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Overview of the management of mitral stenosis

Overview of the management of mitral stenosis
Author:
William H Gaasch, MD
Section Editor:
Catherine M Otto, MD
Deputy Editor:
Susan B Yeon, MD, JD, FACC
Literature review current through: Feb 2022. | This topic last updated: Jun 18, 2020.

INTRODUCTION — Mitral stenosis (MS) is a condition characterized by obstruction of blood flow across the mitral valve from the left atrium to the left ventricle. The mechanical obstruction leads to increases in pressure within the left atrium, pulmonary vasculature, and right side of the heart. Most cases of MS are caused by rheumatic heart disease with mitral commissural adhesion; thickened, immobile mitral valve leaflets; and fibrosis, thickening, shortening, fusion, and calcification of the chordae tendineae. Infrequent causes of MS include mitral annular calcification and congenital MS (including parachute mitral valve). (See "Clinical manifestations and diagnosis of rheumatic mitral stenosis" and "Pathophysiology and natural history of mitral stenosis".)

The medical management and indications for intervention for MS will be reviewed here. Outcomes and management of patients undergoing percutaneous mitral balloon valvotomy and mitral valve surgery for MS are discussed separately. (See "Percutaneous mitral balloon valvotomy for mitral stenosis" and "Surgical and investigational approaches to management of mitral stenosis".)

MONITORING AND EVALUATION — Periodic monitoring is recommended in asymptomatic patients with MS to assess for disease progression and development of indications for intervention. For all patients, the follow-up should include yearly history and physical examination. Follow-up transthoracic echocardiography should be performed with frequency based upon the severity of disease. We agree with the 2014 American Heart Association/American College of Cardiology (AHA/ACC) valve guideline recommendation for echocardiography every three to five years if the mitral valve area (MVA) is >1.5 cm2, every one to two years if the MVA is 1.0 to 1.5 cm2, and once per year if the MVA is <1.0 cm2 [1,2]. The long interval between testing in asymptomatic, stable, mild disease is based in part upon the natural history of MS, as mitral valve area declines at a mean of approximately 0.1 cm2 per year (see "Pathophysiology and natural history of mitral stenosis", section on 'Rate of progression'). More frequent monitoring may be required in patients with concurrent mitral regurgitation and/or disease affecting other valves. All patients should undergo re-evaluation whenever there is a change in clinical status.

Monitoring and evaluation prior to and during pregnancy are discussed separately. (See "Pregnancy in women with mitral stenosis".)

The rationale for monitoring is to optimize timing of mitral valve intervention. The timing of surgical or percutaneous intervention for MS is crucial for the following reasons:

If performed too early, the patient may be put at unnecessary risk of a procedure-related complication with little or no benefit because MS (in the absence of intervention) may remain asymptomatic and stable for many years.

Delaying intervention may cause irreversible pulmonary hypertension and/or right heart failure. The risk of failure to receive necessary corrective intervention was illustrated in a report that included patients in whom valve surgery was indicated but refused [3]. Patient survival with medical therapy was 44 percent at five years, 32 percent at 10 years, and 19 percent at 15 years.

In patients who develop indications for mitral valve intervention, the feasibility of percutaneous mitral balloon valvotomy is assessed by using the Wilkins score and by characterization of commissural calcification. Other criteria for percutaneous mitral balloon valvotomy include absence of left atrial thrombus and lack of moderate to severe mitral regurgitation (MR). (See "Percutaneous mitral balloon valvotomy for mitral stenosis", section on 'Echocardiography'.)

INDICATIONS FOR INTERVENTION — Since MS is a mechanical disorder, its natural history is significantly altered with an improvement in mortality only by intervention with percutaneous mitral balloon valvotomy or surgery [4,5]. This section will discuss indications for intervention for MS. Additional issues related to indications for intervention in pregnant patients with MS and additional discussion of percutaneous mitral balloon valvotomy and mitral valve surgery in patients with MS are discussed separately. (See "Percutaneous mitral balloon valvotomy for mitral stenosis" and "Surgical and investigational approaches to management of mitral stenosis" and "Pregnancy in women with mitral stenosis".)

Our approach — We agree with the recommendations for mitral valve intervention for MS in the 2014 AHA/ACC valve guideline (figure 1 and table 1 and table 2) [1,2], which is similar to the approach in the 2012 ESC valve guidelines [6]. Criteria for valve morphology include the Wilkins score and the pattern of commissural calcification. (See "Percutaneous mitral balloon valvotomy for mitral stenosis", section on 'Echocardiography'.)

We recommend percutaneous mitral balloon valvotomy for symptomatic patients with severe MS (mitral valve area [MVA] ≤1.5 cm2, stage D) in patients with favorable valve morphology, absence of left atrial thrombus, and absence of moderate to severe or severe mitral regurgitation (MR).

