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Acquired Mitral Stenosis Medication

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

Medication Summary

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



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.


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.


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.


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.


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.


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.


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.



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.

Contributor Information and Disclosures

M Silvana Horenstein, MD Assistant Professor, Department of Pediatrics, University of Texas Medical School at Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc

M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Medical Association

Disclosure: Nothing to disclose.


Henry Walters, III, MD Associate Professor of Surgery, Wayne State University School of Medicine; Chief, Department of Surgery, Division of Cardiovascular Surgery, Children's Hospital of Michigan

Henry Walters, III, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American Medical Association, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

Michael D Pettersen, MD Consulting Staff, Rocky Mountain Pediatric Cardiology, Pediatrix Medical Group

Michael D Pettersen, MD is a member of the following medical societies: American Society of Echocardiography

Disclosure: Received income in an amount equal to or greater than $250 from: Fuji Medical Imaging.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Julian M Stewart, MD, PhD Associate Chairman of Pediatrics, Director, Center for Hypotension, Westchester Medical Center; Professor of Pediatrics and Physiology, New York Medical College

Julian M Stewart, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Autonomic Society, American Physiological Society

Disclosure: Received grant/research funds from Lundbeck Pharmaceuticals for none.

Chief Editor

Stuart Berger, MD Medical Director of The Heart Center, Children's Hospital of Wisconsin; Associate Professor, Department of Pediatrics, Section of Pediatric Cardiology, Medical College of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

Ira H Gessner, MD Professor Emeritus, Pediatric Cardiology, University of Florida College of Medicine

Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

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Hemodynamic changes in severe mitral valve stenosis (MS). MS causes an obstruction (in diastole) to blood flow from the left atrium (LA) to the left ventricle (LV). Increased LA pressures are transmitted retrograde to pulmonary veins and pulmonary capillaries, resulting in capillary leak with subsequent development of pulmonary edema. To overcome pulmonary edema, the arterioles constrict, increasing pulmonary pressures. Over time, capillaries develop intimal thickening, causing fixed (permanent) pulmonary hypertension. The right ventricle (RV) hypertrophies to generate enough pressure to overcome the increased afterload. Eventually, the RV fails, which manifests as hepatomegaly and/or ascites, edema of the extremities, and cardiomegaly on radiography.
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