Mitral Regurgitation

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Continuing Education Activity

Mitral regurgitation (MR) is caused by the retrograde flow of blood from the left ventricle (LV) into the left atrium (LA) through the mitral valve (MV), causing a systolic murmur heard best at the apex of the heart with radiation to the left axilla. MR is the most common valvular abnormality worldwide, affecting over 2% of the total population and has a prevalence that increases with age. This activity reviews the evaluation and management of mitral regurgitation and highlights the role of the healthcare team in evaluating and treating patients with this condition.


  • Identify the etiology and epidemiology of mitral regurgitation medical conditions and emergencies.

  • Review the appropriate history, physical, and evaluation of mitral regurgitation.

  • Outline the treatment and management options available for mitral regurgitation.

  • Describe interprofessional team strategies for improving care coordination and communication to advance mitral regurgitation and improve outcomes.


Mitral regurgitation (MR) is caused by the retrograde flow of blood from the left ventricle (LV) into the left atrium (LA) through the mitral valve (MV), causing a systolic murmur heard best at the apex of the heart with radiation to the left axilla. MR is the most common valvular abnormality worldwide, affecting over 2% of the total population and has a prevalence that increases with age.[1][2][3] This article will review and summarize the characteristics, pathophysiology, etiology, management, and treatment of mitral regurgitation. 

Anatomy of Mitral Valve

The mitral valve consists of two leaflets (anterior and posterior) sitting within the annulus. The posterior mitral leaflet originates from the left atrial (LA) endocardium. A subvalvular apparatus, comprising of 2 papillary muscles (anterolateral and posteromedial), arise from the LV myocardium and the chordae tendineae, supporting the leaflets.[4][5] 

Types of MR 

Mitral regurgitation can subdivide into primary and secondary causes.[6] 

Primary Mitral Regurgitation

  • Also called degenerative or organic
  • Any MR resulting from structural deformity of or damage to the leaflets, chordae, and/or papillary muscles causing leaflets to close insufficiently during systole[5]
  • Common causes: papillary muscle rupture, mitral valve prolapse (MVP), or leaflet perforation[5]

Secondary Mitral Regurgitation

  • Also called functional or ischemic
  • Due to a left ventricular wall motion abnormalities (i.e., ischemic cardiomyopathy) or left ventricular remodeling (i.e., dilated cardiomyopathy)[7]
  • No structural problems with the valve itself[8]
  • Leads to mitral annular dilatation or displacement of papillary muscles causing retrograde flow from improperly closed mitral valve leaflets

Carpentier's Classification[3][9][10]

  • Type 1: Normal leaflet motion
    • Caused by annular dilation or leaflet perforation
    • Regurgitation jet directed centrally
  • Type 2: Excessive leaflet motion
    • Caused by papillary muscle rupture, chordal rupture, or redundant chordae
    • Eccentric jet directed away from the involved leaflet
  • Type 3: Restricted leaflet motion
    • IIIa: Leaflet motion restricted in both systole and diastole
      • Caused by rheumatic heart disease commonly
      • Normal papillary muscles
      • Jet may be centrally or eccentrically directed 
    • IIIb: Leaflet motion restricted in systole 
      • Caused by papillary muscle dysfunction or left ventricular dilation
      • Abnormal papillary muscles
      • Jet may be centrally or eccentrically directed


Primary MR


The underlying pathophysiologic basis for degenerative mitral regurgitation is most commonly related to myxomatous degeneration of the mitral valve, resulting in mitral valve prolapse (MVP). MVP can occur either as a primary, non-syndromic process or a secondary, syndromic process. In primary MVP, advancing age is the driving factor responsible for disease progression. Connective tissue diseases such as Marfan syndrome, Ehlers-Danlos syndrome, MASS phenotype, systemic lupus erythematosus (SLE), osteogenesis imperfecta, and pseudoxanthoma elasticum lead to secondary MVP, causing MR.[11] 


Conditions like isolated cleft of the mitral valve [12], double orifice mitral valve, and parachute mitral valve (PMV), which is a congenital valvular anomaly where the chordae tendineae are attached to a single papillary muscle, have been linked to causing MR.[13] While extremely rare, these congenital conditions are well defined in the literature to cause primary MR. 


