Continuing Education Activity

This activity discusses clinical aspects of mitral regurgitation (MR) in terms of etiology, epidemiology, diagnosis, management, and treatment guidelines for clinicians, which should help them understand this common disease comprehensively. It reviews the role of the interprofessional team.

Objectives:

• Explain the etiology of mitral regurgitation.
• Outline the clinical bedside assessment of mitral regurgitation.
• Review the most updated guidelines for the surveillance of mitral regurgitation.
• Describe various treatment strategies such as surgical and transcatheter therapies for mitral regurgitation with their relative risks and benefits.

Introduction

Mitral valve insufficiency or mitral regurgitation (MR) is characterized by the reversal of blood flow from the left ventricle (LV) to the left atrium (LA), typically in the systolic phase of the cardiac cycle. It continues to be a significant issue in cardiovascular health worldwide. Serial advancements in the diagnostic tools, clinical management, and treatment of this valvular lesion have changed the clinical approach over the last several decades. The mitral valve apparatus is a complex but dynamic structure and consists of the mitral annulus, two leaflets, chords, and papillary muscles, which are surrounded by complex anatomy in LA and LV.[1] Disruption in the structural integrity or functional mechanism of this apparatus with or without the involvement of surrounding structures results in MR.[2] This activity will review various aspects of this common clinical cardiovascular entity, including diagnosis, evaluation, and management.

Etiology

Based on the acuity of presentation, mitral regurgitation can be acute or chronic. However, acute MR has a very specific set of etiological reasons such as rupture of the chord/papillary muscle from trauma or ST-segment elevation myocardial infarction (STEMI), or infective endocarditis (IE) leading to leaflet perforation or rupture of the chords.[3] Spontaneous rupture of the chord has also been reported in degenerative mitral valves such as myxomatous degeneration and Marfan syndrome, causing severe acute MR.[4]

In the chronic MR, causative mechanisms can be related to the valvular apparatus itself, causing primary (degenerative/organic) MR versus related to structural changes in LV geometry leading to secondary (functional) MR. Most of the intrinsic abnormalities in the valve arising from local/systemic infection, inflammation, excess growth of the tissue, drug or radiation-induced damage, and calcific degeneration lead to primary MR.[5] Connective tissue disorders, cleft in the mitral leaflets, rheumatic heart disease, and IE are other common etiologies for chronic primary MR.[3] While the predominant cause of primary MR in developing countries continues to be rheumatic heart disease, myxomatous degenerative changes with mitral valve prolapse (MVP) is the commonest etiology of primary MR in developed countries.[6][7] Genetic predisposition causing myxomatous degenerative MR has also been shown in community studies about familial MR.[8] 

In secondary MR, the basic structure of the mitral valve is preserved, but dilatation of LV cavity from various reasons including ischemic and nonischemic cardiomyopathies, increased annular diameter, tethering of papillary muscle, migration of papillary muscles due to structural remodeling of LV, lead to failure of coaptation of mitral leaflets.[3] Ischemic heart disease continues to be an important contributor to secondary MR due to structural remodeling from acute as well as chronic ischemia.[9] More than 10% of patients with coronary artery disease have moderate to severe MR, affecting long-term outcomes with heart failure and mortality.[10] Also, atrial fibrillation and diastolic congestive heart failure (CHF) lead to progressive left atrial and ventricular enlargement and subsequent annular dilatation, causing functional MR.[11] Congenital conditions such as hypertrophic cardiomyopathy also cause specific structural changes in the left ventricle and the left atria, with a variable degree of MR.[12]

Epidemiology

mitral regurgitation is one of the commonest valvular heart disease worldwide as well as in North America, affecting greater than 175 million people worldwide and around 5 million people in the United States.[13][14] Due to the rising proportion of the geriatric population with better life expectancy and overall growth, the prevalence of MR is on the rise.[15] The prevalence increases from less than 1% in the general population at less than 45 years of age, rising to more than 11% in the age group of population greater than 75 years of age, with a significant impact on survival.[16] However, nearly 50% of patients diagnosed with severe MR are not candidates for corrective surgery due to LV dysfunction, old age, and related comorbidities. Moreover, due to the scarcity of advanced skilled facilities, the treatment has been suboptimal for this population.[17] Clinical outcomes highly depend on early diagnosis, timely referral, and medical/surgical interventions.

