Mitral Regurgitation

Steven Douedi; Hani Douedi

Mitral Regurgitation

Author: Steven Douedi Editor: Hani Douedi Updated: 4/30/2024 2:52:38 PM

Introduction

Mitral regurgitation (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] MR is 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 the sound radiating to the left axilla (see Image. Mitral Regurgitation During Systole).

Anatomy of Mitral Valve

The mitral valve consists of 2 leaflets (anterior and posterior) sitting within the annulus. The posterior mitral leaflet originates from the LA endocardium. The leaflets are supported by a subvalvular apparatus comprising 2 papillary muscles (anterolateral and posteromedial) that arise from the LV myocardium and the chordae tendineae.[4][5]

Types of Mitral Regurgitation

Mitral regurgitation is subdivided into primary and secondary.[6]

Primary mitral regurgitation

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

Secondary mitral regurgitation

Also called functional or ischemic
Due to left ventricular wall motion abnormalities (ie, ischemic cardiomyopathy) or left ventricular remodeling (ie, 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

The Carpentier Classification divides mitral regurgitation into 3 types based on the leaflet motion:

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
  - 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 [3][9][10]

Etiology

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Etiology

Primary Mitral Regurgitation

Degenerative: 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, 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, osteogenesis imperfecta, and pseudoxanthoma elasticum lead to secondary MVP, causing MR.[11]

Congenital: 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 as causing primary MR.

Infectious/rheumatic: With an estimation of over 15 million cases worldwide, rheumatic heart disease is prevalent in developing countries due to a lack of medical resources and vaccinations.[14] Chronic rheumatic heart disease 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 Mitral Regurgitation

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, a flattening of the mitral annulus, and lower valve closing forces.[4] Reduced closing forces include LV contractility, altered systolic annular contraction, reduced synchronicity between the 2 papillary muscles, and global LV desynchrony, especially in basal segments.

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

Ischemic mitral regurgitation: Ischemic mitral regurgitation 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 classification, the leaflet dysfunction resulting in the most common form of ischemic mitral regurgitation 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, valvular deformation, and LV and papillary muscle synchronicity.

Congestive heart failure-associated: In a heart failure clinical study of 558 patients with severe congestive heart failure, defined as ejection fraction (EF) less than or equal to 35%, MR was severe in 4.3% of the patients, 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 congestive heart failure and MR.

Atrial fibrillation associated: Results from a retrospective cohort study found atrial fibrillation to cause increased atrial and valve annular size, resulting in functional MR. Of the patients studied, controlling atrial fibrillation and restoring sinus rhythm resulted in an increased reduction of functional MR.[21] A randomized trial also showed that AF had an association 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]

Epidemiology

Mitral regurgitation is a common valvular abnormality occurring in about 10% of the population.[1] Mitral valve prolapse, which is related to myxomatous degeneration of the mitral valve, is the most common cause of primary mitral regurgitation. Accounting for 2% to 3% of the total population, mitral valve prolapse has been cited as the most common cardiac mitral valvular pathology worldwide.[24] In developing countries, rheumatic heart disease remains prevalent and is the most common cause of mitral valvular pathology that results in hospital admissions.[25][26]

Pathophysiology

The definition of MR is a retrograde flow of blood from the LV into the left atrium LA through the MV, causing a systolic murmur heard best at the apex of the heart, with the sound radiating to the left axilla. Mitral regurgitation leads to left ventricular volume overload due to increased stroke volume, caused by increased blood volume within the left atrium and 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 EF is usually observed. However, the effective EF can be considerably lower depending on the regurgitant fraction. Over time, there is a positive feedback loop by which volume overload from MR causes dilation of the ventricle, widening of the mitral annulus, and diminishing coaptation of leaflets, leading to progressive worsening of the MR.

Eventually, volume overload becomes so severe that excitation-contraction coupling of the muscle membrane becomes impaired, and wall stress-related afterload on the left ventricle leads to dilation with decreased contractility, resulting in a reduction of EF. In addition, the regurgitant blood from the left ventricle during systole can eventually cause left atrial enlargement, impairment of left atrial contraction, and subsequent atrial fibrillation, leading to a thrombus in the left atrial appendage.[3][27][28]

History and Physical

Mitral valve regurgitation causes a holosystolic murmur that is heard best at the apex of the heart, with the sound radiating to the left axilla (see Video. Murmur of Mitral Regurgitation). Differentiating the murmur of mitral regurgitation from other systolic murmurs is essential.[29]