With an estimation of over 15 million cases worldwide, rheumatic heart disease (RHD) is extremely common in developing countries due to a lack of medical resources and vaccinations.[14] Chronic RHD is associated with pancarditis and has mitral valve involvement causing regurgitation in almost 100% of cases due to scarring of the valve and valve apparatus.[15][16] 

Secondary MR

Left ventricular dilation due to ischemic or nonischemic cardiomyopathy secondarily impairs leaflet coaptation of a structurally normal MV, resulting in secondary MR. Dysfunction and remodeling can lead to apical and lateral papillary muscle displacement, resulting in leaflet tethering, dilation, and a flattening of the mitral annulus, and lower valve closing forces.[4] Reduced closing forces include a reduction in LV contractility, altered systolic annular contraction, reduced synchronicity between the two papillary muscles, and global LV desynchrony, especially in basal segments.

Papillary Muscle Rupture:

Papillary muscle rupture is a very rare condition seen in 1% to 2% of patients after myocardial infarction (MI) or infective endocarditis. It leads to severe mitral regurgitation due to dysfunction of the papillary muscles.[17][18] 

Ischemic MR (IMR):

IMR results from prior MI associated with normal mitral valve leaflets and chordae. Ischemia of the segments underlying the papillary muscles results in remodeling. This phenomenon causes papillary muscle displacement, which results in a more apical position of the leaflets known as a “seagull sign.”[19] Under Carpentier's classification, the leaflet dysfunction resulting in the most common form of IMR is type IIIb due to restricted motions of the leaflet(s) in systole. 

The degree of exercise-induced increase or decrease in MR relates to changes in LV remodeling and valvular deformation and also to changes in LV and papillary muscle synchronicity.

Congestive heart failure (CHF) Associated:

In a study of 558 patients form a heart failure clinic with severe congestive heart failure (EF less than or equal to 35%), MR was severe in 4.3%, moderate to severe in 12.5%, moderate in 21.9%, mild to moderate in 11.8%, mild in 39.1%, and absent or present in 10.4%.[20] This study identified the correlation between severe CHF and MR and their association. 

Atrial Fibrillation Associated:

A retrospective cohort study found atrial fibrillation (AF) to cause increased atrial and valve annular size, resulting in functional MR. Of the patients studied, controlling AF, and restoring sinus rhythm resulted in an increased reduction of functional MR.[21] A randomized trial also showed that AF had links with worsening valvular disease.[22] 

Hypertrophic Cardiomyopathy: 

Hypertrophic cardiomyopathy (HCM) can also lead to MR. HCM is defined by severe left ventricular hypertrophy, which causes increased papillary muscle mass, bringing them closer together. This phenomenon causes the mitral valve leaflets to become elongated and floppy and pulls the leaflets closer to the left ventricular outflow tract causing regurgitant retrograde flow.[5][23] 


Mitral regurgitation is a common valvular abnormality occurring in about 10% of the total population.[1] Mitral valve prolapse (MVP) related to myxomatous degeneration of the mitral valve is the most common cause of primary MR. It has been cited as the most common cardiac mitral valvular pathology worldwide, accounting for 2% to 3% of the total population.[24] In developing countries, RHD remains prevalent and is the most common cause for mitral valvular pathology resulting in hospital admissions.[25][26]


The definition of mitral regurgitation is a retrograde flow from the left ventricle into the left atrium. Mitral regurgitation leads to left ventricular volume overload due to increased stroke volume, caused by an increase in blood volume within the left atrium and hence an increased preload delivered to the left ventricle during diastole. In chronic progressive MR, ventricular remodeling occurs, allowing maintenance of cardiac output, and an initial increase in ejection fraction (EF) is usually observed. However, depending on the regurgitant fraction, the effective EF can be considerably lower. Over time, there is a positive feedback loop by which volume overload from MR causes ventricular dilatation, widening of the mitral annulus, and diminished coaptation of leaflets, leading to further worsening of MR. Eventually, volume overload becomes so severe that excitation-contraction coupling becomes impaired and wall stress-related afterload on the left ventricle leading to dilatation and decreased contractility, resulting in a reduction of EF.[3][27][28]