We recommend mitral valve surgery (repair, commissurotomy, or valve replacement) in severely symptomatic patients (New York Heart Association [NYHA] class III or IV) with severe MS (MVA ≤1.5 cm2, stage D) who are not high risk for surgery and who are not candidates for or who have failed prior percutaneous mitral balloon valvotomy.

We suggest concomitant mitral valve surgery for patients with severe MS (MVA ≤1.5 cm2, stage C or D) undergoing cardiac surgery for other indications.

We suggest percutaneous mitral balloon valvotomy for asymptomatic patients with very severe MS (mitral valve area ≤1.0 cm2, stage C), favorable valve morphology, absence of moderate to severe MR, and no left atrial thrombus.

We suggest mitral valve surgery for severely symptomatic patients (NYHA class III to IV) with severe MS (MVA ≤1.5 cm2, stage D) who are candidates for percutaneous intervention but are undergoing surgery with cardiopulmonary bypass for other indications (eg, aortic valve disease, coronary artery disease, tricuspid regurgitation, aortic aneurysm).

We also suggest intervention for MS in selected patients in the following clinical settings, although supporting evidence is very limited:

We suggest percutaneous mitral balloon valvotomy for selected asymptomatic patients with severe MS (MVA ≤1.5 cm2, stage C) with new onset atrial fibrillation (AF) and favorable valve morphology, absence of moderate to severe MR, and no left atrial thrombus.

We suggest percutaneous mitral balloon valvotomy for selected symptomatic patients with moderate MS MVA >1.5 cm2 if pulmonary artery wedge pressure is >25 mmHg or mean mitral valve gradient is >15 mmHg during exercise and valve morphology is favorable and there is no more than mild MR and no left atrial thrombus.

We suggest percutaneous mitral balloon valvotomy for selected severely symptomatic patients (NYHA class III to IV) with severe MS (MVA ≤1.5 cm2, stage D) who have a suboptimal valve anatomy and who are not candidates for surgery or at high risk for surgery.

We suggest mitral valve surgery for selected patients with moderate MS (MVA 1.6 cm2 to 2.0 cm2) with mitral valve anatomy unfavorable for percutaneous intervention (echocardiogram score and presence of MR) undergoing cardiac surgery for other indications.

We suggest mitral valve surgery and excision of the left atrial appendage for selected patients with severe MS (MVA ≤1.5 cm2, stage C and D) who have had recurrent embolic events while receiving adequate anticoagulation.

Evidence — The above recommendations are based upon observational data on outcomes for mitral valve surgery (commissurotomy, repair, or replacement) and for percutaneous mitral balloon valvotomy compared with outcomes without intervention [1,6]. Early intervention in selected clinical settings is based upon natural history studies showing that MS is generally progressive (with MVA declining at a mean rate of approximately 0.1 cm2 per year, though there is significant variation in this rate). (See "Surgical and investigational approaches to management of mitral stenosis" and "Percutaneous mitral balloon valvotomy for mitral stenosis" and "Pathophysiology and natural history of mitral stenosis".)

MEDICAL MANAGEMENT

Prevention of thromboembolism

Antithrombotic recommendations — We agree with the antithrombotic recommendations for MS in the 2014 American Heart Association/American College of Cardiology guideline on the management of valvular heart disease and the 2019 guidelines on atrial fibrillation [1,2,7]. These recommendations are similar to those in the 2012 Ninth American College of Chest Physicians (ACCP) consensus conference and 2017 European Society of Cardiology valve guidelines [6,8]. As noted below, scant direct evidence is available to guide antithrombotic therapy in patients with MS.

We recommend anticoagulation (with vitamin K antagonist; target International Normalized Ratio [INR] 2.5) in patients with moderate to severe rheumatic MS and one or more of the following conditions:

Atrial fibrillation (paroxysmal, persistent, or permanent)

Prior embolic event

Left atrial thrombus

Some clinicians also suggest anticoagulation with vitamin K antagonist for patients with mild MS with one or more of the above conditions [9].

Transient subclinical atrial fibrillation (AF) occurs in some patients with MS, and transient AF is a predictor of stroke and systemic embolism [10]. Transient AF and infective endocarditis should be considered as potential causes when embolization occurs in patients with MS who are in sinus rhythm.

Monitoring patients for the development of an indication for percutaneous balloon mitral valvotomy may also help manage the thromboembolic risk since timely percutaneous intervention appears to reduce the risk of systemic embolism in patients with and without AF [11]. (See 'Indications for intervention' above and "Percutaneous mitral balloon valvotomy for mitral stenosis".)

