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Mitral Stenosis Treatment & Management

  • Author: Claudia Dima, MD, FACC; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Nov 06, 2014
 

Medical Care

The goal of medical treatment for mitral stenosis is to reduce recurrence of rheumatic fever, provide prophylaxis for infective endocarditis, reduce symptoms of pulmonary congestion (eg, orthopnea, paroxysmal nocturnal dyspnea), control the ventricular rate if atrial fibrillation is present, and prevent thromboembolic complications.[7]

Because rheumatic fever is the primary cause of mitral stenosis, secondary prophylaxis against group A beta-hemolytic streptococci (GAS) is recommended.[8] Duration of prophylaxis depends on the number of previous attacks, the time elapsed since the last attack, the risk of exposure to GAS infections, the age of the patient, and the presence or absence of cardiac involvement. Penicillin is the agent of choice for secondary prophylaxis, but sulfadiazine or a macrolide or azalide are acceptable alternatives in individuals allergic to penicillin (Tables 1 and 2).

A recent study done in Europe on 315 patients with rheumatic mitral stenosis showed a significantly slower progression of rheumatic mitral stenosis in patients treated with statins compared with patients not taking statins. These findings could have an important impact in the early medical therapy of patients with rheumatic heart disease.[9]

American Heart Association (AHA) guidelines do not recommend infective endocarditis prophylaxis for most patients with rheumatic heart disease.[7, 10] However, the maintenance of optimal oral health care remains an important component of an overall healthcare program. For the relatively few patients with rheumatic heart disease in whom infective endocarditis prophylaxis remains recommended, such as those with prosthetic valves or prosthetic material used in valve repair, the current AHA recommendations should be followed. These recommendations advise the use of an agent other than a penicillin to prevent infective endocarditis in those receiving penicillin prophylaxis for rheumatic fever because oral alpha-hemolytic streptococci are likely to have developed resistance to penicillin.

The indication for antibiotic prophylaxis for endocarditis has also been significantly reduced in the 2012 European Society of Cardiology (ESC) guidelines, although they recommend considering antibiotic prophylaxis for high-risk procedures in high-risk patients.[11]

Initial symptoms of pulmonary congestion can be safely treated by diuretics. Dietary sodium restriction and nitrates decrease preload and can be of additional benefit. Careful use of beta-blockers in patients with a normal sinus rhythm can prolong the diastolic filling time and thus decrease in left atrial pressure. In general, afterload reduction should be avoided as it can cause hypotension.

Atrial fibrillation is common in mitral stenosis and often leads to a rapid ventricular rate with reduced diastolic filling time and increased left atrial pressure. The ventricular rate can be slowed acutely by the administration of intravenous beta-blocker or calcium channel blocker therapy (diltiazem or verapamil). The rate and/or rhythm can be controlled long-term with oral beta-blockers, calcium channel blockers, amiodarone, or digoxin.

In the patient with mild mitral stenosis and recent-onset (< 6 mo) atrial fibrillation, conversion to sinus rhythm can be accomplished with pharmacologic agents or electrical cardioversion. In this circumstance, anticoagulation therapy should be given for at least 3 weeks prior to cardioversion. Alternatively, a TEE can be performed to exclude the presence of left atrial thrombus, prior to cardioversion. Patients who are successfully converted to sinus rhythm should receive long-term anticoagulation and antiarrhythmic drugs. Warfarin should be used for anticoagulation. The novel anticoagulants dabigatran and rivaroxaban have been recently approved for nonvalvular atrial fibrillation; these drugs have not been evaluated in patients with heart valve disease.[12]

According to the 2012 ESC/European Association for Cardio-Thoracic Surgery (EACTS) guidelines, anticoagulant therapy with a target INR in the upper half of the range 2 to 3 is indicated in patients with either permanent or paroxysmal atrial fibrillation. In patients with sinus rhythm, anticoagulation is indicated in those with prior embolism, or those in whom a thrombus is present in the left atrium.[11]

Surgical correction of the mitral stenosis is indicated if embolization is recurrent, despite adequate anticoagulation therapy.

Table 1. Duration of Secondary Rheumatic Fever Prophylaxis (Open Table in a new window)

Category Duration After Last Attack Rating*
Rheumatic fever with carditis and residual heart disease (persistent valvular disease† ) 10 y or until age 40 y (whichever is longer); sometimes lifelong prophylaxis IC
Rheumatic fever with carditis but no residual heart disease (no valvular disease† ) 10 y or until age 21 y (whichever is longer) IC
Rheumatic fever without carditis 5 y or until age 21 y (whichever is longer) IC
*Rating indicates classification of recommendation and level of evidence (eg, IC indicates Class I, level of Evidence C).



