Acquired Mitral Stenosis Treatment & Management

  • Author: M Silvana Horenstein, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Sep 1, 2010
 

Medical Care

  • Asymptomatic patients with mild mitral stenosis (MS) require yearly follow-up care to monitor for disease progression. Yearly evaluation should include physical examination, chest radiography, and echocardiography.
  • For the patient with signs or symptoms of CHF, diuretics may provide benefit.
  • Tachyarrhythmias, such as atrial flutter and atrial fibrillation, usually require medical treatment aimed at restoration and maintenance of sinus rhythm. If this is not possible, therapy may be aimed at decreasing ventricular response and maintaining an acceptable heart rate.
    • Digoxin, beta-blockers, and calcium channel blockers have all been used to slow atrioventricular (AV) node conduction and decrease ventricular rate response.
    • Antiarrhythmics from class I (eg, procainamide, flecainide, propafenone) and class III (eg, sotalol, amiodarone) have been used with variable success in converting to and maintaining sinus rhythm.
    • Thromboembolic complication from chronic atrial arrhythmia can be reduced with anticoagulation using warfarin.
  • Electrophysiologic ablation of atrial fibrillation or flutter circuits may be performed in the catheterization laboratory.
  • Surgical ablation via a Cox-Maze procedure during mitral valve repair or replacement has been shown to be an effective treatment for atrial fibrillation with freedom from atrial fibrillation recurrence of nearly 80% after 10 years.[9]
  • Percutaneous mitral balloon valvuloplasty for acquired MS was first described in 1984 and approved by the US Food and Drug Administration in 1994. Indications for this procedure are similar to those for surgery, including CHF unresponsive to medical management and in asymptomatic patients with a pulmonary artery (PA) systolic pressure of 50 mm Hg or greater at rest or greater than 60 mm Hg with exercise in the absence of a left atrial thrombus or moderate to severe MR.[10] In some centers, the procedure is successful in 80-90% of selected cases. The procedural mortality rate is 1-2%.
  • Hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) have reportedly slowed the progression of rheumatic MS.[11, 12]
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Surgical Care

Surgical intervention is indicated in symptomatic (NYHA functional class III-IV) moderate or severe MS when percutaneous MV balloon valvuloplasty is unavailable or contraindicated because of left atrial thrombus despite anticoagulation or concomitant moderate to severe MR, or when valve morphology is unfavorable for valvotomy.[8]

Surgical procedures include the following:

  • Mitral valvotomy
    • Commissurotomy consists of an incision of fused mitral valve commissures and shaving of thickened mitral valve leaflets.
    • Fused chordae tendineae and papillary muscles can be divided to relieve subvalvular stenosis.
    • Supravalvular tissue contributing to the MS should be resected.
    • Combined valvuloplasty with prosthetic ring annuloplasty is also used with reportedly good results.[13]
  • Mitral valve replacement with mechanical valve or bioprosthesis
    • This is reserved for patients in whom mitral valvotomy is considered unlikely to achieve a satisfactory result, such as in those with moderate to severe MR.
    • Mechanical mitral valve replacement is performed frequently in adolescents and adults in whom anticoagulation with warfarin (Coumadin) is not contraindicated. In older patients in whom warfarin therapy may be relatively contraindicated or in patients who have other contraindications to warfarin therapy, mitral valve replacement can be performed using a bioprosthesis, although these are less durable than mechanical prostheses.
    • Weigh the risk of warfarin therapy against that of bioprosthetic valve deterioration resulting in the need for reoperation. Warfarin is contraindicated during pregnancy.
    • Complications after mitral valve replacement include anticoagulation-related complications, valve thrombosis, valve dehiscence, infective endocarditis, valve malfunction, and embolic events.
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Consultations

Consult a cardiologist and a cardiothoracic surgeon.

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Diet

Salt intake should be restricted and excessive fluid intake minimized to avoid exacerbating signs and symptoms of CHF.

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Activity

Patients with more severe than mild MS should avoid strenuous exertion. Increased heart rate may result in decreased diastolic filling, thereby decreasing cardiac output. Coexistent atrial arrhythmias result in loss of atrial augmentation of LV filling and may further impair cardiac output.

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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, and American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Michael Pettersen, MD  Director of Echocardiography, Division of Cardiology, Children's Hospital of Michigan; Associate Professor of Pediatrics, Wayne State University School of Medicine

Michael Pettersen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, and American Society of Echocardiography

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, and Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Ira H Gessner, MD  Professor Emeritus, Pediatric Cardiology

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, and Society for Pediatric Research

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital 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, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

References

  1. 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. Feb 26 2008;51(8):856-62. [Medline].

  2. 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. Sep 2007;16(5):468-74. [Medline].

  3. 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. Jan 2008;13(1):31-8. [Medline].

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

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

  6. 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. Jul 20 2006;[Medline].

  7. 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. Jul 18 2006;48(2):411-3. [Medline].

  8. 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].

  9. 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. Jun 2010;89(6):1942-9. [Medline].

  10. 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. Oct 7 2008;118(15):e523-661. [Medline].

  11. 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. May 18 2010;121(19):2130-6. [Medline].

  12. 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. May 19 2009;53(20):1874-9. [Medline].

  13. Bernal JM, Pontón A, Diaz B, Llorca J, García I, Sarralde JA, et al. Combined mitral and tricuspid valve repair in rheumatic valve disease: fewer reoperations with prosthetic ring annuloplasty. Circulation. May 4 2010;121(17):1934-40. [Medline].

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

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

  16. 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. Oct 2001;14(10):1033-5. [Medline].

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

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

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

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

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

  22. 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. Dec 1999;48(4):242-3. [Medline].

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

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

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

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

  27. 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. Sep 2007;16(5):468-74. [Medline].

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

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

  30. Villablanca AC. Heart disease during pregnancy. Which cardiovascular changes reflect disease?. Postgrad Med. Nov 1998;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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