Use of anticoagulation in patients with MS in normal sinus rhythm with left atrial enlargement or spontaneous echocardiographic contrast on TEE is controversial since the utility of such treatment in managing the risk of thromboembolism is uncertain.

Direct oral anticoagulants (DOACs), such as dabigatran, are approved for prevention of systemic embolism in adults with nonvalvular AF. We recommend use of warfarin or heparin in adults with MS when anticoagulation is needed because patients with significant mitral valve disease were excluded from the trials of these newer agents. Further study is needed to determine the safety and efficacy of DOAC in this setting. (See 'Evidence' below.)

Evidence — Systemic thromboembolism is a major complication of MS and is the presenting event in some patients. Prior to widespread anticoagulant therapy and surgical treatment in patients with MS, as many as 30 percent of patients with MS experienced an embolic event during the course of the disease. (See "Clinical manifestations and diagnosis of rheumatic mitral stenosis", section on 'Thromboembolism'.)

The role of anticoagulation in patients with MS and AF has been primarily supported by extrapolation of data from AF in patients without MS. (See "Atrial fibrillation in adults: Use of oral anticoagulants".)

Patients with MS have been excluded from most randomized trials examining the efficacy of long-term anticoagulation to prevent thromboembolism in patients with AF. An exception was a substudy of the NASPEAF trial that included 311 patients with MS and AF (with and without prior embolism) and 175 with nonvalvular AF and prior embolism, but this study was limited by small numbers of events [12]. The patients were randomly assigned to anticoagulation therapy (target INR 2.0 to 3.0, median attained value 2.46) or moderate intensity anticoagulation (INR 1.4 to 2.4, median attained value 2.15) in combination with the antiplatelet agent triflusal, which is structurally related to aspirin. The primary end point was a composite of fatal and nonfatal stroke and myocardial infarction, sudden death, or death from bleeding. The following findings were noted at a median follow-up of 2.9 years:

For the whole patient population, combined antiplatelet plus anticoagulant therapy significantly reduced the number of vascular events compared with anticoagulant therapy alone (14 versus 19 events).

Among patients with MS, the event rate was nominally lower with combined therapy than with anticoagulation alone both in patients with (3.5 versus 6.6 percent) and without (0.8 versus 2.5 percent) prior embolism. However, these differences were not statistically significant.

Although left atrial enlargement and spontaneous echocardiographic contrast (along with atrial fibrillation and smaller mitral valve area) have been identified as predictors of thromboembolism in patients with MS [11,13,14], the risks and benefits of anticoagulation for left atrial enlargement or spontaneous echocardiographic contrast in patients with MS in sinus rhythm are uncertain. Spontaneous echocardiographic contrast (SEC) is a marker of blood stasis associated with decreased atrial contractile function and increased risk of left atrial thrombus in patients with MS [15,16]. Among patients with MS, SEC is more frequent among patients in AF although some patients in sinus rhythm also have SEC, other evidence of decreased atrial function, and atrial thrombus. A transesophageal echocardiographic study of 848 patients with moderate to severe MS in sinus rhythm found left atrial thrombus in 7 percent [17].

Findings of an observational study of patients with MS and AF suggest a role for DOAC in this setting [18], but further study is required to determine the safety and efficacy of DOAC in this population. The observational study included a total of 2230 propensity-matched patients, half treated with a DOAC and half treated with warfarin. Thromboembolic events were less frequent in the DOAC group than in the warfarin group (2.22 versus 4.19 percent; adjusted hazard ratio [HR] 0.28, 95% CI 0.18-0.45). The frequency of intracranial hemorrhage was similar in the two groups (0.49 and 0.93 percent; adjusted HR 0.53, 95% CI 0.22-1.26). The mortality rate was significantly lower in the DOAC group (3.45 versus 8.08 percent; adjusted HR 0.41, 95% CI 0.30-0.56).

Pharmacologic therapy for heart failure — The onset of symptoms is an indication for intervention in patients with severe MS. (See 'Indications for intervention' above.)

The role of medical therapy for MS is limited. Pharmacologic therapy is appropriate to improve symptoms and hemodynamic conditions prior to intervention, for persistent symptoms after intervention, and for management of symptoms precipitated by an intercurrent illness or during pregnancy. (See "Pregnancy in women with mitral stenosis", section on 'Clinical management'.)

Diuretic therapy (usually with a loop diuretic) and dietary salt restriction are appropriate when there are manifestations of pulmonary vascular congestion such as exertional shortness of breath, orthopnea, and/or paroxysmal nocturnal dyspnea [19]. At a later stage of MS, right heart failure can occur, with hepatic congestion and peripheral edema. Loop diuretics acutely improve such manifestations of the congestive state [20]. (See "Use of diuretics in patients with heart failure".)