†Clinical or echocardiographic evidence.



Table 2. Secondary Prevention of Rheumatic Fever (Prevention of Recurrent Attacks) (Open Table in a new window)

Agent Dose Mode Rating*
Benzathine penicillin G Children 27 kg (60 lb): 600,000 U



Patients >27 kg: 1,200,000 every 4 wk†



Intramuscular IA
Penicillin V 250 mg bid Oral IB
Sulfadiazine Children 27 kg: 0.5 g qd



Patients >27 kg: 1 g qd



Oral IB
Macrolide or azalide (for individuals allergic to penicillin and sulfadiazine) Variable Oral IC
*Rating indicates classification of recommendation and level of evidence (eg, IA indicates Class I, level of Evidence A).



†In high-risk situations, administration every 3 weeks is justified and recommended.



 

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Diet and Activity

The patient should start a low-salt diet if pulmonary vascular congestion is present.

In most patients with mitral stenosis, recommendations for exercise are symptom limited. Patients should be encouraged to pursue a low-level aerobic exercise program for maintenance of cardiovascular fitness.

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Surgical Care

Surgical therapy for mitral stenosis consists of mitral valvotomy (which can be either surgical or percutaneous) or mitral valve replacement. The surgical mitral valvotomy approach can be through an closed or open technique; the latter technique is rarely used, except in developing countries, and has largely been replaced by the percutaneous balloon commissurotomy.[5]

Asymptomatic patients with moderate or severe mitral stenosis (mitral valve area < 1.5 cm2) and a suitable valve should be considered for percutaneous balloon commissurotomy if the pulmonary arterial systolic pressure is ≥50 mm Hg at rest or ≥60 mm Hg with exercise, or pulmonary capillary wedge pressure is ≥25 mm Hg with exercise.[13]

Symptomatic patients with moderate or severe mitral stenosis (mitral valve area < 1.5 cm2) and suitable valve are also candidates for percutaneous balloon commissurotomy.

ESC/EACTS guidelines recommend percutaneous balloon commissurotomy in symptomatic patients with favorable characteristics, symptomatic patients with contraindications or high risk for surgery, symptomatic patients with unfavorable anatomy but without unfavorable clinical characteristics, and in asymptomatic patients without unfavorable characteristics and a high thromboembolic risk and/or a high risk of hemodynamic decompensation.[11]

Contraindications to percutaneous mitral commissurotomy include mitral valve area >1.5 cm2, left atrial thrombus, more than mild mitral regurgitation, severe or bicommissural calcification, absence of commissural fusion, severe concomitant aortic valve disease or severe combined tricuspid stenosis and regurgitation, and concomitant coronary artery disease requiring bypass surgery.[11]

If percutaneous balloon commissurotomy is not an option, patients should be referred for surgical repair or mitral valve replacement.

Percutaneous balloon valvuloplasty/percutaneous mitral commissurotomy (PMC)

PMC is the procedure of choice for patients with uncomplicated mitral stenosis. Patients with pliable, mobile, relatively thin, minimally calcified mitral leaflets with minimal or no subvalvular stenosis are good candidates for this procedure. A TEE should be performed prior to commissurotomy to clearly define the valve anatomy and exclude the presence of a left atrial thrombus.

The echocardiographic scoring system (Wilkins score) has been used as a valuable tool for patient selection. Leaflet mobility, valvular thickening, valvular calcification, and subvalvular disease are each given a score of 0-4, with higher scores indicating more severe involvement. A total score of less than 8 results in good short- and long-term outcome with balloon valvuloplasty.

With PMC, a catheter is directed into the left atrium after transseptal puncture, and a balloon is directed across the valve and inflated in the orifice. This results in separation of the mitral leaflets. The valve size can be increased up to 2-2.5 cm2.

Improvement in symptoms is noted immediately following the procedure. If symptoms do not improve, the commissurotomy was either ineffective or resulted in mitral regurgitation.

The short- and long-term prognoses are favorable compared with surgical valvotomy.

PMC offers certain advantages over surgical valvotomy, including avoidance of a thoracotomy and general anesthesia and their attendant complications.

The major contraindications to balloon commissurotomy are the presence of thrombus in the left atrium or its appendage, moderate-to-severe mitral regurgitation, and an unfavorable valve morphology (ie, high Wilkins echo score).

Complications of a PMC include embolization, mitral regurgitation, ventricular rupture, residual atrial septal defect, stroke, and death.

Surgical valvotomy/valve replacement

Open surgical commissurotomy allows direct visualization of the mitral valve.

Using current techniques, even severe regurgitant or stenotic valves can often be repaired, with good long-term results. Valves that are not suitable for repair can be replaced using either bioprosthetic or metallic prosthetic valves.

