Myocarditis Medication

Updated: Dec 19, 2016
  • Author: Wai Hong Wilson Tang, MD; Chief Editor: Henry H Ooi, MD, MRCPI  more...
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Medication

Medication Summary

In general, treatment of either acute or chronic myocarditis is aimed at reducing congestion and improving cardiac hemodynamics in heart failure, as well as providing supportive therapy, with the hope of prolonging survival. Treatment of heart failure follows the same treatment regimen regardless of the underlying cause (ie, ACE inhibitors, beta-adrenergic blockers).

Intensive immunosuppressive therapy (eg, corticosteroids, azathioprine, cyclosporine, muromonab-CD3/OKT3) has been shown to have some benefit only in small-scale clinical studies in the treatment of giant cell myocarditis and has not been validated in large clinical trials. At this time, immunosuppressive therapy is not recommended for myocarditis until clear evidence is available from the results of multicenter trials.

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Vasodilators

Class Summary

Vasodilators reduce systemic vascular resistance, allowing more forward flow and improving cardiac output. This, in turn, improves myocardial oxygen supply, resulting in dilatation of epicardial and collateral vessels and improving blood supply to the ischemic myocardium.

Nitroglycerin (Minitran, Nitro-Bid, Nitrostat, Nitro-Dur)

Nitroglycerin is the drug of choice for patients who are not hypotensive. It provides excellent and reliable preload reduction, while higher doses provide mild afterload reduction.

The drug has rapid onset and offset (both within minutes), allowing for rapid clinical effects and rapid discontinuation of effects in adverse reactions.

Sodium nitroprusside (Nitropress)

Sodium nitroprusside is considered an afterload reducer. It is a potent direct smooth muscle–relaxing agent that results primarily in afterload reduction but can cause mild preload reduction. The drug produces improved cardiac output, but it can also cause precipitous decreases in blood pressure. Intra-arterial blood pressure monitoring is strongly recommended.

Sodium nitroprusside is an excellent medication in critically ill patients because of rapid onset and offset of action (within 1-2 min). It is excellent for use in cardiogenic pulmonary edema associated with relative hypertension in myocarditis.

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ACE inhibitors

Class Summary

Following stabilization of heart failure symptoms, initiation of ACE inhibitors is the standard of care to delay disease progression in heart failure. Beta-adrenergic antagonists should be used only following resolution of congestive symptoms and clinical stabilization of the patient's condition.

Ramipril (Altace)

Prevents conversion of Angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Enalapril (Vasotec, Epaned)

Enalapril is a competitive inhibitor of angiotensin-converting enzymes. It reduces angiotensin II levels, causing a decrease in aldosterone secretion.

Quinapril (Accupril)

Prevent conversion of Ang I to Ang II (a potent vasoconstrictor), resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Captopril

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Rapidly absorbed, but bioavailability is significantly reduced with food intake. It achieves a peak concentration in an hour and has a short half-life. The drug is cleared by the kidney.

Impaired renal function requires reduction of dosage. Absorbed well PO. Give at least 1 h before meals. If added to water, use within 15 min.

Can be started at low dose and titrated upward as needed and as patient tolerates.

Lisinopril (Prinivil, Zestril)

Prevent conversion of Ang I to Ang II (a potent vasoconstrictor), resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

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Diuretics

Class Summary

Diuretics reduce preload. The initial drop in cardiac output produced by diuresis causes a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels, and peripheral vascular resistance falls below its pretreatment baseline.

Furosemide (Lasix)

Furosemide is the most commonly used loop diuretic. It increases the excretion of water by interfering with the chloride-binding cotransport system, resulting in inhibition of sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Furosemide reduces preload through diuresis in 20-60 minutes. It may contribute to more rapid preload reduction through a direct vasoactive mechanism, but this is controversial.

As many as half of all patients with cardiogenic pulmonary edema (CPE) are total-body euvolemic. Furosemide is generally administered to all patients with CPE, but it is probably most useful in patients with total-body fluid overload. The oral form has a slower onset of action and, therefore, is generally not considered appropriate for treating these patients.

Torsemide (Demadex)

Acts from within the lumen of the thick ascending portion of the loop of Henle, where inhibits the Na/K/2Cl carrier system. Increases urinary excretion of sodium, chloride, and water, but does not significantly alter glomerular filtration rate, renal plasma flow, or acid-base balance.

Bumetanide

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in ascending loop of Henle. These effects increase urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs following administration, renal vascular resistance decreases, and renal blood flow is enhanced.

Individualize dose to patient. Start at 1-2 mg IV; titrate to as high as 10 mg/d. Rarely, doses as high as 24 mg/d are used for edema but generally are not required for treatment of hyperkalemia.

One mg of bumetanide is equivalent to approximately 40 mg of furosemide.

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Angiotensin II receptor blockers

Class Summary

Angiotensin receptor blockers are as effective as ACE inhibitors in the treatment of heart failure. Their adverse-effect profile is similar to that of ACE inhibitors with regard to renal insufficiency or hyperkalemia but they do not cause potentiation of bradykinin and therefore do not cause cough.

Candesartan (Atacand)

Blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACE inhibitors.

Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function, and delaying onset of end-stage renal disease.

Losartan (Cozaar)

Angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors.

Valsartan (Diovan)

Prodrug that produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. For use in patients unable to tolerate ACE inhibitors.

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Beta-adrenergic blockers

Class Summary

Avoid the use of beta-blockers in the very early treatment of fulminant myocarditis and in the acute phase of decompensated HF. Beta blockers have antiarrhythmic and antihypertensive properties, as well as the ability to reduce ischemia. They minimize the imbalance between myocardial supply and demand by reducing afterload and wall stress. Beta blockers ameliorate dynamic obstruction of the left ventricular outflow tract in patients with apical infarct and hyperdynamic basal segments. These agents work in multiple ways to treat heart failure. They should not be used acutely in patients with cardiogenic shock or signs of heart failure on presentation.

Metoprolol (Lopressor, Toprol XL)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate and ECG.

Carvedilol (Coreg, Coreg CR)

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.

Bisoprolol (Zebeta)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions.

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Inotropic agents

Class Summary

Inotropic drugs may be necessary for severe decompensation, although they are highly arrhythmogenic.

Milrinone

Bi-pyridine positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from both digitalis glycosides and catecholamines. Selectively inhibits phosphodiesterase type III (PDE III) in cardiac and smooth vascular muscle, resulting in reduced afterload, reduced preload, and increased inotropy.

Dobutamine

Produces vasodilation and increases inotropic state. At higher dosages may cause increased heart rate, exacerbating myocardial ischemia.

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