History and Physical

Mitral valve regurgitation is defined as a holosystolic murmur heard best at the cardiac apex with radiation to the left axilla. However, it is essential to differentiate the murmur of mitral regurgitation compared to other systolic murmurs[29]:

  • Mitral valve prolapse (MVP) - early systolic murmur with a mid-systolic click heard best at the cardiac apex.
  • Tricuspid regurgitation (TR) - holosystolic, heard best at the lower left sternal border with radiation to the right lower sternal border. TR, compared to MR, increases on inspiration. 
  • Ventral septal defect (VSD) - holosystolic, the larger the VSD, the quieter the murmur.
  • Aortic stenosis (AS) - mid-systolic, crescendo-decrescendo in character radiating towards the neck. Quieter with Valsalva or standing.
  • Pulmonic stenosis (PS) - This condition demonstrates mid-systolic, crescendo-decrescendo murmur that increases in intensity during inspiration. In severe PS, the S2 heart sound is widely-split.
  • Atrial septal defect (ASD) - mid-systolic, S2 heart sound is fixed-split and does not change with inspiration.
  • Hypertrophic cardiomyopathy (HCM) - mid-systolic, also radiates and is heard best at the left sternal border and is important to distinguish from MR. The murmur of HCM is louder with Valsalva and standing. 

Clinical findings related to MR can divide into two categories: those related to the MR itself and those associated with the underlying cause. It is crucial to maintain a broad differential diagnosis, but, in general, with an initially focused history and physical examination, one can establish whether the MR is acute or chronic and thus significantly narrow the possible etiologies.

Acute Mitral Regurgitation[27][30]

The clinical assessment will elicit findings associated with a precipitous decline in cardiac output and possibly cardiogenic shock. The patient will usually complain of significant dyspnea at rest, exacerbated in the supine position, as well as cough with clear or pink, frothy sputum. They may also endorse symptoms associated with myocardial ischemia, such as chest pain radiating to the neck, jaw, shoulders, or upper extremities, nausea, and diaphoresis. Physical examination may reveal altered mental status, tachycardia (or bradycardia if there is ischemic involvement of the conduction system), hypotension, tachypnea, hypoxemia, and cyanosis.

Additionally, there may be jugular venous distension, diffuse crackles on lung auscultation, and an apical holosystolic murmur with radiation to the axilla on a precordial exam. Acute MR is typically related to either papillary muscle rupture from acute coronary syndrome or fulminant destruction of the valvular apparatus secondary to acute bacterial endocarditis. Thus, further clinical assessment should focus on confirming these potentially devastating conditions.

In the case of acute bacterial endocarditis, there will be signs and symptoms of sepsis, such as fevers and chills. A history of intravenous drug abuse is highly prevalent, and patients may also have comorbid conditions that predispose to immunocompromise such as diabetes mellitus, HIV/AIDS, and alcohol use disorder. Due to embolization of vegetative material, there may be a variety of additional clinical findings depending on the ultimate fate of the emboli - focal neurologic deficits if there is brain involvement, hematuria, or oligoanuria if there is renal involvement, and Janeway lesions or widespread petechiae if there is cutaneous involvement. In contrast to subacute bacterial endocarditis, acute infections typically occur in patients with structurally normal heart valves and, as such, rheumatic heart disease and prosthetic valves are less common in this population. Furthermore, because the route of bacterial delivery to the mitral valve passes through the right side of the heart, concomitant lesions of the tricuspid and pulmonic valves are not uncommon, and these can often be appreciated on physical examination. 

Chronic Mitral Regurgitation[27]

Patients often remain asymptomatic until late in the course. Clinical findings common to all etiologies include fatigue, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, weight gain, widening of pulse pressure, apical holosystolic murmur with radiation to the axilla, dependent edema, displaced apical impulse, and jugular venous distension. In more advanced cases, there may also be syncope or near syncope, cyanosis, clubbing of digits, gross anasarca, hepatomegaly, evidence of ascites with a fluid wave, or shifting dullness, and evidence of pleural or pericardial effusions. These latter findings are reflective of the development of pulmonary hypertension and resultant right ventricular systolic dysfunction from chronic pressure overload. The differential diagnosis is also considerably broader, and specific clinical findings are dependent on the etiology. 



