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Pediatric Viral Myocarditis Medication

  • Author: Edwin Rodriguez-Cruz, MD; Chief Editor: Howard S Weber, MD, FSCAI  more...
 
Updated: Aug 26, 2015
 

Medication Summary

If congestive heart failure is present in a patient with viral myocarditis, 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 (see the Cardiac Output calculator). 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 angiotensin-converting enzyme (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 subjects were treated with immunosuppressive agents. Small series in humans have shown that the condition of patients improves when the patients are treated with these agents.

In a randomized study of 111 patients, the Multicenter Myocarditis Treatment Trial found that left ventricular function and survival did not significantly differ between patients given any of the following 3 treatment modalities[17] :

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

Intravenous gamma globulin may be important in the treatment of acute myocarditis.[18, 19] 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 shown 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 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.

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Cardiac glycosides

Class Summary

These agents may improve left ventricular function by increasing myocardial contraction through inhibition of 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)

 

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

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Diuretics

Class Summary

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

Chlorothiazide (Diuril)

 

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

Spironolactone (Aldactone)

 

Spironolactone is a potassium-sparing diuretic. It acts on the distal convoluted tubule of the kidney as an aldosterone antagonist.

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Angiotensin-converting enzyme (ACE) inhibitors

Class Summary

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 the production of angiotensin II, a potent vasoconstrictor. High levels of angiotensin II have also been associated with cellular damage in patients with myocarditis.

Captopril

 

Captopril reduces afterload and myocyte necrosis. It is beneficial in all stages of chronic heart failure. The drug's pharmacologic effects result in a decrease in systemic vascular resistance, reducing blood pressure, preload, and afterload. Dyspnea and exercise tolerance are improved.

Enalapril (Vasotec)

 

A competitive ACE inhibitor, enalapril reduces angiotensin II levels, decreasing aldosterone secretion. The drug lowers systemic arterial blood pressure, reducing injury caused by elevated blood pressure. It may slow the progression of renal failure by lowering intraglomerular pressure or other intrarenal mechanisms. Enalapril may be used every day or twice per day, which may improve compliance in comparison with a 3-time-per-day medication, such as captopril.

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Adrenergic agonist agents (inotropic agents)

Class Summary

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

Dopamine

 

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).

Dobutamine

 

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

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Cyclic adenosine monophosphate (c-AMP) phosphodiesterase inhibitors

Class Summary

Inotropic effects occur through the inhibition of cyclic adenosine monophosphate (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

 

Inamrinone produces vasodilation and increases the inotropic state. This agent is more likely to cause tachycardia than dobutamine is, and it may exacerbate myocardial ischemia.

Milrinone

 

Milrinone is a bipyridine with positive inotropic and vasodilator effects and little chronotropic activity. Milrinone is different in mode of action from digitalis glycosides and catecholamines.

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Immunomodulatory agents

Class Summary

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

Immunoglobulin (Carimune, Gammagard SD, Octagam, Gamunex, Privigen)

 

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

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Contributor Information and Disclosures
Author

Edwin Rodriguez-Cruz, MD Director, Section of Cardiology, Department of Pediatrics, San Jorge Children’s Hospital, Puerto Rico; Private Practice in Interventional Pediatric Cardiology and Internal Medicine, Centro Pedíatrico y Cardiovascular

Edwin Rodriguez-Cruz, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Echocardiography, Society for Cardiovascular Angiography and Interventions, Society of Pediatric Echocardiography, American College of Physicians-American Society of Internal Medicine, American Medical Association, Puerto Rico Medical Association

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: St Jude's Medical Co.<br/>Received grant/research funds from NOVARTIS for investigator; Received consulting fee from St. Jude Medical Corp. for speaking and teaching.

Coauthor(s)

Robert D Ross, MD Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Division of Pediatric Cardiology, Children's Hospital of Michigan; Professor of Pediatrics, Wayne State University School of Medicine

Robert D Ross, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Society of Pediatric Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Howard S Weber, MD, FSCAI Professor of Pediatrics, Section of Pediatric Cardiology, Pennsylvania State University College of Medicine; Director of Interventional Pediatric Cardiology, Penn State Hershey Children's Hospital

Howard S Weber, MD, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Received income in an amount equal to or greater than $250 from: St. Jude Medical.

Acknowledgements

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.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Hypersensitivity myocarditis. High magnification of myocardium with perivascular infiltrates rich in eosinophils. This patient had a clinical history compatible with drug-induced hypersensitivity myocarditis.
 
 
 
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