Wajahat MIRZA MD,
Mahvash AMER MBBS.


Mitral stenosis is a condition in which the mitral valve leaflets become thickened and the commissures fused along with thickening and shortening of the chordae tendineae. Mitral Stenosis is the leading cause of congestive heart failure in developing countries.

Mitral stenosis is almost always the result of rheumatic fever 1. Isolated involvement of mitral valve occurs in 25% of cases 2 while an additional 40% case have combined mitral stenosis and regurgitation 3. The history of rheumatic fever may or may not be elicited. In patients with rheumatic fever antibiotic prophylaxis with benzathine penicillin or penicillin VK has been shown to prevent recurrence. 4,5. Less common causes include congenital mitral stenosis 6, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), atrial myxoma, malignant carcinoid 7 and bacterial endocarditis. (Table 1)



Pure mitral stenosis (MS) develops in approximately 40% of all patients with rheumatic heart disease. After an episode of rheumatic fever, the latency period is 10-20 years or more before the onset of symptoms. The hall mark of mitral stenosis is comissural fusion 8. The normal area of the mitral valve orifice is 4-6 sq. cm. When this orifice is reduced to 2, increased left atrial pressure (LAP) is necessary for normal transmitral flow. Critical MS occurs when the opening is reduced to 1 sq. cm. At this stage, elevated left atrial pressure (LAP) is required to maintain a normal cardiac output 9 . This increase in LAP raises pulmonary venous and capillary pressures,12 resulting in exertional dyspnea. As the disease progresses, chronic elevation of LAP leads to pulmonary hypertension, tricuspid and pulmonary incompetence and eventual right heart failure.

Progressive dilation of the left atrium predisposes to two further complications 9. One is the development of mural thrombi. These thrombi embolize in 20% of patients. Patients at high risk for embolization are: over 35 years old, those with atrial fibrillation with a low cardiac output and those having a large left atrial appendage. The other significant complication is the development of atrial fibrillation (Afib) which occurs in up to 40% of patients. Loss of atrial contraction with the development of Afib decreases cardiac output by 20%. Since cardiac output is related to heart rate, Afib with a rapid ventricular response decreases diastolic filling time and further compromises cardiac output. The left ventricular function is often normal 11.


In the U.S.: The prevalence of MS has decreased due to the decline in rheumatic fever in the US and developed countries. The mitral valve is the valve most commonly affected with rheumatic heart disease.

Internationally: In underdeveloped areas, MS tends to progress more rapidly. Occasionally, patients can become symptomatic before the age of 20.

Mortality/Morbidity: Without surgical intervention, the progressive nature of the disease

results in an 85% mortality rate twenty years after the onset of symptoms.

Sex: Two-thirds of all patients with MS are female.

Age: The onset of symptoms is usually between the third and fourth decades.

Natural History:

Mitral Stenosis is a progressive disease in most patients. As depicted in figure below an average of 19 years elapses before the onset of dyspnea.


Recognised MS                   Dyspnea         Valve Replacement/PMBV

I--------------------I-------------------I------------------I------------------I Death

Rheumatic Fever

0 ------------Time in years--------19


Before the surgical era the outlook for patients with this disease was unfavourable. From 1925 Rowe et al 17studied 250 patients with mitral stenosis. By 10 years 39% of patients had died, 22% had become more dyspneic, and 16% had developed at least one thromboembolic complication. By 20 years, 79% had died 8% had become more symptomatic, and 26% had developed at least one thromboembolic event. Progression of disease is the rule at least in the symptomatic group. The younger patients follow a more benign course then their old counter parts .


The diagnosis of mitral stenosis is suspected on history and confirmed by physical examination, electrocardiography and echocardiography. Cardiac catheterization may aid the diagnosis and treatment in selected individuals.



The physical exam findings depend on how advanced the disease is and the degree of underlying cardiac decompensation.


Aortic Regurgitation

  • May give diastolic murmur and left sided failure but left ventricle is enlarged and murmur is usually parasternal and high pitched

Chronic Obstructive Pulmonary Disease and Emphysema

  • May have cyanosis and edema, and can occur with MS, Patients with MS are frequently diagnosed as asthmatics.

