Mitral regurgitation

Highlights
Summary Overview

Basics
Definition Epidemiology Aetiology Pathophysiology Classification

Prevention
Secondary

Diagnosis
History & examination Tests Differential Step-by-step Criteria Guidelines Case history

Treatment
Details Step-by-step Emerging Guidelines

Follow Up
Recommendations Complications Prognosis

Resources
References Images Patient leaflets Credits Email Print Feedback Share Add to Portfolio Bookmark Add notes

History & exam

Key factors
presence of risk factors dyspnoea on exertion decreased exercise tolerance lower extremity oedema holosystolic murmur

Other diagnostic factors

orthopnoea paroxysmal nocturnal dyspnoea palpitations fatigue diaphoresis displaced point of maximal impulse pulmonary closure is louder than aortic closure S3 heart sound diminished S1 heart sound History & exam details

Diagnostic tests
1st tests to order
transthoracic echo ECG

Tests to consider
flow convergence method or proximal isovelocity surface area colour Doppler flow transoesophageal echocardiogram left heart catheterisation cardiac MRI Diagnostic tests details

Treatment details
Acute
acute MR emergency surgery preoperative diuretics intra-aortic balloon counterpulsation

Ongoing
asymptomatic chronic MR o o left ventricular ejection fraction >60% and/or left ventricular end-systolic diameter <45 mm angiotensin-converting enzyme (ACE) inhibitors beta-blockers

left ventricular ejection fraction 60% or less and/or left ventricular end-systolic diameter 45 mm or more

surgery symptomatic chronic MR

o o o

left ventricular ejection fraction 30% or more surgery + medical treatment left ventricular ejection fraction <30% medical treatment intra-aortic balloon counterpulsation Treatment details

Summary
Mitral regurgitation (MR) may present with dyspnoea, usually on exertion, palpitations, and/or decreased exercise tolerance. MR. Colour Doppler flow and continuous-wave Doppler studies can assess severity of regurgitation, left ventricular dimensions, size and function of the right ventricle, and pulmonary artery systolic pressure. Surgical treatment is the best available treatment option, although percutaneous approaches have gained significant potential. The most common complications of surgical treatment are failure of repair, prosthetic valve stenosis, endocarditis, and mitral valve patient-prosthesis mismatch. Typically presents as a holosystolic blowing murmur at the apex, radiating to axilla. Transthoracic echo is the diagnostic test of choice in identifying presence, severity, and mechanism of

Definition
The mitral valve apparatus consists of anterior and posterior leaflets, chordae tendineae, anterolateral and posteromedial papillary muscles, and mitral annulus. Any aberrations of the mitral valve apparatus, due to mechanical, traumatic, infectious, degenerative, congenital, or metabolic causes, may lead to mitral regurgitation (MR). Mild to moderate disease can be asymptomatic for many years; however, with progression of the disease, eccentric cardiac hypertrophy occurs, which leads to elongation of the myocardial fibres and increased left ventricular enddiastolic volume. Eventually, prolonged volume overload leads to left ventricular dysfunction and increased left ventricular end-systolic diameter.

Epidemiology
Although the exact incidence and prevalence of MR is unknown it has been suggested that the prevalence probably exceeds 5,000,000 worldwide. [1]

Aetiology
The mitral valve apparatus consists of anterior and posterior leaflets, chordae tendineae, anterolateral, and posteromedial papillary muscles, and mitral annulus. To be inclusive, it also includes the atrial and ventricular myocardium. Mitral valve dysfunction may result from aberrations of any portion of the mitral valve apparatus, due to mechanical, traumatic, infectious, degenerative, congenital, or metabolic causes. MR can be either acute or chronic. Typical causes of acute MR include infective endocarditis, ischaemic papillary muscle dysfunction [2] or rupture, acute rheumatic fever, and acute dilation of the left ventricle due to myocarditis or ischaemia. [2] [3] Common causes of chronic MR include those already listed as well as myxomatous degeneration of the mitral leaflets or chordae tendineae, mitral valve prolapse,View imageView image and mitral annular enlargement.

