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Myocarditis Treatment & Management

  • Author: Wai Hong Wilson Tang, MD; Chief Editor: Henry H Ooi, MD, MRCPI  more...
Updated: Sep 05, 2014

Approach Considerations

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, including with slow rehabilitation and the implementation of evidence-based medical therapy. Repeat assessment with echocardiography may be helpful to determine the persistence of cardiac dysfunction.

Overall, neurohormonal agents are given in a similar manner as in patients presenting with new-onset heart failure. Serial assessment is needed to determine the potential resolution of acute myocarditis, and during the early recovery period, strenuous exercise and digoxin should be avoided. Data regarding the risks of relapse with drug withdrawal following recovery are not available, so it is generally not recommended in practice.


Transfer to a tertiary care center with heart failure/transplant expertise may be warranted in fulminant cases in which surgical support may be necessary.

Deterrence and prevention

Vaccination should reduce the incidence of myocarditis caused by measles, rubella, mumps, poliomyelitis, and influenza. The development of vaccines for other cardiotropic viruses may prevent viral myocarditis in the future.

Diet and activity

Patients should consume a low-sodium diet similar to that for heart failure management. Bedrest and avoidance of athletic activities are recommended from anecdotal experiences (with lower incidence of arrhythmia).


Consultations may be indicated for the following:

  • Cardiothoracic surgery
  • Infectious disease and/or rheumatology consultations

Emergency Department Care

Standard treatment of clinically significant disease includes the detection of dysrhythmia with cardiac monitoring, the administration of supplemental oxygen, and the management of fluid status.

Left ventricular dysfunction developing from myocarditis should be approached in much the same manner as other causes of congestive heart failure (CHF), with some exceptions. In general, sympathomimetic drugs should be avoided, because they increase the extent of myocardial necrosis and mortality.[28] Beta blockers should be avoided in the acutely decompensating phase of illness.

Patients who present with Mobitz II or complete heart block require temporary pacemaker placement. Very few patients require permanent pacer or automatic implantable cardioverter-defibrillator (AICD) placement.


Pharmacologic Therapy

Treatment of myocarditis includes supportive therapy for symptoms of acute heart failure with use of diuretics, nitroglycerin/nitroprusside, and angiotensin-converting enzyme (ACE) inhibitors. Inotropic drugs (eg, dobutamine, milrinone) may be necessary for severe decompensation, although they are highly arrhythmogenic. Long-term treatment follows the same medical regimen, including ACE inhibitors, beta blockers, and aldosterone receptor antagonists. However, in some instances, some of these drugs cannot be implemented initially because of hemodynamic instability.

Withdrawal of the offending agent is called for, if applicable (eg, cardiotoxic drugs, alcohol). Treat underlying infectious or systemic inflammatory etiology. Nonsteroidal anti-inflammatory agents should be avoided in the acute phase, as their use may impede myocardial healing and actually exacerbate the inflammatory process and increase the risk of mortality.

Anticoagulation may be advisable as a preventive measure, as in other causes of heart failure, although no definitive evidence is available.

Antiarrhythmics can be used cautiously, although most antiarrhythmic drugs have negative inotropic effects that may aggravate heart failure. (Supraventricular arrhythmias should be converted electrically.) High-grade ventricular ectopy and ventricular tachyarrhythmia should be treated cautiously with beta blockers and antiarrhythmics.

Patients are usually very sensitive to digoxin and should use it with caution and in low doses. (Digoxin increases expression of proinflammatory cytokines and mortality rate in animal models.)