Beta blockers (or negative chronotropic calcium channel blockers) are used for heart rate control (in patients in atrial fibrillation or sinus rhythm) and to improve dyspnea, though their effect on exercise tolerance is uncertain. These agents can significantly decrease heart rate and cardiac output at rest, causing a decrease in the transmitral gradient, pulmonary venous pressure, and mean pulmonary artery pressure in patients with MS [21]. Beta blockers can blunt the heart rate and cardiac output responses to exercise, while attenuating the rise in transmitral gradient that normally occurs [22]. However, the impact of beta blockers on exercise tolerance is uncertain, with conflicting results from small trials [22,23].

The role of digoxin in patients with MS is limited since most patients have preserved ventricular systolic function [24,25]. Digoxin may be helpful in selected patients who have symptomatic left and/or right ventricular systolic dysfunction as in patients with other causes of systolic heart failure. Digoxin may also be helpful in controlling a rapid ventricular rate during AF, although it should not be considered a first-line drug for this indication. (See "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy" and "Overview of the management of heart failure with reduced ejection fraction in adults" and "Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults", section on 'Digoxin'.)

Management of atrial fibrillation rate and rhythm — In general, the medical management of atrial fibrillation (AF) for patients with MS does not significantly differ from general treatment guidelines. However, because of the exaggerated adverse hemodynamic effects caused by MS, prompt therapy is often necessary. In patients who are hemodynamically unstable, immediate electrical cardioversion is indicated. For hemodynamically stable patients, the initial management consists of controlling the ventricular rate (with a beta blocker, calcium channel blocker [verapamil or diltiazem], or, less preferably, digoxin) and anticoagulation. (See "Overview of atrial fibrillation" and "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy" and 'Antithrombotic recommendations' above.)

When MS is hemodynamically significant (valve area <1.5 cm2), flow across the mitral valve is maintained by two factors: adequate diastolic filling time and higher-than-normal pulmonary venous pressure. AF in patients with MS may be poorly tolerated for two reasons, with the hemodynamic consequences depending upon the severity of the stenosis:

If AF is associated with a rapid ventricular rate, the shortened diastolic filling time causes left atrial and pulmonary pressures to rise, potentially leading to pulmonary edema. (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm".)

The loss of atrial contraction contributes to a decrease in left ventricular filling and an increase in left atrial pressure.

Rate versus rhythm control — A rate control strategy is generally preferred because, based upon studies in patients with nonvalvular AF, outcomes are as good as or perhaps better than with a rhythm control strategy and, with a rhythm control strategy, long-term anticoagulation is still required in most patients. Conversion to sinus rhythm may be necessary if heart rate cannot be adequately controlled with medications. In patients not requiring urgent cardioversion, the decision for rate control versus rhythm control is based upon multiple factors including the duration of AF, hemodynamic response to AF, symptoms, and left atrial size. (See "Rhythm control versus rate control in atrial fibrillation".)

For patients in whom a rhythm control strategy is chosen, issues related to the method of restoration of sinus rhythm, anticoagulation before, during, and after cardioversion, and antiarrhythmic drug therapy to maintain sinus rhythm are discussed separately. (See "Atrial fibrillation: Cardioversion" and "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation" and "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Recommendations".)

Regardless of the initial response to antiarrhythmic therapy, it may become increasingly difficult, if not impossible, to maintain sinus rhythm as the severity of MS progresses. In many patients with MS, the onset of AF may contribute to the onset of symptoms. Percutaneous mitral balloon valvotomy has been suggested by some experts for new AF in patients MS since intervention may aid conversion to sinus rhythm. Catheter AF ablation is an option in selected patients with MS [26]. Patients with indications with mitral valve surgery may undergo concomitant surgical AF ablation. (See "Overview of catheter ablation of cardiac arrhythmias" and "Maintenance of sinus rhythm in atrial fibrillation: Catheter ablation versus antiarrhythmic drug therapy" and "Atrial fibrillation: Surgical ablation" and 'Our approach' above.)

Secondary prevention of rheumatic fever — Patients with rheumatic MS should receive antibiotic prophylaxis for secondary prevention of rheumatic fever. Acceptable regimens and issues related to the duration of prophylaxis are discussed separately. Regardless of whether or not prophylaxis is continued, there should always be a low threshold to test and treat these patients for acute group A streptococcal pharyngitis. (See "Acute rheumatic fever: Treatment and prevention", section on 'Prevention' and "Treatment and prevention of streptococcal pharyngitis in adults and children".)