With bioprosthetic valves, the patient does not require anticoagulation, as long as he or she remains in sinus rhythm; however, 20-40% of these valves fail within 10 years, secondary to structural deterioration.

Mechanical valves are placed in young patients who do not have any contraindications for anticoagulation, and these valves are associated with good long-term durability.

Patients who have chronic atrial fibrillation and who undergo mitral valve surgery can have simultaneous Cox Maze procedure or pulmonary vein ablation, which helps to maintain sinus rhythm in up to 80% of the cases during the postoperative period.

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Consultations

Key members of a multidisciplinary team for structural heart valve disease management include primary cardiologists, interventional cardiologists, cardiac surgeons, noninvasive and heart failure cardiologists, echocardiographers and cardiac imaging specialists, cardiac anesthesiologists, nurse practitioners, physician assistants, research coordinators, administrators, dietary and rehabilitation specialists, and social workers. Each component will need to develop and implement specific protocols depending on the individual patient and specific technical procedure.[15]

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Contributor Information and Disclosures
Author

Claudia Dima, MD, FACC Interventional Cardiology

Disclosure: Nothing to disclose.

Coauthor(s)

Kenneth B Desser, MD &#0134; Former Clinical Professor, Director of Cardiology Fellowship, Banner Good Samaritan Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association, Heart Rhythm Society, Alaska State Medical Association, American College of Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Additional Contributors

L Michael Prisant, MD, FACC, FAHA Cardiologist, Emeritus Professor of Medicine, Medical College of Georgia, Georgia Regents University

L Michael Prisant, MD, FACC, FAHA is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Clinical Pharmacology, American College of Forensic Examiners Institute, American College of Physicians, American Heart Association, American Medical Association

Disclosure: Received honoraria from Boehringer-Ingelheim for speaking and teaching.

Acknowledgements

The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors Holger P Salazar, MD, Senthil Nachimuthu, MD, FACP, and Kiruthika Balasundaram, MBBS, to the development and writing of this article.

References
  1. Iwataki M, Takeuchi M, Otani K, et al. Calcific extension towards the mitral valve causes non-rheumatic mitral stenosis in degenerative aortic stenosis: real-time 3D transoesophageal echocardiography study. Open Heart. 2014. 1(1):e000136. [Medline]. [Full Text].

  2. Marcus RH, Sareli P, Pocock WA, et al. The spectrum of severe rheumatic mitral valve disease in a developing country. Correlations among clinical presentation, surgical pathologic findings, and hemodynamic sequelae. Ann Intern Med. 1994 Feb 1. 120(3):177-83. [Medline].

  3. Henri C, Pierard LA, Lancellotti P, Mongeon FP, Pibarot P, Basmadjian AJ. Exercise Testing and Stress Imaging in Valvular Heart Disease. Can J Cardiol. 2014 Sep. 30(9):1012-1026. [Medline].

  4. Wunderlich NC, Beigel R, Siegel RJ. Management of mitral stenosis using 2D and 3D echo-Doppler imaging. JACC Cardiovasc Imaging. 2013 Nov. 6(11):1191-205. [Medline].

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

  6. Schlosshan D, Aggarwal G, Mathur G, Allan R, Cranney G. Real-time 3D transesophageal echocardiography for the evaluation of rheumatic mitral stenosis. JACC Cardiovasc Imaging. 2011 Jun. 4(6):580-8. [Medline].

  7. [Guideline] Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline 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. J Am Coll Cardiol. 2014 Jun 10. 63(22):e57-185. [Medline]. [Full Text].

  8. [Guideline] Gerber MA, Baltimore RS, Eaton CB, Gewitz M, Rowley AH, Shulman ST, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. 2009 Mar 24. 119(11):1541-51. [Medline].

  9. Antonini-Canterin F, Moura LM, Enache R, Leiballi E, Pavan D, Piazza R. 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].

  10. [Guideline] Nishimura RA, Carabello BA, Faxon DP, et al. ACC/AHA 2008 Guideline update on valvular heart disease: focused update on infective endocarditis: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008 Aug 19. 52(8):676-85. [Medline].

  11. [Guideline] Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease (version 2012): The Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2012 Oct. 33(19):2451-96. [Medline].

  12. Wann LS, Curtis AB, Ellenbogen KA, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran): a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol. 2011 Mar 15. 57(11):1330-7. [Medline].

  13. Feldman T. Rheumatic Mitral Stenosis. Curr Treat Options Cardiovasc Med. 2000 Apr. 2(2):93-104. [Medline].

  14. Rahimtoola SH. Choice of Prosthetic Heart Valve in Adults An Update. J Am Coll Cardiol. 2010 Jun 1. 55(22):2413-2426. [Medline].

