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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.

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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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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

References
  1. Shah B, Sharma M, Kumar R, Brahmadathan KN, Abraham VJ, Tandon R. Rheumatic Heart Disease: Progress and Challenges in India. Indian J Pediatr. 2012 Sep 2. [Medline].

  2. Roberts-Thomson KC, Stevenson IH, Kistler PM, Haqqani HM, Goldblatt JC, Sanders P, et al. Anatomically determined functional conduction delay in the posterior left atrium relationship to structural heart disease. J Am Coll Cardiol. 2008 Feb 26. 51(8):856-62. [Medline].

  3. Selcuk MT, Selcuk H, Maden O, Temizhan A, Aksu T, Dogan M, et al. Relationship between inflammation and atrial fibrillation in patients with isolated rheumatic mitral stenosis. J Heart Valve Dis. 2007 Sep. 16(5):468-74. [Medline].

  4. Ucer E, Gungor B, Erdinler IC, Akyol A, Alper AT, Eksik A, et al. High sensitivity CRP levels predict atrial tachyarrhythmias in rheumatic mitral stenosis. Ann Noninvasive Electrocardiol. 2008 Jan. 13(1):31-8. [Medline].

  5. Movahed MR, Ahmadi-Kashani M, Kasravi B, Saito Y. Increased prevalence of mitral stenosis in women. J Am Soc Echocardiogr. 2006 Jul. 19(7):911-3. [Medline].

  6. Ahmed S, Ayoub EM, Scornik JC, et al. Poststreptococcal reactive arthritis: clinical characteristics and association with HLA-DR alleles. Arthritis Rheum. 1998 Jun. 41(6):1096-102. [Medline].

  7. Gouya H, Cabanes L, Mouthon L, Pavie A, Legmann P, Vignaux O. Severe mitral stenosis as the first manifestation of systemic lupus erythematosus in a 20-year-old woman: the value of magnetic resonance imaging in the diagnosis of Libman-Sacks endocarditis. Int J Cardiovasc Imaging. 2014 Apr 9. [Medline].

  8. Kennedy JL, Mery CM, Kern JA, Bergin JD. Mitral stenosis caused by an amplatzer occluder device used to treat a paravalvular leak. Ann Thorac Surg. 2012 Jun. 93(6):2058-60. [Medline].

  9. Horstkotte D, Fassbender D, Piper C. [Congenital heart disease and acquired valvular lesions in pregnancy]. Herz. 2003 May. 28(3):227-39. [Medline].

  10. Yuce M, Davutoglu V, Ozbala B, Ercan S, Kizilkan N, Akcay M, et al. Fragmented QRS is predictive of myocardial dysfunction, pulmonary hypertension and severity in mitral stenosis. Tohoku J Exp Med. 2010. 220(4):279-83. [Medline].

  11. Ozdemir O, Alyan O, Soylu M, et al. Relation between Sympathetic Overactivity and Left Atrial Spontaneous Echo Contrast in Patients with Mitral Stenosis and Sinus Rhythm. Heart Lung Circ. 2006 Jul 20. [Medline].

  12. Morris MF, Maleszewski JJ, Suri RM, Burkhart HM, Foley TA, Bonnichsen CR, et al. CT and MR imaging of the mitral valve: radiologic-pathologic correlation. Radiographics. 2010 Oct. 30(6):1603-20. [Medline].

  13. Messika-Zeitoun D, Serfaty JM, Laissy JP, et al. Assessment of the mitral valve area in patients with mitral stenosis by multislice computed tomography. J Am Coll Cardiol. 2006 Jul 18. 48(2):411-3. [Medline].

  14. Wu M, Zhang S, Dong A, He Z, Chen S, Chen R. Long-term outcomes of maze procedure plus valve replacement in treating rheumatic valve disease resulting in atrial fibrillation. Ann Thorac Surg. 2010 Jun. 89(6):1942-9. [Medline].

  15. Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD, et al. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2008 Oct 7. 118(15):e523-661. [Medline].

  16. Antonini-Canterin F, Moura LM, Enache R, Leiballi E, Pavan D, Piazza R, et al. Effect of hydroxymethylglutaryl coenzyme-a reductase inhibitors on the long-term progression of rheumatic mitral valve disease. Circulation. 2010 May 18. 121(19):2130-6. [Medline].