Pathophysiology

In primary mitral regurgitation, there is a pathological disruption in the integrity of the mitral valve apparatus, causing regurgitation, whereas, in secondary MR, the problem arises due to structural changes in the left ventricle (LV), causing failure of coaptation of mitral leaflets due to annular dilatation.[18] 

The popular classification defined by Carpentier has given a surgeon's perspective for the corrective approach towards MR based on the leaflet motion of the valve.[19][18] 

• Type I - normal leaflet motion with normal coaptation (leaflet perforation, cleft)
• Type II - abnormal coaptation with excessive leaflet motion (either due to excess of tissue/excess of motion- mitral valve prolapse)
• Type IIIa - abnormal apposition of leaflets due to restricted leaflet motion both in systole and diastole (mostly from organic leaflet issues such as rheumatic heart disease)
• Type IIIb - abnormal apposition of leaflets due to restricted leaflet motion in systole (from LV remodeling)[19] 

Primary MR

Myxomatous degeneration with excessive thickening of mitral valve leaflets causes redundant lengthening of leaflets and prolapse in younger patients, and fibroelastic deficiency leading to chordal rupture causes primary MR in the older population. Barlow disease is in the same spectrum as thickened leaflets and redundant motion.[20] Rheumatic heart disease, drugs, radiation, and connective tissue disorder lead to progressive thickening of mitral leaflets with restrictive movements and loss of central coaptation leading to central primary MR. Progressive calcific degeneration of leaflets and subvalvular apparatus has been found to be another common cause of primary MR in the geriatric population.[21] Leaflet perforation and rupture of a chord can be the severe consequences of IE, leading to severe primary MR.[2]

Secondary MR

Secondary mitral valve insufficiency is the continuum of the underlying myocardial disease process- either as a result of acute or chronic myocardial ischemia or nonischemic cardiomyopathy. Ischemic MR typically arises from obstructive coronary artery disease. Acute ischemic MR happens due to acute myocardial infarction causing disruption in subvalvular apparatus such as ruptured chords or rupture of a papillary muscle. Chronic ischemic MR is a sequela of altered LV geometry, causing displacement of papillary muscles and functional disintegration of the mitral apparatus.[22] Chronic ischemic MR is typically caused by LV remodeling from lateral or inferior myocardial infarction with papillary muscle displacement but intact leaflets and chords. This leads to overall apical displacement of mitral valve apparatus and annular dilatation, resulting in malcoaptation due to a mismatch between tethering forces and closing forces.

Ischemic MR being the largest contributor to secondary MR, nonischemic cardiomyopathy from various reasons also leads to remodeling of LV cavity with progressive dilatation, dyssynchronous contractility, alteration in systolic annular movements, and decreased LV function, eventually causing functional MR. The vicious cycle of MR causing LV dilatation, which leads to further annular dilatation, causes progressive worsening of MR.[23] Interestingly, local LV remodeling causing valvular distortion and excessive mitral valve tenting have been found to be major determinants of the degree of MR instead of LV function and global LV remodeling.[24]

It is very important to understand the complex exchange of causes and mechanisms of MR for accurate prediction of outcomes after surgical intervention because a significant overlap exists between causes and mechanisms of MR. Another recommended approach to evaluate the mechanism of MR is if the issue is leaflet apposition or leaflet coaptation.[18]

History and Physical

Presentation of acute mitral regurgitation is typically quite dramatic with sudden clinical and hemodynamic decompensation from discrete etiology such as papillary muscle rupture from myocardial infarction, blunt trauma to the chest, perforation of the mitral leaflet, etc.[25][26][27] The typical holosystolic murmur can become early systolic or very faint due to the rapid equalization of pressures between LA and LV. Acute MR requires emergent clinical attention with critical care support, and most of them require urgent surgical or percutaneous cardiovascular intervention. 

The majority of patients suffering from chronic MR are asymptomatic, but serial quantitative assessment and follow-up of a patient with asymptomatic MR have shown a significant impact on the survival and clinical outcome.[28] Due to the insidious and slowly progressive nature of chronic MR, patients may not report any specific symptoms and may not notice a progressive decline in functional status during the early phase of the disease by gradual modification of their activities. Bedside evaluation for valvular heart disease is very important as management highly depends on symptoms as well as the severity of valvular lesions. Patients with MR are usually referred due to symptoms of chest pain, shortness of breath, palpitations, leg swelling, or just incidental finding of systolic murmur on physical examination. A thorough history of prior bacterial or viral infections, rheumatic fever, trauma, ischemic events, invasive cardiac/noncardiac procedures and family history with a comprehensive review of systems should be obtained. A detailed physical examination with particular attention to the cardiovascular system, including pulse, apical impulse, jugular veins, edema, signs of congestive heart failure, and assessment of characteristic systolic murmur with other pertinent findings should be documented.[29][3] A characteristic holosystolic murmur present at the apex and radiating to the left axilla can be present most of the time except in cases of MVP where the murmur appears in mid-late systole with or without midsystolic click. The murmur should not be confused with other systolic murmurs such as aortic stenosis, tricuspid regurgitation, pulmonic stenosis, ventricular septal defect, benign flow murmurs, and other cardiac disorders in the spectrum.[30]

Evaluation

Basic 12 lead electrocardiogram may show sinus rhythm or development of atrial arrhythmias, most prevalent being atrial fibrillation, atrial/ventricular enlargement, evidence of acute or chronic ischemia, and conduction disorders such as bundle branch block(s). Chest X-ray may reveal cardiomegaly, chamber enlargement, signs of heart failure, and serial prognostic data.[31]