Nearly all cases of MS are the result of rheumatic involvement of the mitral valve. Although chronic degenerative changes associated with MS may represent a response to turbulent blood flow through the rheumatically deformed valve [27], there is also evidence that repeated episodes of rheumatic carditis contribute to the natural history of MS even when no clinical signs of acute rheumatic fever have been present [28,29]. Thus, preventing repeated attacks of rheumatic fever may play a role in delaying the progression of MS.

The risk for recurrence of rheumatic fever declines with increasing age and the number of years since the patient's most recent attack, and it has been declining in the United States. (See "Acute rheumatic fever: Treatment and prevention", section on 'Prevention'.)

The likelihood of recurrence is positively correlated with a higher number of previous attacks and the presence and severity of pre-existing rheumatic heart disease [30]. Recurrences of rheumatic fever tend to mimic previous attacks for any particular patient such that the absence of carditis during the initial attack usually means it will also not be a feature during future attacks. However, the diagnosis of recurrent rheumatic fever may be difficult since classical criteria for first episodes may not be present.

Prevention of infective endocarditis — As noted in the 2007 American Heart Association guidelines on the prevention of bacterial endocarditis, only patients with the highest risk of the development of endocarditis (eg, patients with prosthetic heart valves, patients with prior endocarditis) are advised to receive antimicrobial prophylaxis [31]. Most patients with native valvular heart disease, including those with MS, are not included in this group and therefore do not require antimicrobial prophylaxis. (See "Antimicrobial prophylaxis for the prevention of bacterial endocarditis".)

Statin therapy — The value of statin therapy in patients with MS is uncertain. A preliminary retrospective observational study found an association between treatment with statins and slower progression of rheumatic MS [32].

NONCARDIAC SURGERY

Preoperative evaluation — The presence of MS has potentially important implications for the perioperative management and prognosis of the patient undergoing noncardiac surgery. Although there are no definitive data, patients with MS who are asymptomatic and do not have pulmonary hypertension or atrial fibrillation probably do not incur an excess risk in noncardiac surgical procedures. By comparison, the prognosis is poor in patients with untreated symptomatic MS.

The following recommendations for patients with asymptomatic severe MS are consistent with the 2014 American Heart Association/American College of Cardiology (AHA/ACC) valve guidelines [1,2]:

Preoperative percutaneous balloon mitral valvotomy is suggested for patients with asymptomatic severe MS who are candidates for percutaneous intervention (including favorable valve anatomy) and undergoing elective moderate- or high-risk noncardiac surgery (table 1).

The risks and benefits of proceeding with elective noncardiac surgery should be considered in asymptomatic patients with severe MS who are not candidates for percutaneous balloon mitral valvotomy (due to unfavorable valve anatomy or other contraindication). Though evidence is limited, it may be reasonable to proceed with moderate-risk elective noncardiac surgery with appropriate intraoperative and postoperative hemodynamic monitoring and management in this setting.

Intervention according to standard guidelines (table 1) is recommended for patients with symptomatic severe MS prior to elective non-cardiac surgery [1,2]. (See 'Our approach' above.)

Perioperative management — Perioperative management of patients with unoperated MS undergoing noncardiac surgery should include attention to the following [1,2] (see "Anesthesia for labor and delivery in high-risk heart disease: Specific lesions", section on 'Mitral stenosis'):

Adequate heart rate control – Tachycardia should be avoided since it shortens diastolic left ventricular filling time across the stenotic mitral valve and can result in reduced cardiac output, exacerbation of the transmitral gradient, and potentially pulmonary congestion. Anesthetic agents and muscle relaxants associated with decreased heart rates are preferred. Among patients with atrial fibrillation, the ventricular rate should be well controlled prior to elective surgery.

Careful management of central blood volume – Pulmonary venous pressure (ie, pulmonary artery balloon occlusion pressure) should be monitored and maintained high enough to allow adequate cardiac output but low enough to avoid pulmonary edema. Because of the obstruction to flow from left atrium to left ventricle, any situation that increases venous return and central blood volume will lead to a rise in pulmonary pressures and congestion. As an example, the Trendelenburg position dramatically increases pulmonary blood flow and can cause overt pulmonary edema. Right heart pressure monitoring during surgery is essential to manage the volume status.

Maintenance of systemic vascular resistance – MS impairs the normal compensatory response associated with a fall in blood pressure, since the stroke volume cannot be substantially increased. As a result, maintenance of systemic vascular resistance is important, since sudden drug-induced reductions in systemic vascular resistance can lead to hypotension.

Avoidance of marked changes in pulmonary vascular resistance – Some degree of pulmonary hypertension is present in patients with MS. However, an increase in pulmonary hypertension (eg, from arterial hypoxemia) may produce frank right ventricular decompensation.

