Acquired Mitral Stenosis Medication

Updated: Apr 29, 2014
  • Author: M Silvana Horenstein, MD; Chief Editor: Stuart Berger, MD  more...
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Medication

Medication Summary

Medical therapy is directed at alleviating symptoms, treating rhythm abnormalities, and preventing thromboembolic complications.

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Diuretics

Class Summary

These agents promote excretion of water and electrolytes by the kidneys. They decrease fluid overload and pulmonary congestion.

Furosemide (Lasix)

Acts by inhibiting absorption of sodium and chloride in proximal and distal tubules and in the loop of Henle, thereby promoting excretion of sodium chloride and water. Acts as a diuretic and antihypertensive.

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Potassium-sparing diuretics

Class Summary

These agents are used to prevent potassium depletion induced by more potent loop diuretics (eg, furosemide).

Spironolactone (Aldactone)

Used to decrease edema resulting from excessive aldosterone excretion. Inhibits aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule, thereby retaining potassium and excreting sodium and water. Serves as a diuretic and antihypertensive agent.

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Inotropic-antiarrhythmic agents

Class Summary

These agents are mainly used in mitral stenosis (MS) in atrial flutter or fibrillation because of its antiarrhythmic properties. Digoxin is not expected to improve overall cardiac function because, in MS patients, heart failure is from mechanical obstruction causing elevated left atrial pressure, with subsequent transmission to RV and, ultimately, failure. Theoretically, digoxin could aid in improving RV dysfunction.

Digoxin (Lanoxin)

Digitalis glycoside that inhibits sodium-potassium ATPase (enzyme that extrudes sodium and brings potassium into myocyte). Resulting increase in intracellular sodium stimulates sodium-calcium exchange, extruding sodium and bringing in calcium with consequent increase in myocyte contractility. Exerts vagomimetic action on sinus and AV nodes (slowing heart rate and conduction). Also decreases degree of activation of sympathetic nervous system and renin-angiotensin system, referred to as the deactivating effect. Therapeutic serum level range is 0.8-2 ng/mL.

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Class II antiarrhythmic agents (beta-blockers)

Class Summary

These agents are used for atrial flutter or fibrillation. Beta-adrenergic receptor blocking agents are used as a second option when digoxin does not stop atrial flutter or fibrillation.

Propranolol (Inderal)

By blocking the beta-adrenergic receptor, these compounds blunt chronotropic, inotropic, and vasodilator responses of any beta-adrenergic stimulation. Beta-blockers lower ventricular rate; therefore, they are used in patients with atrial flutter or fibrillation.

Esmolol (Brevibloc)

Selective beta-1 (cardioselective)–adrenergic receptor blocking agent; may be used with class I antiarrhythmics if digoxin therapy does not abort atrial arrhythmia. Administer in patients needing prompt slowing of ventricular rate in response to atrial flutter or fibrillation and who are most likely to become hemodynamically unstable if left without treatment or in those waiting for the start of the therapeutic effects of digoxin (average, 10 h).

Has rapid onset and short duration of action. Administered IV to stop atrial arrhythmia; afterward, patient is placed on class I antiarrhythmics for maintenance.

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Class IA antiarrhythmics

Class Summary

These agents are used to stop atrial fibrillation and convert it into sinus rhythm. They can also decrease myocardial excitability.

Procainamide (Pronestyl)

Increases effective refractory period by reducing conduction velocity of atrial fibers and, to a lesser extent, the ERP of His-Purkinje and ventricles. Thus, decreases myocardial excitability and may speed AV node conduction (vagolytic effect). Therapeutic serum level range is 4-10 mg/L.

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Class IC antiarrhythmics

Class Summary

These agents are used after digoxin and/or beta-blockers that have not converted atrial arrhythmia.

Propafenone (Rythmol)

Class IC antiarrhythmic drug that exerts local anesthetic effects and has direct stabilizing action on myocardial cell membrane. Reduces upstroke velocity (phase 0) of action potential by reducing rapid inward current carried by sodium ions. Prolongs effective refractory period and reduces spontaneous automaticity. Prolongs AV node conduction and does not affect sinus node.

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Class III antiarrhythmics

Class Summary

These agents decrease rate of sinus node and relax vascular smooth muscle, with concomitant reduction in peripheral vascular resistance (afterload). They may also exert a mild negative inotropic effect.

Amiodarone (Cordarone)

Prolongs duration of myocyte action potential, prolongs myocyte refractory period, and exerts alpha- and beta-adrenergic inhibition. Therapeutic serum level ranges from 0.5-2.5 mg/L.

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Anticoagulants

Class Summary

These agents are used to prevent clot formation secondary to blood stasis because of an enlarged (left) atrium and (left) atrial fibrillation.

Warfarin (Coumadin)

Inhibits vitamin K–dependent clotting factors II, VII, IX, and X and anticoagulant proteins C and S. Anticoagulation effect occurs 24 h after drug administration, but peak effect may happen 72-96 h later. Antidotes are vitamin K and FFP.

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