Echocardiography is the primary and essential diagnostic test for the diagnosis and assessment of mitral regurgitation (American College of Cardiology/American Heart Association (ACC/AHA) [Class I recommendation].[31] Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) provide both qualitative and quantitative analysis. 

Vena contracta is the width of the regurgitant jet as it escapes the regurgitant orifice. It reflects the regurgitant orifice area. Vena contracta greater than 7 mm is consistent with severe MR. Doppler volumetric method is also an option for the quantification of MR. In this method, the regurgitant volume is measured as the difference between the mitral and aortic stroke volumes. Regurgitant volume can be calculated as the product of effective regurgitant orifice (ERO) and MR velocity time integral (VTI). ERO greater than or equal to 0.2 cm^2, regurgitant volume greater than or equal to 30 mL, regurgitant fraction of 50% or higher quantifies as severe MR.[32][33]

Tenting height is the greatest mid-systolic distance from leaflet tips to the annular plane of the mitral valve. The tenting area is defined as the area bounded by the mitral annular plane and the anterior and posterior leaflets at mid-systole. Normal values are a tenting height of less than 0.5 cm, tenting area of 0 cm^2, and anterior and posterior mitral leaflet angles less than 3 degrees. Poor outcomes after mitral valve repair define as a tenting height of greater than or equal to 1 cm, tenting area of greater than 2.5 to 3 cm^2, complex jets, or posterolateral angle of over 45 degrees.[19][34]

The sphericity index is the ratio between the LV end-diastolic volume and the volume of an imaginary sphere, with its diameter extending from the midpoint of the annular plane to the apex. End-diastolic diameter exceeding 65 millimeters (mm), end-systolic diameter over 51 mm, and systolic sphericity index greater than 0.7 predict unfavorable outcomes of MV repair.[34]

An interpapillary distance over 20 mm, posterior papillary fibrosa distance of more than 40 mm, and lateral wall motion abnormality are associated with poor outcome after MV repair surgery.

After the initial echocardiographic evaluation, repeat echocardiography is indicated for patients with moderate or greater MR with or without symptoms, every 6 to 12 months for severe MR, every 1 to 2 years for moderate MR, and every 3 to 5 years for mild MR. Repeat echocardiography is also a recommendation for patients with any degree of MR and a change in clinical status or physical examination findings.[31][35]

Chest Radiography:

In patients with chronic MR, cardiomegaly due to left atrial or right-sided heart enlargement is visible.[27] 

Electrocardiogram (ECG):

Atrial fibrillation (AF) is the most common ECG finding in patients with MR.[27] Patients with AF can also present with more severe MR than patients without arrhythmia.[22] 

Exercise Stress Testing:

In patients with severe, asymptomatic, primary MR, exercise treadmill testing may provide information regarding the patient’s symptom status and exercise tolerance. Exercise echocardiography is useful to assess changes in MR severity and/or pulmonary artery pressure in symptomatic patients with non-severe MR at rest.[27] 

Cardiac Catheterization:

Cardiac catheterization has a role in the assessment of MR when clinical findings are not consistent with noninvasive test results and can be used to quantify MR volume with high accuracy.

Cardiac MRI:

Cardiac MRI is an important and complementary tool for assessing the severity of MR. Cardiac MRI provides an accurate assessment of quantitative measurements, including regurgitant volume and regurgitant fraction. MRI determination of severe MR demonstrates a stronger correlation with left ventricular remodeling (specifically, smaller left ventricular end-diastolic volume following the elimination of MR) than echocardiography. Clinically, cardiac MRI should help to differentiate severe from non-severe MR in patients whose echocardiographic evaluation is not conclusive, particularly if contemplating surgery.[36][37]


B-type natriuretic peptide (BNP) is released by ventricular myocytes in response to increased wall stress and correlates with the severity of symptoms and provides prognostic information in patients with MR. A BNP level may be normal in severe, compensated MR in the absence of symptoms or adverse hemodynamic effects. An elevated BNP level is associated with the composite endpoint of the New York Heart Association (NYHA) class III or IV heart failure (HF) symptoms, LV dysfunction (ejection fraction less than 60%), or death during follow-up of patients with asymptomatic, severe MR.[38]

The patient's history and physical examination should guide the ordering of diagnostic tests.

