Mitral Stenosis Clinical Presentation

  • Author: Claudia Dima, MD; Chief Editor: Richard A Lange, MD   more...
 
Updated: Nov 1, 2010
 

History

  • Symptoms of mitral stenosis usually manifest during the third or fourth decade of life and nearly half of the patients do not recall a history of acute rheumatic fever.
  • Patients are generally asymptomatic at rest during the early stage of the disease. However, factors that increase heart rate such as fever, severe anemia, thyrotoxicosis, exercise, excitement, pregnancy, and atrial fibrillation may result in dyspnea.
  • Nearly 15% of patients develop embolic episodes that are usually associated with atrial fibrillation. Rarely, embolic episodes may occur even in the patient with sinus rhythm. Systemic embolization may lead to stroke, renal failure, or myocardial infarction.
  • Hoarseness can develop from compression of the left recurrent laryngeal nerve against the pulmonary artery by the enlarged left atrium. Also, compression of bronchi by the enlarged left atrium can cause persistent cough.
  • Hemoptysis may occur and is usually not fatal.
  • Pregnant women with mild mitral stenosis may become symptomatic during their second trimester because of the increase in blood volume and cardiac output.
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Physical

  • Presence of mitral facies (pinkish-purple patches on the cheeks) indicate chronic severe mitral stenosis leading to reduced cardiac output and vasoconstriction.
  • Jugular vein distension may be seen. In the patient with sinus rhythm, a prominent a wave reflects increased right atrial pressure from pulmonary hypertension and right ventricular failure. A prominent v wave is seen with tricuspid regurgitation.
  • The apical impulse may be laterally displaced or not palpable, especially in cases of severe mitral stenosis. This can be explained by decreased left ventricular filling. Rarely, a diastolic thrill can be felt at the apex with the patient in the left lateral recumbent position. See the videos below.
    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.
    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.
  • Often a right ventricular lift is palpable in the left parasternal region in the patient with pulmonary hypertension. A P 2 may be palpable in the 2nd left intercostal space.
  • The auscultatory findings characteristic of mitral stenosis are a loud first heart sound, an opening snap, and a diastolic rumble.
    • The first heart sound is accentuated because of a wide closing excursion of the mitral leaflets. The degree of loudness of the first heart sound depends on the pliability of the mitral valve. The intensity of the first heart sound diminishes as the valve becomes more fibrotic, calcified, and thickened.
    • The second heart sound is normally split, and the pulmonic component is accentuated if pulmonary hypertension is present. The opening snap follows the second heart sound. The sudden tensing of the valve leaflets after they have completed their opening excursion causes an opening snap. In patients with elevated left atrial pressure and hence with severe mitral stenosis, the opening snap occurs closer to the second heart sound.
    • The diastolic murmur of mitral stenosis is of low pitch, rumbling in character, and best heard at the apex with the patient in the left lateral position. It commences after the opening snap of the mitral valve, and the duration of the murmur correlates with the severity of the stenosis. The murmur is accentuated by exercise, whereas it decreases with rest and Valsalva maneuver. In patients with sinus rhythm, the murmur increases in intensity during late diastole (so called, presystolic accentuation) due to increased flow across the stenotic mitral valve caused by atrial contraction.
  • A high-pitched decrescendo diastolic murmur secondary to pulmonary regurgitation (Graham Steell murmur) may be audible at the upper sternal border.
  • A pansystolic murmur of TR and an S 3 originating from the right ventricle may be audible in the 4th left intercostal space in the patient with right ventricular dilatation.
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Causes

See Background.

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Contributor Information and Disclosures
Author

Claudia Dima, MD  Cardiovascular Fellow, Department of Cardiology, Banner Good Samaritan Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Kenneth B Desser, MD  Clinical Professor, Director of Cardiology Fellowship, Banner Good Samaritan Medical Center, Phoenix, Arizona

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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, American College of Physicians, American Heart Association, and American Medical Association

Disclosure: Boehringer-Ingelheim Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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

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

Disclosure: Nothing to disclose.

Amer Suleman, MD  Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD  Professor and Executive Vice Chairman, Department of Medicine, Director, Office of Educational Programs, University of Texas Health Science Center at San Antonio

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

Disclosure: Nothing to disclose.

References

  1. 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. Feb 1 1994;120(3):177-83. [Medline].

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

  3. [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. Mar 24 2009;119(11):1541-51. [Medline].

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

  5. [Guideline] Nishimura RA, Carabello BA, Faxon DP, Freed MD, Lytle BW, O'Gara PT. 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. Aug 19 2008;52(8):676-85. [Medline].

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

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

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

  9. [Guideline] 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. J Am Coll Cardiol. Sep 23 2008;52(13):e1-142. [Medline].

  10. Bonow RO, Otto CM. Valvular heart disease. In: Libby P, Bonow RO, Mann DL, Zipes DP. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 2. 8th ed. Philadelphia, PA: WB Saunders; 2008:1646-1657.

  11. Carabello BA. Modern management of mitral stenosis. Circulation. Jul 19 2005;112(3):432-7. [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
CategoryDuration After Last AttackRating*
Rheumatic fever with carditis and residual heart disease (persistent valvular disease† )10 y or until age 40 y (whichever is longer); sometimes lifelong prophylaxisIC
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 carditis5 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)
AgentDoseModeRating*
Benzathine penicillin GChildren 27 kg (60 lb): 600,000 U



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



IntramuscularIA
Penicillin V250 mg bidOralIB
SulfadiazineChildren 27 kg: 0.5 g qd



Patients >27 kg: 1 g qd



OralIB
Macrolide or azalide (for individuals allergic to penicillin and sulfadiazine)VariableOralIC
*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*)
AgentDoseModeDurationRating †
Penicillins
Penicillin V (phenoxymethyl penicillin)Children 27 kg (60 lb): 250 mg bid or tid



Patients >27 kg: 500 mg bid or tid



Oral10 dIB
Amoxicillin50 mg/kg qd (maximum 1 g)Oral10 dIB
Benzathine penicillin GChildren 27 kg (60 lb): 600,000 U



Patients >27 kg: 1,200,000 U



IntramuscularOnceIB
For individuals allergic to penicillin
Narrow-spectrum cephalosporin (cephalexin, cefadroxil)VariableOral10 dIB
Clindamycin20 mg/kg/d divided in 3 doses (maximum 1.8 g/d)Oral10 dIIaB
Azithromycin12 mg/kg qd (maximum 500 mg)Oral5 dIIaB
Clarithromycin15 mg/kg/d divided bid (maximum 250 mg bid)Oral10 dIIaB
*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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