Other Problems to be Considered

  • Atrial Myxoma

Laboratory Studies:

Complete blood count (CBC), in cases of hemoptysis and to rule out anemia

Blood culture, in cases of suspected endocarditis


Imaging Studies:

Chest X-Ray (CXR):

    1. Prominence of pulmonary arteries,
    2. Enlargement of right ventricle and
    3. Evidence of CHF (interstitial edema with kerley B lines).

Electrocardiogram (EkG):



Transthoracic two dimensional echocardiography is the most sensitive and specific non-invasive method for diagnosing mitral stenosis 25. With 2 dimensional echocardiography mitral valve area can be calculated using different techniques. With two dimensional ECHO, the size of the mitral orifice can be measured along with cardiac chamber sizes. The addition of color Doppler can evaluate the transvalvular gradient, pulmonary artery pressure and accompanying mitral regurgitation 22. Different methods used for mitral valve area assessment 20 are in Table 2







Direct measurement

measurement in short axis view

most reliable, operator dependant

Pressure half time

(P ½ )

P ½ =0.29 x Deceleration time

*MVA= 220/ P ½ time

Unreliable in conditions with elevated left ventricle end diastolic pressure

Continuity Equation

assumption blood flow through different valves is equal


D2 LVOT x 0.785x TVI LVOT


In regurgitant lesions reliability decreases

PISA (Proximal Isovelocity Surface Area)

MVA= 2 x 3.14 r 2 x V1

Very reliable, operator dependant

*= mitral valve area


Two dimensional echocardiography is also useful in qualitative assessment of the valve. It can also be used to assess whether the valve is suitable for percutaneous mitral balloon valvuloplasty. An MGH (Massachusetts General Hospital) score of greater then 8-10 signify a poor outcome. Please see table 3 for MGH criteria



Leaflet Mobility

Leaflet thickening


Subvalvular Apparatus

Transesophageal echocardiography (TEE) is useful for detecting vegetations smaller than 5 mm or thrombi in the left atrium not seen with transthoracic echocardiography.


Cardiac Catheterization:


Males with age greater than 35 years

Post menopausal females

Positive risk factors

History of illicit cocaine use

Prior PMBV (Percutaneous Mitral Balloon Valvuloplasty

Strong clinical suspicion of coronary artery disease


Hemodynamic findings at the time of catheterization may include 12:


Emergency Department Care: 24,26,27,28

Upright posture

Rate Control:

Diuresis for signs of pulmonary edema



Cardiology Consult:

For known or suspected mitral stenosis with hemodynamic instability, arrhythmia or embolization.

For new onset or progression of symptoms.


The goal of medical therapy is to control the rapid ventricular rate. In atrial fibrillation, the drug of choice is digitalis, however, a beta-blocker or calcium channel blocker may need to be added.

Cardiac Glycosides - These agents alter the electrophysiologic mechanisms responsible for arrhythmia. 

Drug Name Digoxin (Lanoxin) -

It is the drug of choice for rapid atrial fibrillation. It is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the Cardiovascular system. Its effects on the myocardium involve both a direct action on cardiac muscle that increases myocardial systolic contractions and indirect actions that result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Adult Dose

Loading dose: 0.25 mg IV q6 up to 1 mg

Maintenance dose: 0.125 mg-0.25 mg qd

Pediatric Dose

Between 2-5 y: Load 30-40 ug/kg PO

Between 5-10 y: Load 20-35 ug/kg PO

Older than 10 y: Load 10-15 ug/kg PO

IV doses are 80% of po doses Maintenance dosing is 25-35% of po loading doses


Avoid use in patients with documented hypersensitivity to this medication or related products and those diagnosed with beriberi heart disease, idiopathic hypertrophic subaortic stenosis, or constrictive pericarditis, or carotid sinus syndrome. 


Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate,erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil.

Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid.


C - Safety for use during pregnancy has not been established.


Exercise caution in patients with renal insufficiencies, and electrolyte abnormalities

Hypokalemia may reduce the positive inotropic effect of digitalis.

