Myocarditis in Emergency Medicine Medication
- Author: David S Howes, MD; Chief Editor: David FM Brown, MD more...
Medication Summary
Current medical therapy for myocarditis primarily involves managing complications, chiefly thromboembolism, dysrhythmia, and congestive heart failure (CHF), and is addressed in detail in the corresponding eMedicine articles; there are a few specific aspects of treatment specific to 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.[19] 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. The identification of one of these entities by endomyocardial biopsy should lead to a plan for immunosuppression.[20, 21]
A great amount of research is currently focused 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 IVIG 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.[22]
Medication treatment specific for myocarditis is an area of avid research, mostly focusing on immunomodulators as discussed below, but many areas are being explored.
Angiotensin converting enzyme inhibitors
Class Summary
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.[20]
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.
Calcium channel blockers
Class Summary
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.[23]
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.
Loop diuretics
Class Summary
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.
Cardiac glycosides
Class Summary
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.
Beta-adrenergic blockers
Class Summary
Beta-blockers should be avoided in the acutely decompensated phase of CHF and in fulminant cases of myocarditis but show long-term improvements in mortality in all other patients.[18, 20]
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.
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