Pathophysiology
Chronic MR can be mild or moderate and can be asymptomatic for many years; however, with progression of the disease to severe, eccentric cardiac hypertrophy occurs, which leads to elongation of the myocardial fibres and increased left ventricular end-diastolic volume. This is a compensatory mechanism that allows an increase in total stroke volume to maintain adequate cardiac output. Additionally, both left ventricular and left atrial enlargement will accommodate the regurgitant volume at a lower filling pressure, which prevents pulmonary congestion. In this stage of the disease, which may last for 7 to 10 years, patients are typically asymptomatic. Eventually, prolonged volume overload leads to left ventricular dysfunction and increased left ventricular end-systolic diameter. However, even in this phase of the disease, left ventricular ejection fraction usually remains above 50% to 60%. [1] [4]

Classification
Acute MR Results from acute disruption of mitral valve leaflets, chordae tendineae, or papillary muscles following MI, trauma, infective endocarditis, rheumatic

fever, or other causes that suddenly disrupt the mitral valve apparatus causing sudden changes in haemodynamics and symptoms. There is no actual classification cut-off point between acute and chronic, because acute MR occurs suddenly within seconds after chordal or papillary muscle rupture and results in immediate symptoms. Chronic MR Occurs over many years and results in volume overload and left ventricular dysfunction.

Secondary prevention
Routine antibiotic prophylaxis for infective endocarditis prior to routine oral, GI, or GU procedures may be offered, depending on the patient's risk profile. [21]

History & examination

Key diagnostic factorshide all
presence of risk factors (common)

Key risk factors include mitral valve prolapse, hx of rheumatic heart disease, infective endocarditis, hx of cardiac trauma, hx of MI, hx of congenital heart disease, hx of ischaemic heart disease, left ventricular systolic dysfunction, hypertrophic cardiomyopathy, and anorectic/dopaminergic drugs.

dyspnoea on exertion (common)

There are no pathognomonic features to diagnose MR by history; however, this is a common presenting symptom of mitral regurgitation.

decreased exercise tolerance (common)

There are no pathognomonic features to diagnose MR by history; however, this is a common presenting symptom of mitral regurgitation.

lower extremity oedema (common)

There are no pathognomonic features to diagnose MR by history; however, this is a common presenting symptom of mitral regurgitation.

holosystolic murmur (common)

MR usually presents as a holosystolic, blowing murmur at the apex that radiates to the axilla. Other diagnostic factorshide all fatigue (common)

There are no pathognomonic features to diagnose MR by history; however, this is a common presenting symptom of mitral regurgitation.

displaced point of maximal impulse (common) Indicates severe and chronic MR. orthopnoea (uncommon)

There are no pathognomonic features to diagnose MR by history; however, this is a common presenting symptom of mitral regurgitation.

paroxysmal nocturnal dyspnoea (uncommon)

There are no pathognomonic features to diagnose MR by history; however, this is a common presenting symptom of mitral regurgitation.

palpitations (uncommon)

There are no pathognomonic features to diagnose MR by history; however, this is a common presenting symptom of mitral regurgitation.

diaphoresis (uncommon) In severe cases, usually with acute MR. pulmonary closure is louder than aortic closure (uncommon) Occurs as right-sided pressures increase. S3 heart sound (uncommon) Occurs in the presence of left ventricular dysfunction. diminished S1 heart sound (uncommon)

Chronic MR is also associated with laterally displaced apical impulse (with left ventricular dilation) and diminished S1. factorshide all

Risk

Strong mitral valve prolapse

May result from abnormal elasticity with redundancy and enlargement of various portions of the mitral valvular apparatus, including the mitral annulus, chordae tendineae, and leaflets. [4] [5] [6] View imageView imageView imageView image

hx of rheumatic heart disease

Leads to leaflet thickening and valvular and subvalvular fibrosis, and various degrees of systolic and diastolic restriction of leaflet motion.

In most cases of restriction involving both leaflets, the jet of MR is central. In some patients, the posterior leaflet is more restricted and the jet direction is posterior.

infective endocarditis

There is leaflet or chordal disruption, flail, and perforations. These often cause MR with associated nodular hypermobile densities (vegetations), which are the echocardiographical hallmarks of the disease.

hx of cardiac trauma Sharp or blunt trauma may result in structural damage to the mitral valve apparatus. hx of MI Myocardial infarction may result in structural damage to the mitral valve apparatus. hx of congenital heart disease

Such as anterior mitral valve cleft, which is commonly associated with septum primum atrial septal defect.

hx of ischaemic heart disease

In the setting of MI and ischaemic heart disease, the left ventricle undergoes remodelling and enlargement, which leads to MR. This is caused by apical tethering of normal leaflets.

