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Pediatric Nonviral Myocarditis Medication

  • Author: Stuart Berger, MD; Chief Editor: P Syamasundar Rao, MD  more...
 
Updated: Mar 30, 2015
 

Medication Summary

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. Drugs used in the treatment of patients with myocarditis include the following:

  • Dopamine
  • Epinephrine
  • Milrinone
  • Digoxin
  • Furosemide
  • Nitroprusside
  • Captopril
  • Warfarin
  • Enoxaparin
  • Aspirin
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Inotropic agents

Class Summary

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.

Dopamine

 

Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation are produced by higher doses. After initiating therapy, increase the dose by 1-4 mcg/kg/min every 10-30 minutes until the optimal response is obtained. More than 50% of patients are satisfactorily maintained on doses of less than 20 mcg/kg/min.

Epinephrine (Adrenalin)

 

Epinephrine 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.

Milrinone

 

Digoxin (Lanoxin)

 

Digoxin is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It directly acts 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

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 have resulted in edema or ascites. These agents cause preload reduction through diuresis.

Furosemide (Lasix)

 

Furosemide is the mainstay of diuresis (reducing preload) in acute CHF. It increases the excretion of water by interfering with the chloride-binding cotransport system, resulting in the inhibition of sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.

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Afterload-reducing agents

Class Summary

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

Nitroprusside (Nitropress)

 

Nitroprusside is a potent vasodilating agent and increases inotropic activity of the heart. At higher dosages, it may exacerbate myocardial ischemia by increasing the heart rate.

Captopril

 

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.

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Anticoagulants

Class Summary

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

Warfarin (Coumadin)

 

Warfarin interferes with hepatic synthesis of vitamin K–dependent coagulation factors. It is used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain an international normalized ratio (INR) in the range of 2-2.5.

Enoxaparin (Lovenox)

 

Enoxaparin is a low ̶ molecular-weight derivative of heparin. It is used to prevent deep venous thrombosis (DVT), which may lead to pulmonary embolism in patients undergoing surgery who are at risk for thromboembolic complications. Enoxaparin enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, it preferentially increases the inhibition of factor Xa.

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Antiplatelet Agents

Class Summary

Probable mechanisms that underlie the therapeutic benefits of aspirin include inhibition of platelet aggregation.

Aspirin (Bayer Aspirin, Ecotrin, Aspirtab, Aspercin, Bufferin )

 

Aspirin inhibits prostaglandin synthesis, which prevents the 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.

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Contributor Information and Disclosures
Author

Stuart Berger, MD Medical Director of The Heart Center, Children's Hospital of Wisconsin; Associate Professor, Department of Pediatrics, Section of Pediatric Cardiology, Medical College 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, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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.

Chief Editor

P Syamasundar Rao, MD Professor of Pediatrics and Medicine, Division of Cardiology, Emeritus Chief of Pediatric Cardiology, University of Texas Medical School at Houston and Children's Memorial Hermann Hospital

P Syamasundar Rao, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, American College of Cardiology, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

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 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, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, Texas Pediatric Society, Cardiac Electrophysiology Society

Disclosure: Nothing to disclose.

References
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  2. Shamna RB, Lalitha AV, Lini B. Myocarditis in Children. Indian J Pediatr. 2013 Sep 26. [Medline].

  3. Libman E, Sacks B. A hitherto undescribed form of valvular and mural endocarditis. Arch Intern Med. 1974. 33:701-37.

  4. Klugman D, Berger JT, Sable CA, et al. Pediatric patients hospitalized with myocarditis: a multi-institutional analysis. Pediatr Cardiol. 2010 Feb. 31(2):222-8. [Medline].

  5. Sachdeva S, Song X, Dham N, Heath DM, DeBiasi RL. Analysis of clinical parameters and cardiac magnetic resonance imaging as predictors of outcome in pediatric myocarditis. Am J Cardiol. 2015 Feb 15. 115(4):499-504. [Medline].

  6. Crossman DJ, Ruygrok PN, Hou YF, Soeller C. Next-generation endomyocardial biopsy: the potential of confocal and super-resolution microscopy. Heart Fail Rev. 2015 Mar. 20(2):203-14. [Medline].

  7. [Guideline] Heart Failure Society Of America. Myocarditis: Current treatment. J Card Fail. 2006 Feb. 12(1):e120-2. [Medline].

  8. Frustaci A, Pieroni M, Chimenti C. Immunosuppressive treatment of chronic non-viral myocarditis. Ernst Schering Res Found Workshop. 2006. 343-51. [Medline].

  9. Miller JR, Lancaster TS, Eghtesady P. Current approaches to device implantation in pediatric and congenital heart disease patients. Expert Rev Cardiovasc Ther. 2015 Apr. 13(4):417-27. [Medline].

 
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Myocarditis with scarring, autopsy. The image is a short axis gross photograph of an 8-year-old child with clinical myocarditis showing scarring of both ventricles, more prominent in the left. The fibrosis shows a random distribution with epicardial, myocardium, and pericardial involvements.
 
 
 
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