PHYSICAL ACTIVITY AND EXERCISE — Most patients with significant MS are symptomatic with exertion, leading them to adopt a more sedentary lifestyle. However, all patients should be encouraged to participate in at least a low level exercise regimen to maintain cardiovascular fitness. Patients should be informed that sudden death in MS is extremely rare, which may alleviate certain fears about exercising.

Each patient's exercise tolerance will vary depending upon the severity of their disease (table 2) and the intensity and type of exercise (figure 2) [33]. More specific recommendations for participation in competitive sports from the 36th Bethesda Conference are as follows [34]:

Patients in sinus rhythm with mild MS with peak pulmonary artery systolic pressures less than 50 mmHg can participate in all competitive sports.

Patients with moderate MS who are in sinus rhythm or atrial fibrillation (AF) and have peak pulmonary artery systolic pressures less than 50 mmHg can participate in low and moderate static and low and moderate dynamic competitive sports (class IA, IB, IIA, and IIB) (figure 2).

Patients with severe MS who are in sinus rhythm or AF and patients with peak pulmonary artery systolic pressures greater than 50 mmHg should not participate in competitive sports.

Patients with MS of any severity who are in or have a history of AF and are treated with anticoagulation should not participate in competitive sports associated with a risk of bodily contact or possible trauma (table 3).

PREGNANCY — Pregnancy is associated with hemodynamic changes that may be poorly tolerated in women with MS, particularly in those with more advanced disease. This issue is discussed in detail separately. (See "Pregnancy in women with mitral stenosis".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Mitral stenosis in adults (The Basics)")

SUMMARY AND RECOMMENDATIONS

Mitral stenosis (MS) is a condition characterized by obstruction of blood flow across the mitral valve from the left atrium to the left ventricle. The mechanical obstruction leads to increases in pressure within the left atrium, pulmonary vasculature, and right side of the heart. (See 'Introduction' above and "Clinical manifestations and diagnosis of rheumatic mitral stenosis".)

The timing of surgical or percutaneous intervention for MS is crucial to avoid the risks of unnecessarily early intervention as well as the risk of irreversible pulmonary hypertension and/or right heart failure from delaying necessary intervention. (See 'Monitoring and evaluation' above.)

In asymptomatic patients with MS, routine follow-up echocardiography is recommended every three to five years if the mitral valve area (MVA) is >1.5 cm2, every one to two years if the MVA is 1.0 to 1.5 cm2, and once per year if the MVA is <1.0 cm2. More frequent monitoring may be required in patients with concurrent mitral regurgitation and/or disease affecting other valves. All patients should undergo re-evaluation whenever there is a change in clinical status. (See 'Monitoring and evaluation' above.)

We recommend long-term oral anticoagulation (with vitamin K antagonist; target International Normalized Ratio 2.5, range 2.0 to 3.0) in patients with MS who have a prior embolic event, left atrial thrombus, or paroxysmal, persistent, or permanent atrial fibrillation (AF). (See 'Antithrombotic recommendations' above.)

In general, rate and rhythm control of AF for patients with MS does not significantly differ from general treatment guidelines for patients without MS. However, because of the exaggerated adverse hemodynamic effects caused by MS, prompt therapy is often necessary. (See 'Management of atrial fibrillation rate and rhythm' above.)

Pharmacologic therapy is not a substitute for valve intervention in patients with MS and is only appropriate for stabilization purposes prior to intervention, to treat hemodynamic decompensation due to an intercurrent illness, or for persistent symptoms after intervention. In these settings, diuretics and beta blockers may improve symptoms. (See 'Pharmacologic therapy for heart failure' above.)

We recommend percutaneous mitral valvotomy for symptomatic patients with severe MS (mitral valve area [MVA] ≤1.5 cm2, stage D) in patients with favorable valve morphology, no left atrial thrombus, and less than moderate mitral regurgitation (MR). (See 'Our approach' above.)

We recommend mitral valve surgery (repair, commissurotomy, or valve replacement) in severely symptomatic patients (New York Heart Association class III or IV) with severe MS (MVA ≤1.5 cm2, stage D) who are not high risk for surgery and who are not candidates for or who have failed prior percutaneous mitral valvotomy. (See 'Our approach' above.)

Patients with rheumatic MS should receive antibiotic prophylaxis for secondary prevention of rheumatic fever. (See 'Secondary prevention of rheumatic fever' above.)

Preoperative percutaneous mitral valvotomy is suggested for patients with asymptomatic severe MS who are candidates for percutaneous intervention, (including favorable valve anatomy) if they are undergoing elective moderate- or high-risk noncardiac surgery. (See 'Noncardiac surgery' above.)