The length of mitral tissue, including the leaflets, chordae, and papillary muscle, is fixed. As the left ventricle dilates, often after MI, the left ventricular wall and papillary muscles are displaced outwards, which tethers the joining surfaces of the mitral valve downwards, reducing the amount of leaflet tissue available for coaptation.

In many cases, the result is a central, or in some cases a posterior, direction of the MR jet. In rare cases, a focal infarction may cause elongation or disruption of the papillary muscle, leading to excessive leaflet motion (often involving both leaflets), most commonly on the medial side of both leaflets from medial papillary muscle abnormalities.

left ventricular systolic dysfunction The mechanism for this risk factor is the same as for ischaemic heart disease. hypertrophic cardiomyopathy Caused by systolic anterior motion of the mitral valve.View image anorectic/dopaminergic drugs

Certain anorectic and other dopaminergic or serotonergic drugs such as ergotamine, pergolide, and cabergoline have been shown to cause MR.

Diagnostic tests
1st tests to orderhide all
Test

transthoracic echo atrial size, other valvular abnormalities, and right ventricular systolic pressure. [8]

Visualisation determines severity of valve dysfunction, mechanism, presence of flail, left ventricular size and func

ECG fibrillation). [8]

All patients must undergo ECG examination as a routine screening as well as for any rhythm disturbance (e.g., a

Tests to considerhide all

Test

flow convergence method or proximal isovelocity surface area

Colour Doppler tracks the location of increases in velocity and shows this as a proximal zone of colour aliasing. A

of this convergence zone when its shape is hemispheric allows estimation of the surface area of the hemisphere colour Doppler flow Small central jet <4 cm^2 or <20% of the left atrial area is considered mild.

Vena contracta width <0.3 cm is considered mild; >0.7 cm is considered severe. transoesophageal echocardiogram MR is graded as 1+ (mild), 2+ (mild to moderate), 3+ (moderate to severe), and 4+ (severe). Patients suspected of having pulmonary hypertension and/or poor left or right ventricular function may have echocardiogram or cardiac catheterisation to calculate pulmonary hypertension. left heart catheterisation MR is graded as 1+ (mild), 2+ (mild to moderate), 3+ (moderate to severe), and 4+ (severe).

All patients at risk of ischaemic heart disease should undergo cardiac catheterisation to check for disease in coro echocardiogram or cardiac catheterisation to calculate pulmonary hypertension. cardiac MRI

arteries. Patients suspected of having pulmonary hypertension and/or poor left or right ventricular function may h

Patients with poor left or right ventricular function and/or mitral annular/leaflet calcification may undergo cardiac M

Differential diagnosis
Condition Differentiating signs/symptoms Differentiating tests

Acute coronary syndrome (ACS)

There may be a history of angina or cardiovascular disease, relief of symptoms with rest or nitrates, and risk factors such as family history, smoking, DM, and hyperlipidaemia.

ECG shows ST segment elevation (in ACS with ST elevation) Cardiac enzymes are raised.

without ST elevation), tall or inverted T waves, or new left bund

The patient with ACS typically presents with central crushing chest pain lasting >20 minutes, often

associated with nausea, sweatiness, dyspnoea, and palpitations. Infective endocarditis

Typically presents with a new murmur, or change in the nature of an existing one, with fever, anaemia, splenomegaly, or clubbing.

Blood cultures are positive in infective endocarditis.

An FBC may show anaemia, raised neutrophils, and raised ES

Echo shows vegetations if larger than 2 mm, giving a cause fo

Mitral stenosis

Presents with dyspnoea, fatigue, palpitations, and chest pain.

CXR: mitral stenosis may show pulmonary oedema, but other enlarged left atrium and mitral valve calcification.

ECG: patients with mitral stenosis can present with atrial fibrilla present, too.

Distinguishing features are a malar flush, a low volume pulse, a tapping and undisplaced apex beat, loud S1 with an opening snap.

Echo is diagnostic for mitral stenosis.

The murmur is a rumbling middiastolic one, which can be distinguished from the Austin Flint murmur by the absence of the opening snap and loud S1.

Aortic stenosis

Presentation includes dyspnoea, dizziness, fainting, and congestive cardiac failure.