  17. Antonini-Canterin F, Leiballi E, Enache R, Popescu BA, Rosca M, Cervesato E, et al. Hydroxymethylglutaryl coenzyme-a reductase inhibitors delay the progression of rheumatic aortic valve stenosis a long-term echocardiographic study. J Am Coll Cardiol. 2009 May 19. 53(20):1874-9. [Medline].

  18. Geldenhuys A, Koshy JJ, Human PA, Mtwale JF, Brink JG, Zilla P. Rheumatic mitral repair versus replacement in a threshold country: the impact of commissural fusion. J Heart Valve Dis. 2012 Jul. 21(4):424-32. [Medline].

  19. Bernal JM, Ponton A, Diaz B, et al. Combined mitral and tricuspid valve repair in rheumatic valve disease: fewer reoperations with prosthetic ring annuloplasty. Circulation. 2010 May 4. 121(17):1934-40. [Medline].

  20. Cho IJ, Hong GR, Lee S, Byung-Chul C, Ha JW, Chung N. Predictors of prognosis in patients with mild to moderate paravalvular leakage after mitral valve replacement. J Card Surg. 2014 Mar. 29(2):149-54. [Medline].

  21. Acar J, Michel PL, de Gevigney G. [When is surgery needed for minimally symptomatic or asymptomatic acquired valvulopathy?]. Presse Med. 2000 Nov 13. 29(34):1867-75. [Medline].

  22. Ananthasubramaniam K, Iyer G, Karthikeyan V. Giant left atrium secondary to tight mitral stenosis leading to acquired Lutembacher syndrome: a case report with emphasis on role of echocardiography in assessment of Lutembacher syndrome. J Am Soc Echocardiogr. 2001 Oct. 14(10):1033-5. [Medline].

  23. Boudoulas H, Vavuranakis M, Wooley CF. Valvular heart disease: the influence of changing etiology on nosology. J Heart Valve Dis. 1994 Sep. 3(5):516-26. [Medline].

  24. Bruce CJ, Nishimura RA. Clinical assessment and management of mitral stenosis. Cardiol Clin. 1998 Aug. 16(3):375-403. [Medline].

  25. Bruce CJ, Nishimura RA. Newer advances in the diagnosis and treatment of mitral stenosis. Curr Probl Cardiol. 1998 Mar. 23(3):125-92. [Medline].

  26. Carabello BA, Crawford FA Jr. Valvular heart disease. N Engl J Med. 1997 Jul 3. 337(1):32-41. [Medline].

  27. Cheng TO. Percutaneous versus surgical treatment of atrial septal defect and of mitral stenosis: Cost-effectiveness in developing versus developed countries. Int J Cardiol. 2006 Jul 5. [Medline].

  28. Denbow CE, Barton EN, Smikle MF. The prophylaxis of acute rheumatic fever in a pair of monozygotic twins. The public health implications. West Indian Med J. 1999 Dec. 48(4):242-3. [Medline].

  29. Keat A. Reactive arthritis. Adv Exp Med Biol. 1999. 455:201-6. [Medline].

  30. Mackie SL, Keat A. Poststreptococcal reactive arthritis: what is it and how do we know?. Rheumatology (Oxford). 2004 Aug. 43(8):949-54. [Medline].

  31. Oechslin E, Turina J, Lauper U, et al. [Cardiovascular disease in pregnancy]. Ther Umsch. 1999 Oct. 56(10):551-60. [Medline].

  32. Ozen S, Bakkaloglu A, Yilmaz E, et al. Mutations in the gene for familial Mediterranean fever: do they predispose to inflammation?. J Rheumatol. 2003 Sep. 30(9):2014-8. [Medline].

  33. Selcuk MT, Selcuk H, Maden O, Temizhan A, Aksu T, Dogan M, et al. Relationship between inflammation and atrial fibrillation in patients with isolated rheumatic mitral stenosis. J Heart Valve Dis. 2007 Sep. 16(5):468-74. [Medline].

  34. Shulman ST, Ayoub EM. Poststreptococcal reactive arthritis. Curr Opin Rheumatol. 2002 Sep. 14(5):562-5. [Medline].

  35. Sokoloski MC. Tachyarrhythmias Confined to the Atrium. Clinical Pediatric Arrhythmias. 1999. 78-96.

  36. Villablanca AC. Heart disease during pregnancy. Which cardiovascular changes reflect disease?. Postgrad Med. 1998 Nov. 104(5):149-56. [Medline].

 
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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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