REFERENCES

  1. 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; 63:e57.
  2. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC Focused Update of the 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 Clinical Practice Guidelines. J Am Coll Cardiol 2017; 70:252.
  3. Horstkotte D, Niehues R, Strauer BE. Pathomorphological aspects, aetiology and natural history of acquired mitral valve stenosis. Eur Heart J 1991; 12 Suppl B:55.
  4. Ellis LB, Singh JB, Morales DD, Harken DE. Fifteen-to twenty-year study of one thousand patients undergoing closed mitral valvuloplasty. Circulation 1973; 48:357.
  5. Orrange SE, Kawanishi DT, Lopez BM, et al. Actuarial outcome after catheter balloon commissurotomy in patients with mitral stenosis. Circulation 1997; 95:382.
  6. Baumgartner H, Falk V, Bax JJ, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J 2017; 38:2739.
  7. January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2019; 74:104.
  8. Whitlock RP, Sun JC, Fremes SE, et al. Antithrombotic and thrombolytic therapy for valvular disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012; 141:e576S.
  9. Iung B, Leenhardt A, Extramiana F. Management of atrial fibrillation in patients with rheumatic mitral stenosis. Heart 2018; 104:1062.
  10. Karthikeyan G, Ananthakrishnan R, Devasenapathy N, et al. Transient, subclinical atrial fibrillation and risk of systemic embolism in patients with rheumatic mitral stenosis in sinus rhythm. Am J Cardiol 2014; 114:869.
  11. Chiang CW, Lo SK, Ko YS, et al. Predictors of systemic embolism in patients with mitral stenosis. A prospective study. Ann Intern Med 1998; 128:885.
  12. Pérez-Gómez F, Salvador A, Zumalde J, et al. Effect of antithrombotic therapy in patients with mitral stenosis and atrial fibrillation: a sub-analysis of NASPEAF randomized trial. Eur Heart J 2006; 27:960.
  13. Boonyasirinant T, Phankinthongkum R, Komoltri C. Clinical and echocardiographic parameters and score for the left atrial thrombus formation prediction in the patients with mitral stenosis. J Med Assoc Thai 2007; 90 Suppl 2:9.
  14. Acartürk E, Usal A, Demir M, et al. Thromboembolism risk in patients with mitral stenosis. Jpn Heart J 1997; 38:669.
  15. Rittoo D, Sutherland GR, Currie P, et al. A prospective study of left atrial spontaneous echo contrast and thrombus in 100 consecutive patients referred for balloon dilation of the mitral valve. J Am Soc Echocardiogr 1994; 7:516.
  16. Goswami KC, Yadav R, Bahl VK. Predictors of left atrial appendage clot: a transesophageal echocardiographic study of left atrial appendage function in patients with severe mitral stenosis. Indian Heart J 2004; 56:628.
  17. Manjunath CN, Srinivasa KH, Panneerselvam A, et al. Incidence and predictors of left atrial thrombus in patients with rheumatic mitral stenosis and sinus rhythm: a transesophageal echocardiographic study. Echocardiography 2011; 28:457.
  18. Kim JY, Kim SH, Myong JP, et al. Outcomes of Direct Oral Anticoagulants in Patients With Mitral Stenosis. J Am Coll Cardiol 2019; 73:1123.
  19. Bruce CJ, Nishimura RA. Newer advances in the diagnosis and treatment of mitral stenosis. Curr Probl Cardiol 1998; 23:125.
  20. Austin SM, Schreiner BF, Kramer DH, et al. The acute hemodynamic effects of ethacrynic acid and furosemide in patients with chronic postcapillary pulmonary hypertension. Circulation 1976; 53:364.
  21. Meister SG, Engel TR, Feitosa GS, et al. Propranolol in mitral stenosis during sinus rhythm. Am Heart J 1977; 94:685.
  22. Stoll BC, Ashcom TL, Johns JP, et al. Effects of atenolol on rest and exercise hemodynamics in patients with mitral stenosis. Am J Cardiol 1995; 75:482.
  23. Klein HO, Sareli P, Schamroth CL, et al. Effects of atenolol on exercise capacity in patients with mitral stenosis with sinus rhythm. Am J Cardiol 1985; 56:598.
  24. Toutouzas P. Left ventricular function in mitral valve disease. Herz 1984; 9:297.
  25. Gaasch WH, Folland ED. Left ventricular function in rheumatic mitral stenosis. Eur Heart J 1991; 12 Suppl B:66.
  26. Nair M, Shah P, Batra R, et al. Chronic atrial fibrillation in patients with rheumatic heart disease: mapping and radiofrequency ablation of flutter circuits seen at initiation after cardioversion. Circulation 2001; 104:802.
  27. Stapleton JF. Natural history of chronic valvular disease. In: Cardiovascular Clinics. Valvular heart disease: comprehensive evaluation and management, Frankl WS, Brest AN (Eds), FA Davis, Philadelphia 1986. p.128.
  28. Edwards WD, Peterson K, Edwards JE. Active valvulitis associated with chronic rheumatic valvular disease and active myocarditis. Circulation 1978; 57:181.
  29. Clawson, BJ. Rheumatic heart disease. An analysis of 796 cases. Am Heart J 1940; 20:454.
  30. Dickinson GM, Bisno AL. Antimicrobial prophylaxis of infection. Infect Dis Clin North Am 1995; 9:783.
  31. Wilson W, Taubert KA, Gewitz M, et al. Prevention of Infective Endocarditis. Guidelines From the American Heart Association. A Guideline From the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation 2007; 115 published online April 19, 2007. www.circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.106.183095v1 (Accessed on May 04, 2007).
  32. Antonini-Canterin F, Moura LM, Enache R, et al. Effect of hydroxymethylglutaryl coenzyme-a reductase inhibitors on the long-term progression of rheumatic mitral valve disease. Circulation 2010; 121:2130.
  33. Mitchell JH, Haskell W, Snell P, Van Camp SP. Task Force 8: classification of sports. J Am Coll Cardiol 2005; 45:1364.
  34. Bonow RO, Cheitlin MD, Crawford MH, Douglas PS. Task Force 3: valvular heart disease. J Am Coll Cardiol 2005; 45:1334.
Topic 8139 Version 24.0