Calcium, if administered IV, may produce arrhythmias in digitalized patients. Hypercalcemia predisposes the patient to digitalis toxicity and hypocalcemia can make digoxin ineffective until serum calcium levels are normal.

Magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity. Patients diagnosed with incomplete A-V Block may progress to complete block when treated with digoxin. Exercise caution in patients diagnosed with hypothyroidism, hypoxia, and acute myocarditis. 


Beta-Blockers - Inhibit chronotropic, inotropic and vasodilatory responses to beta-adrenergic stimulation.

Drug Name

Metoprolol (Lopressor) - It is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions.

During IV administration, carefully monitor blood pressure, heart rate and ECG.

Adult Dose

5 mg IV and repeat in 10 min up to 15 mg

Pediatric Dose

Safety and efficacy in children have not been established.


Avoid use in patients with documented hypersensitivity to this drug or related products and those diagnosed with  uncompensated congestive heart failure, bradycardia, asthma, cardiogenic shock, and A-V conduction abnormalities.


Aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease its  bioavailability and plasma levels, possibly resulting in a decreased pharmacologic effect. Conversely, haloperidol, hydralazine, loop diuretics, and MAO inhibitors may increase metoprolol levels and thus its toxicity or pharmacologic effects.


C - Safety for use during pregnancy has not been established.


Beta-adrenergic blockade may reduce the signs and symptoms of acute hypoglycemia and may decrease the clinical signs of hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid  storm. Monitor the patient closely and withdraw the drug slowly.

During the IV administration, carefully monitor blood pressure, heart rate, and ECG.

Calcium Channel Blocker - In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers inhibit movement of calcium ions across the cell membrane depressing both impulse formation (automaticity) and conduction velocity. 

Drug Name

Diltiazem (Cardizem CD, Cardizem SR, Tiazac, and Dilacor) - During the depolarization, it inhibits the calcium ion from entering the slow channels or the voltage-sensitive areas of the vascular smooth muscle and myocardium.

Adult Dose

0.25 mg/kg IV over 2 min.

Rebolus after 15 min if needed with 0.35 mg/kg.

Pediatric Dose

Safety and efficacy in children have not been established.


Avoid use in patients with documented hypersensitivity to this drug or related products and in those diagnosed with severe CHF, sick sinus syndrome or second- or third-degree AV block, and hypotension (less than 90 mm Hg systolic).


Diltiazem may increase carbamazepine, digoxin, and cyclosporine levels when administered concurrently. Diltiazem, when administered concurrently with amiodarone, can cause bradycardia and a decrease in cardiac output. Similarly, diltiazem when administered concurrently with beta blockers may increase cardiac depression.

Cimetidine may increase diltiazem levels.

Diltiazem may increase theophylline levels.


C - Safety for use during pregnancy has not been



Exercise caution when administering to patients with impaired renal or hepatic function. Diltiazem may increase LFTs and hepatic injury may occur.

Further Inpatient Care:


Bacterial endocarditis prophylaxis for dental and invasive procedures must be continued for life. Appropriate treatment of streptococcal pharyngitis to lessen the occurrence of rheumatic fever should be instituted promptly. Prophylaxis against recurrent streptococcal infection (and recurrent rheumatic fever) in patients with a history of rheumatic fever should be given for at least 25 years



Medical/Legal Pitfalls:

Severity of disease is underestimated during periods of tachycardia because a decrease in cardiac output leads to a decrease in the intensity of the murmur. Failure to give patients with mitral valve disease antibiotic prophylaxis for beta-hemolytic streptococcal infections and prophylaxis for infective endocarditis. Failure to aggressively treat anemia or infections in patients with MS.



  1. Kinkare, S.G. and Kulkarni, H.L. : Quantitative study of mitral valve in chronic rheumatic heart disease. Int. J. Cardiology. 16:271, 1987

  2. Hortskotte, D. Niehues, R., and Strauer, B.E.: Pathomorphological aspects, aetiology and natural history of acquired mitral valve stenosis. Eur. Heart J. 12:55, 1991

  3. Braunwald E., Valvular heart disease 4th ed. E. Braunwald (ed). Philaedelphia, Saunders, 1992, p1007

  4. Taranta A., Kleinberg E., Feinstein, AR, : A long term epidemiologic study of subsequent prophylaxis, streptococcal infections and clinical sequalae Ann. Intern. Med. (suppl 5):47-57, 1964.