  15. Holmes DR Jr, Mack MJ. Transcatheter valve therapy a professional society overview from the american college of cardiology foundation and the society of thoracic surgeons. J Am Coll Cardiol. 2011 Jul 19. 58(4):445-55. [Medline].

  16. Horstkotte D, Niehues R, Strauer BE. Pathomorphological aspects, aetiology and natural history of acquired mitral valve stenosis. Eur Heart J. 1991 Jul. 12 Suppl B:55-60. [Medline].

 
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M-mode across the mitral valve showing a flat E-F slope resulting from elevated left atrial pressure throughout diastole due to a significant gradient across the mitral valve. Increased thickness and calcification of anterior leaflet of the mitral valve and decreased opening of the anterior and posterior leaflets in diastole are also shown.
Parasternal long-axis view demonstrating calcification and doming in diastole of the anterior valve leaflet and mild restriction in the opening of posterior mitral valve leaflet.
Apical 4-chamber view demonstrating restricted opening of the anterior and posterior mitral valve leaflet with diastolic doming of anterior leaflet with left atrial enlargement.
Transesophageal echocardiogram with continuous wave Doppler interrogation across the mitral valve demonstrating an increased mean gradient of 16 mm Hg consistent with severe mitral stenosis.
Apical 4-chamber view with color Doppler demonstrating aliasing in the atrial side of the mitral valve consistent with increased gradient across the valve. This figure also shows mitral regurgitation and left atrial enlargement.
Magnified view of the mitral valve in apical 4-chamber view revealing restricted opening of both leaflets.
Transesophageal echocardiogram in an apical 3-chamber view showing calcification and doming of the anterior mitral leaflet and restricted opening of both leaflets.
Transesophageal echocardiogram in an apical 3-chamber view with color Doppler interrogation of the mitral valve revealing aliasing, which is consistent with increased gradient across the mitral valve secondary to stenosis. Also shown in this image, a posteriorly directed jet of severe mitral regurgitation.
Table 1. Duration of Secondary Rheumatic Fever Prophylaxis
Category Duration After Last Attack Rating*
Rheumatic fever with carditis and residual heart disease (persistent valvular disease† ) 10 y or until age 40 y (whichever is longer); sometimes lifelong prophylaxis IC
Rheumatic fever with carditis but no residual heart disease (no valvular disease† ) 10 y or until age 21 y (whichever is longer) IC
Rheumatic fever without carditis 5 y or until age 21 y (whichever is longer) IC
*Rating indicates classification of recommendation and level of evidence (eg, IC indicates Class I, level of Evidence C).



†Clinical or echocardiographic evidence.



Table 2. Secondary Prevention of Rheumatic Fever (Prevention of Recurrent Attacks)
Agent Dose Mode Rating*
Benzathine penicillin G Children 27 kg (60 lb): 600,000 U



Patients >27 kg: 1,200,000 every 4 wk†



Intramuscular IA
Penicillin V 250 mg bid Oral IB
Sulfadiazine Children 27 kg: 0.5 g qd



Patients >27 kg: 1 g qd



Oral IB
Macrolide or azalide (for individuals allergic to penicillin and sulfadiazine) Variable Oral IC
*Rating indicates classification of recommendation and level of evidence (eg, IA indicates Class I, level of Evidence A).



†In high-risk situations, administration every 3 weeks is justified and recommended.



Table 3. Primary Prevention of Rheumatic Fever (Treatment of Streptococcal Tonsillopharyngitis*)
Agent Dose Mode Duration Rating
Penicillins
Penicillin V (phenoxymethyl penicillin) Children 27 kg (60 lb): 250 mg bid or tid



Patients >27 kg: 500 mg bid or tid



Oral 10 d IB
Amoxicillin 50 mg/kg qd (maximum 1 g) Oral 10 d IB
Benzathine penicillin G Children 27 kg (60 lb): 600,000 U



Patients >27 kg: 1,200,000 U



Intramuscular Once IB
For individuals allergic to penicillin
Narrow-spectrum cephalosporin (cephalexin, cefadroxil) Variable Oral 10 d IB
Clindamycin 20 mg/kg/d divided in 3 doses (maximum 1.8 g/d) Oral 10 d IIaB
Azithromycin 12 mg/kg qd (maximum 500 mg) Oral 5 d IIaB
Clarithromycin 15 mg/kg/d divided bid (maximum 250 mg bid) Oral 10 d IIaB
*Sulfonamides, trimethoprim, tetracyclines, and fluoroquinolones are not acceptable.



† Rating indicates classification of recommendation and level of evidence (eg, IB indicates Class I, level of Evidence B)



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