Mitral valve prolapse: a late systolic murmur heard best at the cardiac apex but with a mid-systolic click
Tricuspid regurgitation: a high-pitched, blowing, holosystolic murmur heard best at the lower left sternal border, with radiation to the right lower sternal border; increases with inspiration
Ventral septal defect: a holosystolic murmur (The more significant the ventral septal defect, the quieter the murmur.)
Aortic stenosis: a mid-systolic, crescendo-decrescendo murmur with radiation toward the neck; gets quieter with Valsalva maneuver or standing
Pulmonic stenosis: mid-systolic, crescendo-decrescendo murmur, increases in intensity during inspiration (In severe pulmonic stenosis, the S2 heart sound is widely split.)
Atrial septal defect: mid-systolic murmur with a fixed split S2 heart sound; does not change with inspiration
Hypertrophic cardiomyopathy: mid-systolic murmur, heard best medial to the cardiac apex; radiates to the left sternal border; murmur is louder with Valsalva and standing

Clinical findings related to MR are divided into 2 categories: those related to the MR itself and those associated with the underlying cause. Maintaining a broad differential diagnosis is important; 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

The clinical assessment of the acute onset of mitral regurgitation 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 accompanied by 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, jugular venous distension, diffuse crackles on lung auscultation, and an apical holosystolic murmur with radiation to the axilla on a precordial exam may be present.

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 them to immunocompromise, such as diabetes mellitus and alcohol use disorder. Due to the embolization of vegetative material, there may be a variety of additional clinical findings depending on the ultimate fate of the emboli. Brain involvement of the emboli will produce focal neurologic deficits; renal involvement will result in hematuria or oliguria; and cutaneous involvement will result in Janeway lesions or widespread petechiae. 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 by auscultation of murmurs on physical examination.[27][30]

Chronic Mitral Regurgitation

Patients with chronic mitral regurgitation often remain asymptomatic until late in the course of the disease. Clinical findings common to all etiologies include fatigue, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, dependent edema, weight gain, jugular venous distension, widening of pulse pressure, displaced apical impulse and apical holosystolic murmur with radiation to the axilla. In more advanced cases, there may also be syncope or near syncope, cyanosis, clubbing of digits, hepatomegaly, evidence of ascites with a fluid wave or shifting dullness, gross anasarca, 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, with specific clinical findings dependent on the etiology.[27]

Evaluation

Several tools are used to evaluate mitral regurgitation; the patient’s history and physical examination should guide the ordering of diagnostic tests.

Echocardiogram

Echocardiography is the primary and essential diagnostic test for diagnosing and assessing mitral regurgitation.[31] Transthoracic echocardiography and transesophageal echocardiography provide qualitative and quantitative analysis.

Various methods are available to quantify MR. One such method involves measuring the vena contracta, which represents the width of the regurgitant jet as it exits the regurgitant orifice. This provides insight into the regurgitant orifice area (eg, vena contracta greater than 7 mm is consistent with severe MR).

The Doppler volumetric method is also an option for quantifying MR. This method measures the regurgitant volume as the difference between the mitral and aortic stroke volumes. Regurgitant volume can be calculated as the product of effective regurgitant orifice area (EROA) and MR velocity time integral. Severe MR is quantified as:

EROA greater than or equal to 0.2 cm²
Regurgitant volume greater than or equal to 30 mL
Regurgitant fraction of 50% or higher [32][33]

After the initial echocardiographic evaluation, repeat echocardiography is indicated for patients with moderate or greater MR with or without symptoms every:

Severe: 6 to 12 months
Moderate: 1 to 2 years
Mild: 3 to 5 years

Repeat echocardiography is also a recommendation for patients with any degree of MR and a change in clinical status or physical examination findings.[31][34]

Following MV repair, successful mitigation of MR can be quantified via several tools. One method is measuring tenting height, which 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. In the healthy heart, normal values are:

Tenting height of less than 0.5 cm
Tenting area of 0 cm²
Angles of the anterior and posterior mitral leaflet are less than 3 degrees

Poor outcomes after MV repair are defined as:

Tenting height of greater than or equal to 1 cm
Tenting area of greater than 2.5 to 3 cm²
Complex jets
Posterolateral angle of over 45 degrees [19][35]

The sphericity index can also quantify the successful mitigation of MR following MV repair. 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 mm, end-systolic diameter over 51 mm, and systolic sphericity index greater than 0.7 predict unfavorable outcomes of MV repair.[35]

Successful MV repair can also be quantified by assessing distance and wall motion. An interpapillary distance of over 20 mm, posterior papillary fibrosis distance of more than 40 mm, and lateral wall motion abnormality are associated with poor outcomes after MV repair surgery.