  5. Taranta A., Kleinberg E., Feinstein, AR,: Rheumatic fever in children and adolescents. Relationship of the rheumatic rate per streptococcal infections to pre-existing clinical features of patients. Ann. Int. Med. (suppl 5): 58-67, 1964

  6. Ruckman, R. N., and Van Praagh, R.: Anatomic types of congenital mitral stenosis: Report of 49 autopsy cases with consideration of diagnostic and surgical implications. Am. J. Cardiol. 42:592, 1978

  7. Roberts, W.C., Sjoerdsma, A.: The cardiac diseases associated with carcinoid syndrome (carcinoid heart disease). Am. J. Med. 36:5-34. 1964

  8. Waller, B. F., : Rheumatic and non rheumatic conditions producing valvular heart disease. In Frankl, W.S., and Brest, A. N., (eds): Cardiovascular clinics. Valvular Heart Disease: Comprehensive evaluation and management. Philaedelphia, F.A. Davis, 1986, pp. 3-104.

  9. Meisner, J.S., Keren G., Pajaro, O.E., Mani A. et al: Atrial contribution to ventricular filling in mitral stenosis. Circulation 84: 1469-1480, 1991

  10. Beyer, R.W., Olmos A, Bermudez RF, Noll HE, Mitral valve resistance as a hemodynamic indicator in mitral stenosis. Am. J. Card. 69: 775-779, 1992

  11. Gaasch WH, Folland ED: Left ventricular function in rheumatic mitral stenosis. Eur Heart J 12 (suppl B): 66-69, 1991

  12. Abbo KM, Caroll JD, Hemodynamics of mitral stenosis: A review. Cathetrization and Cardiovascular Diagnosis, Suppl. 2:16-25, 1994

  13. Barrington WW, Bashore T, Wooley CF: Mitral Stenosis Mitral dome excursion at M1 and mitral opening snap - The concept of reciprocal heart sounds. Am. Heart J. 115:1280-90, 1988

  14. Ebringer R, Pitt A, Anderson ST, Hemodynamics factors inflencing opening snap interval in mitral stenosis. British Heart Journal, 32:350-354, 1970

  15. Cooksey JD, Dunn M, Massie E, Clinical vectorcardiography and electrocardiography. 2nd ed. Chicago, Year book publishers, 1977. P272

  16. Cueto J, Toshima J, Et al: Vectorcardiographic studies in acquired valvular heart disease with reference to diagnosis of right ventricular hypertrophy. Circulation 33: 588, 1967

  17. Row JC, Bland EF, Sprague HB, Ehite PD: The course of mitral stenosis without surgery: ten and twenty year perspectives. Ann Intern Med 52:741, 1960

  18. Wilkins GT, Weyman AE, Abascal VM, Block PC, Palacios IF. Percutaneous balloon dilatation of the mitral valve-an analysis of echocardiographic variables related to outcome and the mechanism of dilatation. Br Heart J 1988; 60: 299-308.

  19. Smith AD, Handshoe R, Handshoe S, et al: Comparative accuracy of two dimensional echocardiography and Doppler pressure half time methods in assessing severity of mitral stenosis in patients with and without prior commissurotomy. Circulation 73:100, 1986.

  20. Feigenbaum H, Echocardiography in Heart Disease, 4th ed, Philadelphia, Saunders, 1992, p81.

  21. Abernathy W, Willis P: Thromboembolic Complications of Rheumatic Heart Disease. Cardiovasc Clin 1973; Vol 5: P.131-175.