CXR: aortic stenosis may show LVH, but other features include

ECG: aortic stenosis may show P mitrale, LVH with strain patte block, or complete AV block.

Echo is diagnostic for aortic stenosis.

Characteristic signs are a slow rising pulse, heaving but undisplaced apex beat, left ventricular heave, and an ejection systolic murmur that radiates toward the carotids and can have an ejection click.

Aortic or pulmonic valve disease

Aortic or pulmonic ejection clicks best heard to the right and left of the upper sternum, respectively. Click timing not affected by dynamic manoeuvres.

Echo is diagnostic for bicuspid aortic valve and pulmonic valvu

Atrial myxoma

May have symptoms of weight loss, fever, and malaise. Examination may reveal a diastolic tumour plop or diastolic murmur.

Heterogeneous masses may be sessile, typically in left atrium. leukocytosis.

echo may yield more detail than transthoracic echo. Laboratory

Step-by-step diagnostic approach

Diagnosis and severity are established by symptoms and quantitative findings on echocardiography. [7]

Presentation
There are no pathognomonic features to diagnose MR by history; however, dyspnoea on exertion, orthopnoea, paroxysmal nocturnal dyspnoea, lower extremity oedema, palpitations, fatigue, and diaphoresis are common presenting symptoms.

Physical examination
MR usually presents as a holosystolic, blowing murmur at the apex that radiates to the axilla. Chronic MR is also associated with laterally displaced apical impulse (with left ventricular dilation) and diminished S1.

Transthoracic echocardiogram
This is the definitive test for determining the presence, severity, and mechanism of flail, as well as evaluating left ventricular size and function, left atrial size, other valvular abnormalities, and right ventricular systolic pressure. [7] [8] View imageView imageView image It is also useful for assessing serial changes in left ventricular size and function, and evaluating the patient after a change in symptoms. Some newer systems can produce real-time 3D images in addition to standard 2D images.View imageView imageView imageView image

Measures of flow
Spatial mapping, flow convergence, pulmonary vein velocity patterns, vena contracta width, continuous-wave Doppler density and shape, and quantification of antegrade valvular flow volumes can be used to further assess severity. A weighted average of multiple methods is often used. Flow convergence method, also called the proximal isovelocity surface area method, involves looking at the colour images on the left ventricular side of the mitral regurgitant images. [9] [10][11] [12] View imageView imageView image This flow convergence zone is the location where the blood is accelerating to go across the regurgitant orifice, as it undergoes a pressure drop from left ventricular pressure to left atrial pressure. Analysis of this convergence zone when its shape is hemispheric allows estimation of the

surface area of the hemisphere; it calculates the actual size of the regurgitant lesion, a fundamental parameter of valve integrity, which may be less loaddependent than other methods. A regurgitant orifice area over 0.4 cm^2 is indicative of severe regurgitation, whereas <0.2 cm^2 is considered mild. Pulmonary vein flow profiles are also useful for determining severity. [13] The normal pulmonary vein pattern is to have flow velocity during ventricular systole higher than antegrade flow velocity during diastole, a pattern that persists in mild and sometimes moderate MR. As the regurgitation progresses, pulmonary vein systolic velocity becomes blunted, with systolic velocity less than diastolic velocity, and sometimes with cessation of systolic flow. In patients with severe MR, systolic flow is often reversed, with flow away from the left atrium during ventricular systole. This occurs due to the large V wave on left atrial pressure and a transient reversal of flow back into the pulmonary parenchyma during ventricular systole.

Transoesophageal echocardiogram
May be needed to better assess the severity and aetiology in rare occasions where the degree of symptoms does not match transthoracic echocardiogram findings. [7] [14] A stress echocardiogram is often useful for determining the severity and impact of the disease on the patient's exercise haemodynamics.

ECG
All patients must undergo ECG examination as a routine screening as well as for any rhythm disturbance (e.g., atrial fibrillation). [8]

Catheterisation and MRI

All patients at risk of ischaemic heart disease should undergo cardiac catheterisation to check for disease in coronary arteries. [7] Patients suspected of having pulmonary hypertension and/or poor left or right ventricular function should have cardiac catheterisation to calculate pulmonary hypertension. Patients with poor left or right ventricular function and/or mitral annular/leaflet calcification may undergo cardiac MRI.

Click to view diagnostic guideline references.