Electrocardiogram

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

Chest Radiography

In patients with chronic MR, cardiomegaly due to left-atrial or right-sided heart enlargement is visible on anterior-posterior x-ray views.[27]

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 pulmonary artery pressure in those symptomatic with non-severe MR at rest.[27]

Cardiac Catheterization

Cardiac catheterization can quantify MR volume with high accuracy when clinical findings are inconsistent with noninvasive test results.

Cardiac Magnetic Resonance Imaging

Cardiac magnetic resonance imaging (MRI) is an important and complementary tool to other modalities for assessing the severity of MR. Cardiac MRI accurately assesses quantitative measurements, including regurgitant volume and regurgitant fraction. Cardiac 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 differentiate severe from non-severe MR in patients whose echocardiographic evaluation is inconclusive, particularly if contemplating surgery.[36][37]

Biomarkers

In response to heightened wall stress, ventricular myocytes release the biomarker B-type natriuretic peptide (BNP), which correlates with symptom severity and offers prognostic insights for individuals with MR. A BNP level may be normal in severe, compensated MR without 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 symptoms, LV dysfunction (ejection fraction less than 60%), or death during follow-up of patients with asymptomatic, severe MR.[38]

Treatment / Management

The choice of medical versus surgical management of mitral regurgitation depends on the condition’s severity, chronicity, comorbidities, and etiology. While some pharmacologic agents can be 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) or the American Heart Association (AHA).[31] Primary severe MR and ischemic severe MR usually receive treatment with valve surgery.[31][39] (A1)

Medical Management of Mitral Regurgitation

Angiotensin-converting enzyme inhibitors (ACE) and angiotensin II receptor blockers (ARBs) have been used in those who are asymptomatic to delay the progression of MR.[40] The belief is that ACE inhibitors and ARBs can decrease regurgitant volume and LV size in patients with chronic primary MR.[41][42] However, there are limited supporting results from studies, and their overall role in treating MR is discouraged.[31][39][43] Some study results have concluded no improvement or survival benefit in patients with MR using ACE inhibitors or ARBs and have even shown worsening outcomes for some.[44][45] In the setting of hypertrophic cardiomyopathy or mitral valve prolapse, vasodilators have demonstrated an increase in the severity of MR.[46](A1)

Beta-blockers for the treatment of MR have also been studied, with results revealing little to no benefit with beta-blocking agents in primary MR; some results have shown increased survival benefit with these agents in secondary MR.[47] One study evaluating the beta blocker carvedilol supported its use after demonstrating the preservation of LV function, remodeling, and decreased regurgitant volume.[48] The ACC/AHA does not have specific recommendations regarding using beta-blockers in patients with MR.[31] (A1)

Loop diuretics are believed to be helpful in conjunction with other pharmacologic agents to further decrease afterload and regurgitant volume, but further studies are necessary to support this association properly.[41] (A1)

Surgical Management of Mitral Regurgitation

The decision whether 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 surgery. Patients with functional causes of MR, such as ischemia, generally require coronary artery bypass grafting.[2][49] Patients with acute, symptomatic MR or an EROA of at least 4 cm² require surgical intervention.[28] Surgery for MR is indicated in patients with LV function deterioration or an end-systolic diameter of 45 mm.[50] Patients diagnosed with primary severe MR require surgery when symptomatic with an ejection fraction over 30% or asymptomatic with an EF of 30% to 60%.[51] (B3)

Mitral valve repair has 2 aims:

An acceptable surface area of mitral valve leaflet coaptation
Essential annular dilatation of 5 to 8 mm [50]

The ACC and AHA generally recommend mitral valve repair over replacement due to decreased recurrence of MR after repair.[31][52] Available data reveal decreased morbidity and mortality after surgical repair over replacement.[53] However, mitral valve replacement is favorable over repair when there is extensive tissue destruction, which can occur in some cases of infective endocarditis.[49] Nevertheless, the newest AHA guidelines clearly state that “mitral valve replacement is preferable to a poor repair.”(A1)

With respect to surgical replacement of the mitral valve, mechanical prostheses are usually preferable to bioprosthetics due to increased durability and less complicated insertion. Postoperatively, both types require anticoagulation, with bioprosthetic valve replacement requiring only temporary anticoagulation and lifelong anticoagulation with warfarin for mechanical valves.[54]