Immunosuppression has not been demonstrated to change the natural history of infectious myocarditis. The Heart Failure Society of America 2010 guideline recommends against routine use of immunosuppressive therapy.[4] Three large-scale prospective clinical trials on immunosuppressive strategies have been performed in patients with myocarditis, none of which showed significant benefits (National Institutes of Health [NIH] prednisone trial[29] , Myocarditis Treatment Trial[23] , and Intervention in Myocarditis and Acute Cardiomyopathy [IMAC] trial[30] ). Empirical treatment with immunosuppression for systemic autoimmune disease, especially in giant cell myocarditis and sarcoid myocarditis, is often given based on evidence from small series.[24, 31]

Ongoing studies will determine if antiviral agents, immunosuppressants, or immunoabsorption therapies are beneficial in specific patient populations, although some small series have provided preliminary evidence demonstrating their potential efficacies.

In the previously mentioned study by Klugman et al, treatment rates among pediatric patients were as follows[11] :

  • Intravenous immunoglobulin (IVIG) - 49.1% of patients
  • Milrinone - 45% of patients
  • Epinephrine - 35% of patients
  • Mechanical ventilation - 25% of patients
  • Extracorporeal membrane oxygenation - 7% of patients
  • Cardiac transplantation - 5% of patients

Klugman and colleagues also found that IVIG did not affect survival rates, even in patients with extreme illness scores.


Surgical Care

Complete heart block is an indication for temporary transvenous pacing. Implantable defibrillators rarely are indicated in lymphocytic myocarditis unless extensive scarring has occurred. In the case of frequent nonsustained or polymorphic ventricular ectopy or tachyarrhythmia, temporary or wearable defibrillator support (eg, LifeVest) may be considered.

Myocarditis carries a low threshold for ventilatory and circulatory support (such as intra-aortic balloon pump) because of the rapidly progressive course of decompensation and the potential for reversal. In extreme cases, circulatory support with a ventricular assist device or percutaneous circulatory support (such as TandemHeart or Impella) has been reported.

Left ventricular assistive devices (LVADs) and extracorporeal membrane oxygenation may be indicated for short-term circulatory support if needed for cardiogenic shock.[5]

For cardiac transplantation, survival rates have not been shown to be decreased in patients with acute myocarditis, although retrospective observations have been made that more posttransplant acute rejections and subsequent posttransplant vasculopathy may occur in these patients.

Transplantation has been shown to be particularly beneficial to those with biopsy-proven giant cell myocarditis; the 5-year survival rate after transplantation was 71%, despite a 25% incidence of posttransplantation recurrence, as seen in 9 of 34 patients in the Multicenter Giant Cell Myocarditis study.


Long-Term Monitoring

Ongoing, chronic inflammation may cause dilated cardiomyopathy and subsequent heart failure. Patients with a history of myocarditis should be monitored at intervals of 1-3 months initially, with gradual return of physical activity.

Any evidence of residual cardiac dysfunction or remodeling should be treated in the same manner as chronic heart failure. The role of medical therapy in those with complete resolution of cardiac structure and performance within a short time is less well established, although conservatively, most would still receive ACE inhibitors or beta blockers at a minimum.

Contributor Information and Disclosures

Wai Hong Wilson Tang, MD Professor of Medicine, Section of Heart Failure and Cardiac Transplantation Medicine, Cleveland Clinic Foundation

Wai Hong Wilson Tang, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society for Clinical Investigation, International Society for Heart and Lung Transplantation, Heart Failure Society of America

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.


Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

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.

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.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, 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: Nothing to disclose.

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

David S Howes, MD Professor of Medicine and Pediatrics, Section Chief and Emergency Medicine Residency Program Director, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eric M Kardon, MD, FACEP Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, 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.

George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center

George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

James B Young, MD Chairman, Professor of Medicine, Department of Medicine, Cleveland Clinic Foundation

Disclosure: National Institute of Health Grant/research funds Independent Contractor

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H and E, low power, showing numerous lymphocytes with associated myocyte damage (photo courtesy of Dr. Donald Weilbaecher)
H and E, high power, showing toxoplasmosis (numerous purple granular-like structures within a myocyte)
H and E, high power, showing lymphocytes, histiocytes and a multinucleated giant cell representing sarcoidosis (a diagnosis of exclusion)
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