Diagnostic criteria

Flow convergence method or proximal isovelocity surface area (PISA)

Flow convergence method or PISA [10] [11] [12] View imageView imageView image involves looking at the colour images on the left ventricular side of the mitral regurgitant images. This flow convergence zone is the location where the blood is accelerating to go across the regurgitant orifice, as it undergoes a pressure drop from left ventricular pressure to left atrial pressure. With this area of flow acceleration, colour Doppler tracks the location of increases in velocity and shows this as a proximal zone of colour aliasing. Analysis of this convergence zone when its shape is hemispheric allows estimation of the surface area of the hemisphere, which is derived from a measurement of the radius (R) and the aliasing velocity (V), numerically extracted from the colour bar reflecting machine settings. When this is combined with the maximum velocity, the size of the regurgitant orifice can be calculated according to the formula 2PiR^2V divided by maximum velocity through the valve obtained by continuous-wave Doppler. The advantage of this formula is that it calculates the actual size of the regurgitant lesion, a fundamental parameter of valve integrity, which may be less load-dependent than other methods. Severity
A regurgitant orifice area >0.4 cm^2 is indicative of severe regurgitation, whereas <0.2 cm^2 is considered mild. A regurgitant fraction of <30% is considered mild and >50% is considered severe. A regurgitant volume of <30 mL is considered mild and >60 mL is considered severe.

Colour Doppler jet area

Small central jet <4 cm^2 or <20% of the left atrial area is considered mild. Vena contracta width >0.7 cm with large central jet is considered severe.

Doppler vena contracta width

<0.3 cm is considered mild. >0.7 cm is considered severe.

Severity of symptoms: New York Heart Association classification

I - No symptoms and no limitation in ordinary physical activity (e.g., shortness of breath when walking, stair climbing). activity. III - Marked limitation in activity due to symptoms, even during less than ordinary activity (e.g., walking short distances; 20-100 m). Comfortable only at rest. IV - Severe limitations. Experiences symptoms even while at rest; mostly bed-bound patients. II - Mild symptoms (mild shortness of breath and/or angina pain) and slight limitation during ordinary

Case history
A 52-year-old woman presents with dyspnoea on exertion, fatigue, and occasional palpitations. She has no prior cardiac history. She denies chest pain, orthopnoea, paroxysmal nocturnal dyspnoea, or lower extremity oedema. On physical examination her jugular venous distension is around 12 cm and her lungs are clear to auscultation. Cardiac examination reveals a slightly displaced apical impulse with a palpable P2. Cardiac auscultation reveals III/VI holosystolic murmur at the apex that radiates to the axilla with diminished S1 and P2 greater than A2.

Other presentations
Acute MR is serious and rare. It may occur in the setting of acute MI and leads to high left atrial pressure and pulmonary oedema secondary to reduced left atrial compliance. It usually presents as a sudden and marked increase in CHF symptoms, with weakness, fatigue, dyspnoea, and sometimes respiratory failure and shock. It is usually associated with peripheral vasoconstriction, pallor, and diaphoresis. Occasionally no murmur is heard, because the lack of left atrial compliance leads to equalisation of pressures between the left atrium and ventricle midway through systole. Chronic MR is associated with a laterally displaced apical impulse (with left ventricular dilation), diminished S1, with or without S3, with or without right ventricular heave, and palpable P2 (if pulmonary hypertension has developed).

Treatment Options

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment Patient group acute MR line 1st Treatmenthide all

emergency surgery

Surgery is indicated for acute MR. Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

Treatment may include preoperative diuretics and, in severe acute cases, intra-aortic balloon counterpulsation. Primary Options valvuloplasty OR annuloplasty OR mechanical valve and anticoagulation OR bioprostheses

adjunct [?]

preoperative diuretics

Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. The diuretic most commonly prescribed for MR is furosemide. Primary Options furosemide : 20-200 mg orally once to twice daily OR indapamide : 2.5-5 mg orally once daily

adjunct [?]

intra-aortic balloon counterpulsation

Severe acute MR associated with hypotension is an

Treatment approach
There is no accepted medical treatment for asymptomatic patients with MR. In general, the treatment of symptomatic MR is surgery.

Acute MR
Acute MR presents as a medical emergency and immediate surgery is indicated. Prior to surgery, afterload reduction using diuretics may be required to stabilise the patient. Severe acute MR associated with hypotension is an indication for intra-aortic balloon counterpulsation.

