administer as in adults

Furosemide should not be given in the same IV line as inamrinone because it may cause precipitation of the compounds; do not dilute in solutions containing glucose
Coadministration with diuretics, may result in hypovolemia and decrease in filling pressure; cardiac glycosides have additive effects on amrinone

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

Like other inotropic agents, this drug may aggravate outflow tract obstructions; inamrinone should be monitored for hypotension, thrombocytopenia, and hepatotoxicity; GI symptoms, including nausea, vomiting, abdominal pain, and anorexia, are some of the more common adverse drug reactions


Milrinone (Primacor)

Bipyridine positive inotropic effect and vasodilator with little chronotropic activity. Different in mode of action from both digitalis glycosides and catecholamines.

Adult

Loading dose: 50 mcg/kg (undiluted) IV over 10-15 min
Maintenance dose: 0.375-0.75 mcg/kg/min IV; titrate to effect

Pediatric

Administer as in adults

Milrinone precipitates in presence of furosemide

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

Like any other inotropic agent, this drug may aggravate outflow tract obstructions; use with caution in patients with a history of ventricular arrhythmias, atrial flutter, or atrial fibrillation; ventricular arrhythmias, supraventricular arrhythmias, hypotension, and headaches are some of the more common adverse drug reactions

Immunomodulatory agents

Immune globulin is a purified preparation of gamma globulin. It is derived from large pools of human plasma and is comprised of 4 subclasses of antibodies, approximating the distribution of human serum.


Immune globulin (Carimune, Gammagard SD, Gammar-P, Gamunex, Polygam S/D)

Use of these agents in myocarditis is not widely accepted. Clinical studies have shown IVIG may improve left ventricular function and survival in children.

Adult

2 g/kg IV as a single dose

Pediatric

Administer as in adults

May interfere with immune response to live virus vaccine (MMR) and reduce efficacy (do not administer within 3 mo of vaccine)

Documented hypersensitivity; IgA deficiency

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

These agents may cause anaphylactic reactions, especially in IgA-deficient patients (procure low IgA product); flushing of the face, chills, nausea, dyspnea, and tachycardia, are the most common adverse effects seen with IVIG administration; other less common adverse effects include chest tightness, dizziness, fever, headache, and diaphoresis; initial infusion rate, maximum infusion rate, maximum concentration, and contraindications are based on the specific IVIG product; consult package insert

More on Myocarditis, Viral

Overview: Myocarditis, Viral
Differential Diagnoses & Workup: Myocarditis, Viral
Treatment & Medication: Myocarditis, Viral
Follow-up: Myocarditis, Viral
References
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Further Reading

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Keywords

viral myocarditis, myocardium, adenovirus, enterovirus, coxsackievirus, active myocarditis, borderline myocarditis, drug hypersensitivity, Starling law, congestive heart failure, cardiac failure, chronic myocarditis, dilated cardiomyopathy, arrhythmia, pericarditis, heart murmur, atrioventricular valve regurgitation, hepatomegaly, sepsis, somnolence, seizures, oliguria, failure to thrive, diaphoresis, end organ damage, chest pain, cytomegalovirus, Epstein-Barr virus, hepatitis C, herpes, HIV, human immunodeficiency virus, influenza, measles, mumps, parvovirus B19, poliomyelitis virus, rubella, varicella

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Contributor Information and Disclosures

Author

Edwin Rodriguez-Cruz, MD, Assistant Professor, Department of Pediatrics, San Juan Bautista Medical School and Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Prediatrics, Hospital El Maestro and San Juan Bautista Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Cardiology, Cardiovascular Center of Puerto Rico and the Caribbean and Veterans Affairs Hospital and Medical Center of Puerto Rico
Edwin Rodriguez-Cruz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, American Society of Echocardiography, Puerto Rico Medical Association, Society of Cardiac Angiography and Interventions, and Society of Pediatric Echocardiography
Disclosure: Nothing to disclose.

Coauthor(s)

Robert D Ross, MD, Co-Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Division of Pediatric Cardiology, Professor, Children's Hospital of Michigan and Wayne State University
Robert D Ross, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, and Society of Pediatric Echocardiography
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA, Professor, Departments of Pediatrics (Cardiology), Cardiovascular Sciences, and Molecular and Human Genetics, Baylor College of Medicine; Chief of Pediatric Cardiology, Foundation Chair in Pediatric Cardiac Research, Texas Children's Hospital
Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Cardiology, American College of Sports Medicine, American Heart Association, American Medical Association, American Society of Human Genetics, Cardiac Electrophysiology Society, Heart Rhythm Society, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, and Texas Pediatric Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Ameeta Martin, MD, Clinical Associate Professor, Department of Pediatric Cardiology, University of Nebraska College of Medicine
Ameeta Martin, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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