  22. Bortolotti U, Valente M, Agozzino L: Rheumatoid Mitral Stenosis Requiring Valve Replacement. Am Heart J 1984; Vol 107: P.1049

  23. Braunwald E: Valvular Heart Disease. Heart Disease: A Text of Cardiovascular Medicine 1997; Vol 2: P.1007-1017.

  24. Braunwald E: Valvular Heart Disease. Harrison's Principles of Internal Medicine 1991;P.938-942.

  25. Duchak J, Chang S, Feigenbaum H: The Posterior Mitral Valve ECHO and the Echocardiographic diagnosis of Mitral Stenosis. Am J Cardio 1972; Vol 29: P.628-632.

  26. Dunmire S, Ahrens B: Endocarditis and Acquired Valvular Heart Disease. Emergency Medicine Concepts and Clinical Practice 1992; Vol 2: P.1492-1493.

  27. Gassach W, O'Rourke R, Cohn L: Mitral Valve Disease. The Heart Arteries and Veins 1994; 8th Ed: P.1483-1491.

  28. Janz T: Valvular Heart Disease: Clinical approach to acute decompensation of left-sided lesions. Ann Emerg Med 1988; 17: P.201.

  29. Kern M, Lewis L: Valvular Heart Disease. Principles and Practice of Emergency Medicine 1992; Vol 1: P.1313-1328.

  30. Ornato J: Valvular Heart Disease. The Clinical Practice of Emergency Medicine 1996;p 612-616.



1) Segal BL; Likoff W; Kingsley B. Echocardiography: Clinical application in mitral stenosis. JAMA, 193:161, 1966. Early description of the M-mode findings for mitral stenosis.

2) Nichol PM; Gilbert BW; Kisslo JA. Two-dimensional echocardiographic assessment of mitral stenosis. Circulation, 55:120, 1977. Initial article detailing the advantage of two-dimensional echocardiography in assessing the presence and severity of rheumatic mitral stenosis.

3) Holen J; Aaslid R; Landmark K; Simonsen S. Determination of pressure gradient in mitral stenosis with a non-invasive ultrasound Doppler technique. Acta Med Scand 199:455-460, 1976. Original description of Doppler measurement of transmitral pressure gradients.

4) David D; Lang RM; Marcus RH; et al. Doppler echocardiographic estimation of transmitral pressure gradients in mitral stenosis. Am J Cardiol 67:1161-1164, 1991. Detailed study of pressure-velocity relations across the stenotic mitral valve.

5) Libanoff AJ; Rodbard S. Evaluation of the severity of mitral stenosis and regurgitation. Circulation 33:218-226, 1966. Original description of pressure half-time with catheterization data.

6) Hatle L; Angelsen B; Tromsdal A. Non-invasive assessment of atrioventricular pressure half-time by Doppler ultrasound. Circulation 60:1096-1104, 1979. Application of pressure half-time concept to Doppler data.

7) Thomas JD; Wilkins GT; Choong CYP; et al. Inaccuracy of mitral pressure half- time immediately after percutaneous mitral valvotomy: Dependence on transmitral gradient and left atrial and ventricular compliance. Circulation 78:980-993, 1988. Evaluation of pressure half-time before and after mitral balloon commissurotomy illustrating reciprocal changes in left atrial and left ventricular compliance after valvuloplasty.

8) Rodriguez L. Validation of the proximal flow convergence method: Calculation of orifice area in patients with mitral stenosis. Circulation, in press. Application of the PISA method to determine mitral valve area.

9) Nakatani S; Masuyama T; Kokama K; Kitabatake A; Fujii K; Kamada T. Value and limitations of Doppler echocardiography in the quantification of stenotic mitral valve area: Comparison of the pressure half-time and the continuity equation methods. Circulation, 77-78, 1988. Important article describing the utility of the continuity equation to determine mitral valve area in rheumatic mitral stenosis.

10) Braverman AC; Thomas HD; Lee RT. Doppler echocardiographic estimation of mitral valve area during changing hemodynamic conditions. The article explains the effect of exercise on Doppler values of peak velocity, pressure half-time and mitral valve area as determined by the continuity equation and pressure half-time methods.




Keren G; Pardes A; Miller HI; Scherez H; Laniado S. Pulmonary venous flow determined by Doppler echocardiography in mitral stenosis. Am J Cardiol 65:246, 1990.


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First published 27.3.2000

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