Mitral stenosis (MS) is a structural anomaly of the mitral valve resulting in a decreased cross-sectional area of the valve. The stenosis impairs blood flow from the left atrium to the left ventricle, progressively causing left atrial distension, pulmonary venous congestion, pulmonary hypertension, and congestive heart failure. MS is most commonly a complication of rheumatic fever and is slowly progressive. Patients typically remain asymptomatic for years until the mitral valve area becomes critically reduced. Patients with severe stenosis often present with atrial fibrillation and (dyspnea, fatigue, orthopnea). Asymptomatic patients are initially managed conservatively and the mitral valve is regularly monitored with transthoracic echocardiography. Once symptoms develop or the valve area decreases to 1.5 cm2, percutaneous valvuloplasty or surgical intervention may be considered. Occasionally, patients with MS have heart failure secondary to tachycardia or increased cardiac demand and require urgent medical management.
- Most commonly due to
- Calcification of the mitral valve annulus
- Autoimmune diseases: systemic lupus erythematosus, rheumatoid arthritis
- Some conditions may mimic mitral stenosis: bacterial endocarditis of the mitral valve with large vegetation, left atrial myxoma
- Degenerative aortic stenosis
|American College of Cardiology/American Heart Association stages of mitral stenosis |
|Stage||Definition||Symptoms||Mitral valve area (cm2)||Associated findings|
|A|| || || || |
|B|| || |
|C|| || |
|D|| || || |
- Mitral valve stenosis → obstruction of blood flow into the left ventricle (LV) → limited diastolic filling of the LV (↓ end-diastolic LV volume) → decreased stroke volume → decreased cardiac output (forward heart failure)
- Mitral valve stenosis → increase in left atrial pressure → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary edema → pulmonary hypertension → backward heart failure and right ventricular hypertrophy
Patients with MS typically progress over many years from being asymptomatic to having symptoms of profound heart failure. Acute symptoms may occur in patients with or an increased cardiac output secondary to pregnancy, sepsis, or exercise.
- Symptoms of embolic disease (e.g., stroke, mesenteric ischemia)
- Later stages
Examination findings 
- Mitral facies
- Sequelae of embolic disease (e.g., focal neurologic deficits, cool and cyanotic extremity)
- Irregular heart rhythm secondary to atrial fibrillation
- pitting edema , bibasilar rales , e.g., lower limb
Auscultation (see “ ”)
- Diastolic murmur heard best at the 5th left intercostal space at the midclavicular line (the apex)
- Loud first heart sound (S1)
- Opening snap
- A shorter interval between S2 and opening snap indicates more severe disease; occurs because left atrial pressure is greater than left ventricular end-diastolic pressure (LVEDP).
- All patients with suspected mitral stenosis should undergo transthoracic echocardiography (TTE).
- Chest x-ray and ECG may show characteristic changes depending on the stage and extent of disease.
- Laboratory studies are typically nonspecific, although they may support a diagnosis of associated heart failure.
Transthoracic echocardiography (TTE) 
- TTE is the most important test for diagnosing and guiding the treatment of mitral stenosis.
- Characteristic findings include:
- MVA, valve pressure gradient, and presence or absence of symptoms and pulmonary artery hypertension are used to grade the severity of disease.
- Often normal
- Characteristic findings include:
Chest x-ray (PA and lateral views) 
Left atrial enlargement
- The main bronchi appear elevated and have > 90% angulation (splayed).
- Straightening or convexity of the left cardiac border
- Double density sign
- X-ray features of right ventricular enlargement 
- BNP or NT-proBNP: Levels increase in proportion to disease severity. 
- CBC: Leukocytosis may indicate an underlying infectious (e.g., infective endocarditis) or inflammatory process.
- BMP: may demonstrate evidence of renal impairment 
- Liver chemistries: may show elevations secondary to
- CRP: suggests ongoing inflammation in rheumatic heart disease 
Additional evaluation 
Further studies are indicated in select patients when TTE findings are unclear or do not correlate with symptoms, or when an intervention is planned.
- Indicated to confirm the diagnosis if TTE examination is technically suboptimal
- Used prior to intervention to identify:
Stress testing 
- Useful when symptoms do not correlate with echocardiographic findings, e.g.:
- Exercise stress testing is preferred over pharmacological stress testing.
The following recommendations are for rheumatic MS. For all other causes of MS, early consultation with cardiology is recommended as treatment can vary significantly.
- Initial management
- General cardiac care and serial TTEs until signs or symptoms of disease progression occur 
- In case of acute heart failure: immediate medical stabilizations and treatment of the precipitating cause
- Indications for interventional management include:
- Symptomatic MS
- MVA decreasing to < 1.5 cm2
- New-onset pulmonary hypertension
- Abrupt onset of acute heart failure symptoms in patients with MS is usually secondary to tachycardia or increased cardiac output.
- Heart failure symptoms are managed using standard therapy, e.g., diuretics.
- Nitrates may reduce pulmonary congestion but should be used with caution (see “Management of acute heart failure” for further information and dosages). 
Patients with mitral stenosis often develop acute heart failure following the onset of atrial fibrillation. Rapid and progressive treatment of atrial fibrillation is necessary in patients with severe mitral stenosis.
Many patients with mild to moderate disease can be managed conservatively for years. Patients should remain under the care of cardiology with regular monitoring of valve function.
Serial TTE examinations 
- Serial TTEs are performed to monitor the progression of MS and guide the timing of interventions.
- Patients typically do not develop symptoms until they have severe disease.
- Early detection prevents irreversible cardiac changes.
- Asymptomatic patients
- Every 3–5 years if MVA is > 1.5 cm2
- Every 1–2 years if MVA is 1–1.5 cm2
- Annually if MVA is < 1 cm2
- TTE should be repeated earlier if symptoms develop or change.
Optimizing medical therapy 
- Patients should receive guideline-directed medical therapy (GDMT) for any concurrent heart failure.
- Screen for and treat all cardiac risk factors, e.g., diabetes, hyperlipidemia, and hypertension.
- Consider heart rate control (e.g., beta blockers) in younger patients in sinus rhythm with high resting or exercise-induced heart rates.
- Treat atrial fibrillation with rate control.
- Anticoagulation with a vitamin K antagonist (VKA) to a target INR of 2.5 is indicated if any of the following are present: 
- It is controversial whether anticoagulation is indicated for patients with MS who do not have one of the above features.
- For dosages, see “Anticoagulation in atrial fibrillation”.
- Infectious endocarditis (IE) prophylaxis 
- Management of rheumatic heart disease
Patients with severe or symptomatic MS should be considered for intervention.
- Asymptomatic patients with MVA ≤ 1.5 cm2 and either of the following:
- Symptomatic patients with:
- MVA ≤ 1.5 cm2
- MVA > 1.5 cm2 and hemodynamically significant MS on stress test
- Percutaneous mitral valve balloon commissurotomy (PMBC) 
- Surgical interventions include open commissurotomy and mitral valve (mechanical or bioprosthetic) replacement.
- Contraindicated if there is a prohibitively high surgical risk
- Atrial fibrillation → thromboembolic events
- Progressive congestion of the lungs, pulmonary edema, pulmonary hypertension
- Congestive heart failure
- Enlarged left atrium (rare) → esophageal compression, recurrent laryngeal nerve palsy
We list the most important complications. The selection is not exhaustive.