Treatment / Management

Medical versus surgical management of mitral regurgitation depends on the severity, chronicity, comorbidities, and etiology. While some pharmacologic agents are used in MR, the evidence for their use is not strong, and they do not have a recommendation from the American College of Cardiology (ACC) and American Heart Association (AHA).[31] Primary severe MR and ischemic MR usually receive treatment with valve surgery.[31][39] 


Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) have been used to delay MR progression in asymptomatic patients.[40] The belief is that ACEI/ARBs can decrease regurgitant volume and left-ventricular size in chronic primary MR patients.[41][42] However, there are limited supporting studies, and their overall role in MR is not recommended.[31][39][43] Some studies have concluded no improvement or survival benefit in patients with MR using ACEI/ARBs and have even shown worsening outcomes for some patients.[44][45] In the setting of hypertrophic cardiomyopathy or mitral valve prolapse, vasodilators have demonstrated an increase in the severity of MR.[46]

Beta-blockers in the setting of MR treatment have also been studied. There is little to no benefit demonstrated with beta-blocking agents in primary MR; however, there have been some studies showing increased survival benefit with these agents in secondary MR.[47] One study evaluating carvedilol supported the use as it demonstrated the preservation of left ventricular function and remodeling as well as decrease regurgitant volume.[48] The ACC/AHA do not have specific recommendations regarding the use of beta-blockers in patients with MR.[31] 

With medical management, loop diuretics are believed to be useful also with other pharmacologic agents to further decrease afterload and regurgitant volume; however, further studies are necessary to support this association properly.[41] 


The decision to operate is dependent on the underlying cause of MR. Patients with valvular damage due to chordal or papillary muscle rupture or infective endocarditis require MR surgery. Patients with functional causes of MR, such as ischemia, generally require coronary artery bypass grafting (CABG).[2][49] Patients with acute, symptomatic MR, or an effective regurgitant orifice of at least 40 mm^2, require surgical intervention.[28] MR surgery is also indicated in patients who have deterioration of LV function or an end-systolic diameter of 4.5 cm.[50] Patients diagnosed with primary severe MR require surgery when they are symptomatic with an ejection fraction over 30% or asymptomatic with an EF of 30% to 60%.[51] 

Mitral valve repair has two aims: have an acceptable surface area of mitral valve leaflet coaptation, 5 to 8 mm being essential and correct annular dilatation.[50] 

The American College of Cardiology (ACC) and American Heart Association (AHA) generally recommend mitral valve repair over replacement due to decreased recurrence of MR after repair.[31][52] There is also some data revealing a decrease in morbidity and mortality after surgical repair over replacement.[53] Mitral valve replacement is favorable over repair when there is extensive tissue destruction, which can present in some cases of infective endocarditis.[49] In regards to a replacement, mechanical prostheses are usually preferable to bioprosthetics due to increased durability and less complicated insertion; however, both require anticoagulation after placement.[54] 

Mitraclip is another surgical procedure proven to be effective and has low morbidity and mortality in patients considered high-risk for repair or replacement.[54] Mitraclip can decrease the mitral valve area leading to stenosis, and therefore, an area of under 4.0 cm^2 is a contraindication for this procedure.[55]

Differential Diagnosis

  • Congestive heart failure exacerbation
  • Acute coronary syndrome (ACS)
  • Hemodynamically unstable dysrhythmia
  • Cardiac tamponade
  • Pneumothorax
  • Pulmonary embolism
  • Septic shock
  • Thyrotoxicosis/thyroid storm


The following staging data is from the 2017 AHA/ACC updated guidelines for the management of mitral regurgitation[7][31]:

Grade A:

  • At risk of mitral regurgitation (i.e., infective endocarditis, MVP)
  • Normal valve leaflets, chords, and annulus in patients with coronary disease or cardiomyopathy
  • Hemodynamics: No MR jet or small central jet area less than 20% LA on doppler, small vena contracta less than 0.30 centimeters (cm) 
  • Cardiac findings: normal or mildly dilated left ventricular size with fixed (infarction) or inducible (ischemia) abnormalities of regional wall motion, primary myocardial disease with LV dilation and systolic dysfunction
  • Symptoms resulting from coronary ischemia or heart failure (HF) may be present that respond to revascularization and appropriate medical therapy

Grade B:

  • Progressive mitral regurgitation
  • Regional wall motion abnormalities demonstrating mild tethering of mitral leaflet and annular dilation with slight loss of central coaptation of the mitral leaflets
  • Hemodynamics: effective regurgitant orifice (ERO) less than 0.40 cm^2, regurgitant volume below 60 mL, Regurgitant fraction under 50%    
  • Cardiac findings: Regional wall motion abnormalities with reduced LV systolic function, LV dilation, and systolic dysfunction due to primary myocardial disease
  • Symptoms as described in Grade A

Grade C:

  • Asymptomatic severe mitral regurgitation
  • Regional wall motion abnormalities and/or LV dilation that show severe tethering of mitral leaflet, annular dilation with significant loss of central coaptation of the mitral leaflets
  • Hemodynamics: ERO greater than or equal to 0.40 cm^2, regurgitant volume greater than or equal to 60 mL, regurgitant fraction under 50%
  • Cardiac findings as described in grade B
  • Symptoms as described in grade A

Grade D:

  • Symptomatic severe mitral regurgitation
  • Regional wall motion abnormalities and/or LV dilation that show severe tethering of mitral leaflet, and annular dilation with significant loss of central coaptation of the mitral leaflets
  • Hemodynamics: ERO greater than or equal to 0.40 cm^2, regurgitant volume greater than or equal to 60 mL, regurgitant fraction greater than or equal to 50%
  • Cardiac findings as described in grade B
  • HF symptoms due to mitral regurgitation persist even after revascularization and optimization of medical therapy, decreased exercise tolerance, exertional dyspnea 


Mitral regurgitation is a common yet debilitating condition that leads to increased morbidity and mortality.[56] A study of 144 patients, found that the 5-year mortality of patients with MR was an impressive 30% compared to 13% of the age-matched control group. The study also determined that patients with functional mitral regurgitation had an overall increase in morbidity and mortality than those with structural MR.[57] 

With medical treatment alone, a study of patients aged 50 and older calculated a yearly mortality rate for moderate and severe organic mitral regurgitation as 3% and 6%, respectively.[6]

Mitral valve repair and replacement surgeries have been extensively studied and have shown significant improvement in symptoms and mortality. 

  • A study of 83 asymptomatic patients undergoing early valve surgery with a mean subject age of 56-years, found residual mitral regurgitation requiring re-repair in 1%, and patients requiring a permanent pacemaker was 4%. The 10-year survival rate after mitral valve surgery was 91.5%.[58]
  • Patients with degenerative or RHD with a mean age of 57-years-old undergoing mitral valve repair had comparable survival rates with individuals in the general population. A study of 125 mitral valve repairs determined early mortality in 2.4% and 10-year-survival of 84.3% postoperatively.[59]
  • The greatest predictor of survival and improvement of symptoms after MV surgery is pre-operative ejection fraction over 60%.[60]

MR repair is associated with increased survival and decreased morbidity and mortality compared to MR replacement.[54][61] A systematic review and meta-analysis of patients with severe MR with a reduced ejection fraction (under 40%) used a comparison of MR repair surgery versus MR replacement surgery regarding operative mortality. In patients undergoing mitral valve repair, the operative mortality was determined to be 5% and following MR replacement 10%.[53] 


Complications of mitral regurgitation include:

  • Heart failure and related symptoms (i.e., shortness of breath)
  • Atrial fibrillation
  • Stroke due to arrhythmias 
  • Pulmonary artery hypertension 
  • Dilation of the heart and cardiomegaly 

Complications of mitral valve surgery/replacement:

  • Infections (including infective endocarditis)
  • Bleeding
  • Clotting and stenosis of new valve
  • Valve dysfunction
  • Arrhythmias 
  • Stroke
  • Death

Postoperative and Rehabilitation Care

If no complications (i.e., infection, bleeding, etc.) arise during the procedure or hospitalization, most patients can be discharged within one-week postoperatively.

