Myocarditis Treatment & Management
- Author: Wai Hong Wilson Tang, MD; Chief Editor: Henry H Ooi, MD, MRCPI more...
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:
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. 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.
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. 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 , Myocarditis Treatment Trial , and Intervention in Myocarditis and Acute Cardiomyopathy [IMAC] trial ). 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 :
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.
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.
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.
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.
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