eMedicine Specialties > Emergency Medicine > Cardiovascular
Myocarditis: Treatment & Medication
Updated: Aug 5, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Emergency Department Care
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.
- Standard treatment of clinically significant disease includes the detection of dysrhythmia with cardiac monitoring, supplemental oxygen, and managing fluid status.
- Left ventricular dysfunction developing from myocarditis should be approached in much the same manner as other causes of CHF with some exceptions (see Medication).
- 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, but studies that have used carvedilol have shown decreases in the expression of several different histochemicals, subsequent inflammatory myocyte infiltrate, and mortality.
- Patients who present with Mobitz II or complete heart block require pacemaker placement. Some authors also suggest the placement of automatic implantable cardioverter-defibrillators (AICDs) in patients with significant, persistent decreases in left ventricular (LV) function.
Consultations
Patients who require emergency room treatment for new-onset CHF, dysrhythmia, or cardiogenic shock should be admitted to the hospital with continuous cardiac monitoring and cardiology consultation.
Medication
Medical therapy for myocarditis is an area of avid research interest but with little success in human trials. Treatment primarily involves managing the complications of myocarditis, chiefly thromboembolism, dysrhythmia, and CHF, and is addressed in detail in the corresponding eMedicine Journal articles; little is specific to myocarditis except for a few specific aspects of the treatment of myocarditis-related CHF.
Despite continued research interest in immunosuppressives for treatment of myocarditis, no randomized controlled trial, of which there have been several, has shown any short- or long-term benefit to all patients. However, in the subset of patients with cardiac sarcoid, hypersensitivity myocarditis, and giant cell myocarditis, general immunosuppression likely can play a significant role in preventing progression and reversing inflammation.
A great amount of research is currently focussed on immune modulators that target particular steps in the immune cascade without eliminating the ability of the body's defenses to shed virus. Immunomodulating therapy, such as IV-IG and interferon alfa and beta, show great promise in animal models, research trials, and limited clinical experience. In research trials, of interferon beta, patients have had elimination of viral genome and have gained and maintained improved LV function after treatment. These therapies are not yet used outside of research protocols.
Medication treatment specific for myocarditis is an area of avid research, mostly focussing on immunomodulators as discussed below, but many areas are being explored. An interesting Chinese study demonstrated a potent antiviral effect against coxsackievirus replication from a polyphenol extracted from the spice tumeric.
Angiotensin converting enzyme inhibitors
These agents are beneficial in the management of blood pressure and LV function in heart failure. Captopril, in particular, has been shown to be beneficial in the treatment of significant LV dysfunction. Other ACE inhibitors have not shown the same effect in animal trials, indicating captopril's oxygen radical scavenging properties in the morbidity effect.
Captopril (Capoten)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Adult
6.25-12.5 mg PO tid; not to exceed 150 mg tid
Pediatric
0.15-0.3 mg/kg PO bid/tid
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; renal impairment
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
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in renal impairment, valvular stenosis, or severe CHF
Calcium channel blockers
Although they have limited use in ischemic causes of CHF, calcium channel blockers may prove to be useful in myocarditis-related myopathies. Amlodipine, in particular, perhaps due to its effect on nitric oxide, showed benefit in animal models and in a placebo controlled trial.
Amlodipine (Norvasc)
Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias.
Adult
2.5-5 mg PO qd
10 mg PO qd maximum
Pediatric
Not established
Fentanyl and alcohol may increase hypotensive effects; calcium channel blocker may increase cyclosporine levels; H2 blockers (cimetidine), erythromycin, nafcillin, and azole antifungals may increase toxicity (avoid combination or monitor closely); carbamazepine may reduce bioavailability (avoid this combination); rifampin may decrease levels (monitor and adjust dose of calcium channel blocker)
Documented hypersensitivity
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
Adjust dose in renal or hepatic impairment; may cause lower extremity edema; allergic hepatitis has occurred but is rare
Loop diuretics
These agents are used for management of fluid overload.
Furosemide (Lasix)
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; titrate up to 600 mg/d for severe edematous states
Pediatric
1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg
Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication
Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
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
Perform frequent serum electrolyte, CO2, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter
Cardiac glycosides
These agents decrease AV nodal conduction primarily by increasing vagal tone. They may aid in the dysrhythmia and CHF aspects of myocarditis.
Digoxin (Digitek, Lanoxicaps, 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
0.125-0.375 mg PO qd
Pediatric
<5 years: Not established
5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
Maintenance dose: Use 25-35% of PO loading dose
Many medications can alter levels of digoxin, which has a fairly narrow therapeutic window
Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome
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
Patients with myocarditis seem to be particularly sensitive to digoxin toxicity
Beta-adrenergic blockers
Beta-blockers should be avoided in the acutely decompensated phase of CHF and fulminant case of myocarditis but show long-term improvements in mortality.
Carvedilol (Coreg)
Nonselective beta- and alpha-adrenergic blocker. Also has antioxidant properties. Does not appear to have intrinsic sympathomimetic activity. May reduce cardiac output and decrease peripheral vascular resistance. Shown to be of benefit in patients with heart failure. Some evidence suggests it is even more beneficial than metoprolol.
Adult
6.25-50 mg PO bid as tolerated (maximum of 75 mg/d if <85 kg, 100 mg/d if >85 kg)
Pediatric
Not established
Rifampin, barbiturates, cholestyramine, colestipol, NSAIDs, salicylates, and penicillins may decrease effects; carvedilol may increase effects of antidiabetic agents, digoxin, and calcium channel blockers; concurrent administration with clonidine may increase blood pressure and decrease heart rate; carvedilol may decrease effect of sulfonylureas; cimetidine, fluoxetine, paroxetine, and propafenone may increase carvedilol levels
Documented hypersensitivity; hypotension; bradycardia; AV/SA node disease; cardiogenic shock; overt cardiac 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
Caution in congestive heart failure being treated with digitalis, diuretics, or ACE inhibitors (AV conduction may be slowed); discontinue if liver impairment occurs; caution in peripheral vascular disease, hyperthyroidism, and diabetes mellitus
More on Myocarditis |
| Overview: Myocarditis |
| Differential Diagnoses & Workup: Myocarditis |
 Treatment & Medication: Myocarditis |
| Follow-up: Myocarditis |
| References |
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Further Reading
Keywords
myocarditis, heart inflammation, dilated cardiomyopathy, inflammatory changes in the heart muscle, myocyte necrosis, viral myocarditis, acute myocarditis, inflammatory myocarditis, Chagas disease, coxsackievirus B, influenza virus, echovirus, herpes simplex virus, varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, hepatitis C, HIV, diphtheria, Bartonella species, Brucella species, Leptospira species, Salmonella species, endocarditis, Borrelia burgdorferi, toxic myocarditis, parasitic myocarditis