Chronic MR: asymptomatic patients

There is no accepted medical treatment for asymptomatic patients with preserved left ventricular function; however, these patients are closely monitored for risk factors such as hypertension. Asymptomatic patients with impaired left ventricular function are usually treated with angiotensin-converting enzyme (ACE) inhibitors and betablockers. Indications for surgery include depressed left ventricular function and elevated left atrial pressures. For asymptomatic patients, surgery is indicated if they have a depressed left ventricular ejection fraction of 60% or less and/or left ventricular end-systolic diameter 45 mm or more. [7] Given the operative risk associated with mitral valve repair, mitral valve surgery for asymptomatic patients with severe MR who have elevated left atrial pressures with pulmonary hypertension and/or atrial fibrillation may be considered. In general, the threshold for surgical treatment of MR has been declining because of significant success with mitral valve repair with low operative risk. Surgical options include: [15]
Valve repair: valvuloplasty or annuloplasty [16] Valve replacement: mechanical valve and anticoagulation [17] or bioprostheses.

Chronic MR: symptomatic patients

All patients should be treated with ACE inhibitors, [18] beta-blockers, and diuretics. Once the patient is stabilised, the treatment of choice is surgery, indicated for all patients with New York Heart Association class II, III, and IV symptoms.

However, patients with ejection fraction of <30% are at significant risk, and medical therapy to treat CHF may be elected. The American College of Cardiology/American Heart Association guidelines recommend medical therapy alone for patients with symptomatic MR with ejection fraction <30%.

Emerging treatments
Percutaneous mitral valve repair This is an emerging procedure that involves treating MR without open heart surgery, using catheter-based approaches. Currently, the edge-to-edge mitral e-clip is undergoing phase II trials. In the next decade many of the current emerging techniques may become available for routine use.

Monitoring
Asymptomatic patients are closely monitored for risk factors such as hypertension. Post-treatment follow-up is necessary following mitral valve repair or replacement to assess the effectiveness of the repair early. The recommended first visit is around 3 to 4 weeks after the operation and then yearly in asymptomatic patients. Baseline echo is essential at 3 to 4 weeks.

Complications
Complicationhide all

atrial fibrillation Occurs as the result of left atrial enlargement. Treated with rate control and proper anticoagulation. pulmonary hypertension see our comprehensive coverage of Idopathic pulmonary arterial hypertension Occurs as the result of left-sided failure and pressure overload. Mitral valve repair or replacement is the only treatment. postoperative stroke see our comprehensive coverage of Overview of stroke May be caused by manipulation of the ascending aorta.

prosthesis stenosis May result from pannus formation or degenerative disease. LV dysfunction and CHF see our comprehensive coverage of Congestive heart failure, acute exacerbation There is an increase in LV end-diastolic volume as a compensatory mechanism in early stages; however, as time progresses LV dysfunction occurs, accompanied by impaired ejection and increased end-systolic volume. With time there may be further LV dilation and increased LV filling pressure. Eventually this leads to reduced forward flow and increased LV filling pressure. Mitral valve repair or replacement is the only treatment. [20] recurrent MR or perivalvular regurgitation after valve replacement 1% per year may require reoperation. Recurrent MR may occur as a result of progressive degenerative disease, lack of use of an annuloplasty ring, the use of chordal shortening instead of artificial chordae or transposition, and lack of use of a sliding plasty for posterior annulus dilatation. prosthesis dysfunction after valve replacement May be related to surgical procedure, endocarditis, or acute MI. postoperative endocarditis see our comprehensive coverage of Infective endocarditis Both early and late. Usually caused by Staphylococcus within days of the operation.

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Prognosis
There is a 1% per-year risk of reoperation after mitral valve repair or replacement. The risk of mortality is lower with mitral valve repair than with replacement. MR may remain asymptomatic for many years. Progression of mitral valve disease is variable and depends on progression of lesions or mitral annulus size. Severe MR also has a variable prognosis, but most experts agree that left ventricular (LV) dysfunction will occur within 6 to 10 years. For flail posterior mitral leaflet at 10 years, 90% of the patients are dead or require MV operation.

All patients with MR may be offered antibiotic prophylaxis prior to dental and/or urological procedures, depending on their risk profiles.