References

1 : 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.

2 : 2017 AHA/ACC Focused Update of the 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 Clinical Practice Guidelines.

3 : Pathomorphological aspects, aetiology and natural history of acquired mitral valve stenosis.

4 : Fifteen-to twenty-year study of one thousand patients undergoing closed mitral valvuloplasty.

5 : Actuarial outcome after catheter balloon commissurotomy in patients with mitral stenosis.

6 : 2017 ESC/EACTS Guidelines for the management of valvular heart disease.

7 : 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.

8 : Antithrombotic and thrombolytic therapy for valvular disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.

9 : Management of atrial fibrillation in patients with rheumatic mitral stenosis.

10 : Transient, subclinical atrial fibrillation and risk of systemic embolism in patients with rheumatic mitral stenosis in sinus rhythm.

11 : Predictors of systemic embolism in patients with mitral stenosis. A prospective study.

12 : Effect of antithrombotic therapy in patients with mitral stenosis and atrial fibrillation: a sub-analysis of NASPEAF randomized trial.

13 : Clinical and echocardiographic parameters and score for the left atrial thrombus formation prediction in the patients with mitral stenosis.

14 : Thromboembolism risk in patients with mitral stenosis.

15 : A prospective study of left atrial spontaneous echo contrast and thrombus in 100 consecutive patients referred for balloon dilation of the mitral valve.

16 : Predictors of left atrial appendage clot: a transesophageal echocardiographic study of left atrial appendage function in patients with severe mitral stenosis.

17 : Incidence and predictors of left atrial thrombus in patients with rheumatic mitral stenosis and sinus rhythm: a transesophageal echocardiographic study.

18 : Outcomes of Direct Oral Anticoagulants in Patients With Mitral Stenosis.

19 : Newer advances in the diagnosis and treatment of mitral stenosis.

20 : The acute hemodynamic effects of ethacrynic acid and furosemide in patients with chronic postcapillary pulmonary hypertension.

21 : Propranolol in mitral stenosis during sinus rhythm.

22 : Effects of atenolol on rest and exercise hemodynamics in patients with mitral stenosis.

23 : Effects of atenolol on exercise capacity in patients with mitral stenosis with sinus rhythm.

24 : Left ventricular function in mitral valve disease.

25 : Left ventricular function in rheumatic mitral stenosis.

26 : Chronic atrial fibrillation in patients with rheumatic heart disease: mapping and radiofrequency ablation of flutter circuits seen at initiation after cardioversion.

27 : Chronic atrial fibrillation in patients with rheumatic heart disease: mapping and radiofrequency ablation of flutter circuits seen at initiation after cardioversion.

28 : Active valvulitis associated with chronic rheumatic valvular disease and active myocarditis.

29 : An analysis of 796 cases

30 : Antimicrobial prophylaxis of infection.

31 : Antimicrobial prophylaxis of infection.

32 : Effect of hydroxymethylglutaryl coenzyme-a reductase inhibitors on the long-term progression of rheumatic mitral valve disease.

33 : Task Force 8: classification of sports.

34 : Task Force 3: valvular heart disease.