Mitraclip is another surgical procedure proven to be effective and has low morbidity and mortality in patients considered to be at high risk for repair or replacement.[54] Mitraclip can decrease the mitral valve area, leading to stenosis, and therefore, an area of under 4 cm² is a contraindication for this procedure.[55]

Differential Diagnosis

Clinical findings related to MR can be divided into 2 categories: those related to the MR itself and those associated with the underlying cause. Maintaining a broad differential diagnosis is crucial. In general, with an initially focused history and physical examination, one can establish whether the MR is acute or chronic and significantly narrow the possible etiologies that can include the following:

Congestive heart failure exacerbation
Acute coronary syndrome
Hemodynamically unstable dysrhythmia
Cardiac tamponade
Pneumothorax
Pulmonary embolism
Septic shock
Thyrotoxicosis or thyroid storm

The differential diagnosis of chronic mitral regurgitation is also considerably broader, and specific clinical findings depend on the etiology.

Staging

The following staging data for MR is from the 2020 AHA/ACC updated guidelines for managing heart valve disease, including mitral regurgitation:

Stage A

At risk of mitral regurgitation (ie, infective endocarditis, mitral valve prolapse)
Normal valve leaflets, chords, and annulus in patients with coronary disease or cardiomyopathy
Hemodynamics: no MR jet or a small central jet area less than 20% LA on Doppler; small vena contracta less than 3 mm; MR grade can be described as trace or trivial
Cardiac consequences: none or those that are unrelated to the valvular changes
Patients at this stage remain asymptomatic [7][31]

Stage B

Progressive mitral regurgitation occurs in this stage.
ECG assessment of mitral valve anatomy demonstrates mild tethering of mitral leaflets and annular dilation with a normal to slight loss of central coaptation that may be associated with prior infective endocarditis (IE.)
Hemodynamics: EROA is less than 0.4 cm2, regurgitant volume below 60 mL, and regurgitant fraction below 50%. There might be a central regurgitant jet that is only 20% to 40% in magnitude or a late systolic eccentric jet. The venta contracta should not exceed 7 mm in width in all cases. MR grade is 1+ to 2+.
Cardiac consequences: Left atrial enlargement begins at this stage. Left ventricular dimensions and pulmonary pressures are usually not affected.
Patients at this stage remain asymptomatic.

Stage C

Asymptomatic severe mitral regurgitation occurs in this stage.
ECG assessment of mitral valve anatomy shows a flail leaflet or severe mitral valve prolapse (MVP) and loss of central coaptation due to leaflet restriction. Causes can be prior IE or a history of chest irradiation.
Hemodynamics: EROA is greater than or equal to 0.4 cm2, regurgitant volume is greater than or equal to 60 mL, regurgitant fraction is greater than or equal to 50%, central regurgitant jet that is greater than 40%, or there is a pansystolic eccentric jet. MR grade is 2+ to 3+.
Cardiac consequences: patients at this stage are categorized as C1 (preserved ejection fraction greater than 60%, LV end-systolic diameter is less than 40 mm, or C2 (reduced ejection fraction less than or equal to 60% or LV end-systolic diameter is greater than 40 mm). Both categories exhibit moderate to severe LA enlargement with some LV distension.
Patients at this stage remain largely asymptomatic. Some patients may experience symptoms upon severe physical exertion.

Stage D

Symptomatic severe mitral regurgitation defines this stage.
ECG assessment of mitral valve anatomy is similar to stage C with increased severity and extent.
Hemodynamics: EROA is greater than 0.4 cm², regurgitant volume greater than or equal to 60 mL, regurgitant fraction greater than or equal to 50%, vena contracta greater than or equal to 7 mm, central regurgitant jet that is greater than 40%, or a pansystolic eccentric jet. MR grade is 3+ to 4+.
Cardiac changes as described in grade C with evidence of pulmonary hypertension
Heart failure symptoms due to mitral regurgitation persist even after revascularization and optimization of medical therapy, decreased exercise tolerance, and exertional dyspnea.

Prognosis

Mitral regurgitation is a common yet debilitating condition that leads to increased morbidity and mortality, and research is valuable for finding new techniques for managing this condition.[56] Mitral valve repair and replacement surgeries have been extensively studied and have shown significant improvement in symptoms and mortality.