Postoperative guidelines have undergone study, and the following are the recommendations[62][63]:

  • A postoperative echocardiogram should be performed soon after the procedure before discharge and is periodically necessary to assess left-ventricular function, especially if symptoms arise.
  • Lifelong anticoagulation, particularly with warfarin, is indicated for mechanical or prosthetic valve replacements.
  • Clinicians should initiate antibiotic prophylaxis for infective endocarditis with patients who have a mechanical or prosthetic valve prior to dental, oral, or upper respiratory tract procedures or in patients with a history of endocarditis.[27]

Exercise therapy (ET) and cardiac rehabilitation after heart valve surgery has been extensively studied and is a general recommendation. Some data supports improved exercise capacity, and ejection fraction, however further studies are needed to develop a definite correlation.[64][65][66][67]

In a retrospective study of 105 patients undergoing heart valve surgery, the mean-time to return to work was about five months. Analysis of these patients also showed improved ejection fraction, 78.4% of patients studied were categorized in NYHA Stage I or II as compared with 38.1% before heart valve surgery.[68]


A cardiologist is necessary for the diagnosis and medical management of MR, and a cardiothoracic surgeon consult would be necessary if planning surgery.

Deterrence and Patient Education

Patients should know the symptoms associated with severe MR and when to seek medical attention. Patients with MR should also be aware of the indications for surgery and treatment. While patients diagnosed with moderate or severe secondary mitral regurgitation may benefit from surgery, leading to improved symptoms and quality of life, there has been no survival benefit from the surgery. In most cases, it is not indicated or performed.[31]

  • In the elderly population (defined as over 60-years-old), studies have shown that surgeons opt not to perform surgery due to no survival benefit. Several factors affect treatment decisions; in a study of 1741 MR patients, only 60.31% received surgical treatment. This number decreased to 54.71% in the greater than 60-year-old age group.[69]
  • Another study of 396 patients diagnosed with severe MR, 49% were not operated on due to comorbid conditions.[70]
  • Factors such as impaired left-ventricular ejection fraction, older age, and comorbid conditions should factor into the surgical decision-making process. 

It is essential to consult with a cardiologist regarding MR management as patient treatment options can vary depending on several factors discussed.

Enhancing Healthcare Team Outcomes

Mitral valve regurgitation is an increasingly common valvular disease associated with a wide range of causes and symptoms. Due to comorbidities, MR has a significant mortality rate, especially in the elderly population, and the only definitive treatment is surgical.[6] MR is universally under-diagnosed and treated, leading to its increased prevalence.[56] [Level 3] The American College of Cardiology (ACC) and American Heart Association (AHA) have developed evidence-based guidelines in the diagnosis and management of valvular diseases.[31] [Level 1]

Interprofessional healthcare team members should recognize early diagnosis and management have proven to be lifesaving, and advancements in medicine and valvular studies have attributed to a significant decrease in morbidity and mortality of this disease. [Level 1] Developing a team of specialized healthcare providers, such as cardiologists and cardiac surgeons, has shown to significantly improve patient care due to efficiency in the management of the patient and the decision-making process.[71] [Level 4] Cardiology nurses monitor patients, provide education, and facilitate team communication, reporting all observations to the appropriate clinical staff. Pharmacists review dosing, check for interactions, and also provide patient and healthcare team education. Also, the care of patients does not end in the operating room as cardiac rehabilitation, and postoperative care requires a group of health professionals that are crucial for improved patient outcomes and morale. These interprofessional team strategies can improve the outcomes for patients with mitral valve regurgitation. [Level 5]

(Click Image to Enlarge)
<p>Mitral Regurgitation During Systole

Mitral Regurgitation During Systole. Retrograde flow of blood through the mitral valve from the left ventricle to the left atrium. (1) Mitral valve (2) Left Ventricle (3) Left Atrium (4) Aorta.

J Heuser, Public Domain, via Wikimedia Commons

<p>Contributed by K Humphreys</p>


Steven Douedi


Hani Douedi


4/7/2023 2:54:20 PM



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