Several pertinent studies follow:

A study of 144 patients with mitral regurgitation found that the 5-year mortality was a remarkable 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]
Another study of patients 50 and older with medical treatment alone for mitral regurgitation calculated a yearly mortality rate for moderate and severe organic mitral regurgitation as 3% and 6%, respectively.[6]
A study of 83 patients (asymptomatic, mean age of 56, and undergoing early mitral valve surgery) found residual mitral regurgitation requiring re-repair in 1%, and 4% required a permanent pacemaker. The 10-year survival rate after surgery was 91.5%.[58]
Patients with degenerative or rheumatic heart disease and a mean age of 57 years undergoing mitral valve repair had comparable survival rates with individuals in the general population. A study of 125 mitral valve repairs determined postoperative early mortality in 2.4% of the patients and a 10-year survival rate of 84.3%.[59]
A systematic review and meta-analysis of patients with severe MR with a reduced ejection fraction (under 40%) compared mitral valve repair surgery versus mitral valve replacement surgery regarding operative mortality. In one study of patients undergoing mitral valve repair, the operative mortality was determined to be 5%. However, the mortality rate following mitral valve replacement was estimated to be 10%.[53]

The greatest predictor of survival and improvement of symptoms after MV surgery was shown to be a pre-operative ejection fraction over 60%.[60] Mitral valve repair is associated with increased survival and decreased morbidity and mortality compared to mitral valve replacement.[54][61]

Complications

Complications of mitral regurgitation include:

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

Complications of mitral valve surgery or replacement include:

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

Postoperative and Rehabilitation Care

Most patients can be discharged postoperatively if no complications (ie, infection or bleeding) arise during the procedure or hospitalization.

Postoperative guidelines have undergone study, and the following are the recommendations:

A postoperative ECG should be performed soon after the procedure before discharge and is periodically necessary to assess left ventricular function, especially if symptoms arise.
Lifelong anticoagulation, typically with warfarin, is indicated for mechanical or prosthetic valve replacements.
Clinicians should initiate antibiotic prophylaxis for infective endocarditis before dental, oral, or upper respiratory tract procedures in patients with a mechanical or prosthetic valve or a history of endocarditis.[27][62][63]

Exercise therapy and cardiac rehabilitation after heart valve surgery have been extensively studied and are generally recommended. 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 who underwent heart valve surgery, the mean time for them to return to work was about 5 months. These patients also showed improved ejection fraction, with 78.4% of patients studied categorized in NYHA stage I or II compared with 38.1% before heart valve surgery.[68]

Consultations

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

Deterrence and Patient Education

Patients could benefit from understanding the symptoms indicative of severe MR and recognizing when to seek medical assistance. Additionally, it is valuable for patients with MR to understand the criteria for surgery and available treatment options. While patients diagnosed with moderate or severe secondary mitral regurgitation may benefit from surgery, with an improvement in symptoms and quality of life, there has been no proven survival benefit from surgery. In most cases, it is not indicated or performed.[31]

In the older adult population (eg, 60+), study results have shown that surgeons opt not to perform this surgery due to no survival benefit. Several factors affect treatment decisions. In a study of 1741 patients with mitral regurgitation, only 60.31% received surgical treatment. This number decreased to 54.71% in the age group greater than 60.[69]
In another study of 396 patients diagnosed with severe mitral regurgitation, 49% were not operated on due to comorbid conditions.[70]
Surgical decision-making should consider impaired left-ventricular ejection fraction, older age, and comorbid conditions.

Consult with a cardiologist regarding the management of mitral regurgitation, as patient treatment options can vary depending on several factors.

Enhancing Healthcare Team Outcomes

Mitral valve regurgitation is an increasingly common valvular heart disease associated with a wide range of causes and symptoms. Due to comorbidities, MR has a significant mortality rate, especially in the population older than 60, and the only definitive treatment is surgery.[6] MR is universally under-diagnosed and under-treated, leading to its increased prevalence.[56] The ACC and AHA have developed evidence-based guidelines for evaluating, diagnosing, and managing valvular diseases.[31]

Interprofessional healthcare team members should recognize that early diagnosis and management have proven to be lifesaving, and advancements in medicine and valvular studies have contributed to a significant decrease in morbidity and mortality of this disease. Developing a team of specialized healthcare professionals, such as cardiologists and cardiac surgeons, has significantly improved patient care due to efficiency and efficacy in managing the patient and the decision-making process.[71]

Nurses trained in cardiology monitor patients, provide education, and facilitate team communication, reporting all observations to the appropriate clinical staff. Pharmacists review the dosing and potential interactions of medications and educate patients and the healthcare team. Patient care does not end in the operating room; postoperative care and cardiac rehabilitation require a team of healthcare professionals who are crucial for improved patient outcomes and morale.

Media

(Click Image to Enlarge)

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>

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