Echocardiography, including transthoracic (TTE), transesophageal (TEE), and 3-dimensional (3D) mode, remains the "gold standard" modality of investigation for both diagnoses as well as management of MR.[32] The parasternal long-axis view in TTE cuts through middle scallops of anterior and posterior leaflets (A2 and P2), but the short-axis views at multiple levels in the ventricle give more information about leaflets and commissures, with a better definition of underlying pathology. [21] Apart from the mechanism and severity of MR, it also provides crucial information about the preferred treatment approach with the likelihood of success, comprehensive review of adjacent structures including pulmonary veins, left ventricle remodeling, ejection fraction, development of pulmonary hypertension, and left atrial indices.[33] Progressive MR leads to increased pressure in LA and volume overload, which leads to the development of pulmonary hypertension and right ventricular failure.[34] The widespread availability of echocardiography services has made it the screening as well as a monitoring tool for MR. Given its inherent advantages in image quality and accuracy, TEE has higher predictability for the anatomy of MR lesions as well as surgical outcomes as compared to TTE.[7] En face views obtained by 3D-TEE are able to provide specific information regarding the location, anatomy, and mechanism of MR.[21] In the case of equivocal evaluation at rest, exercise echocardiography is indicated to assess response to exercise.[34] Decreased exercise capacity, exercise-induced severe MR, pulmonary hypertension, wall motion abnormalities, and development of atrial fibrillation are some of the key criteria for MV surgery.[22]

In acute MR, TTE plays a crucial role in urgent bedside assessment of the underlying mechanism of MR, intracardiac pressures, and ventricular function. Due to the sudden onset of MR, an acute increase in LA pressure leads to pulmonary edema, and hyperdynamic LV function is noted. The murmur can be holosystolic or early systolic or barely audible due to the rapid equalization of pressures in LA and LV. If TTE is suboptimal, TEE provides very specific information, including vegetations or abscess, in case of infective endocarditis. [3]

The severity of MR by qualitative and quantitative measures can be assessed by TTE with various methods of grading as follows:[35]

1. Color Doppler Method

• A. Regurgitant jet area- The area of LA occupied by the MR jet gives an approximate estimation of the severity of MR, but the correlation is weak. In acute MR, the jet may not appear wide and large due to the rapid equalization of pressures. Also, the MR jet area highly depends on blood pressure, LA enlargement, LV systolic function, and eccentricity. Also, technical limitations in echocardiography itself can cause alterations in the jet area. In general, a central jet that occupies less than 20% of the LA area is considered trace or mild MR, and jet penetrating pulmonary veins is labeled severe MR. Eccentric jets should not be evaluated by these criteria.
• B. Vena contracta method- The high velocity, laminar flow at or just downstream of MR jet, is the narrowest portion of MR jet, and severity can be reliable as it is independent of flow rate and driving pressure of MR. Measurement of vena contracts (VC) is done in the plane perpendicular to the commissural lane in multiple images. In general, VC less than 0.3 cm is considered mild, greater than 0.7 cm as severe MR, and between 0.3 to 0.7 cm as moderate MR, but then other parameters need to be considered for confirmation.
• C. Flow convergence or PISA (proximal isovelocity surface area) method- Based on a complex hydrodynamic equation, PISA can be estimated on TTE/TEE after adjustment of the Nyquist limit and hemispheric shell of highest velocity and the minimum area is measured. Effective regurgitant orifice area (EROA) is calculated from PISA measured by parallel alignment of continuous wave (CW) Doppler signal to MR jet and selection of appropriate aliasing velocity, as large errors can be introduced if aliasing velocity and alignment of CW signal are not accurate. It is a reliable method mostly for central MR jets and circular orifice. By convention, EROA ≥ 0.4 cm is graded as severe MR, 0.20 to 0.39 cm moderate, and less than 0.20 cm mild MR.

2. Pulsed Doppler Method (Pulsed Wave (PW) method)

The pulsed Doppler method is based on the principle that, in the absence of significant valvular regurgitant lesion(s) and intracardiac shunt, stroke volume (SV) through any cardiac valve should be the same to maintain a uniform cardiac output. So, to compensate for regurgitant flow volume, SV through the pertinent valve increases proportionately. SV, through any valvular annulus, is calculated by the cross-sectional area of the annulus and velocity-time integral (VTI) of the flow-through that annulus. Except for the tricuspid annulus, all other three valves have near-circular annuli with minor variations. SV is then calculated from these annuli, and SV of normal aortic or pulmonic valve is subtracted from SV of the mitral valve to obtain regurgitant volume (RV). Regurgitant fraction (RF) can be calculated from the ratio of RV to SV through the mitral valve. RV less than 30 ml is mild, and greater than 60 ml is severe. Errors can be introduced with incorrect measurements of the annulus, angulation, and VTI.

3. Continuous Wave Doppler Method

Apart from PISA, as mentioned above, the peak velocity of 4 to 6 m/s and the density of the jet have been directly correlated with significant MR. Also, early peaking of maximal systolic velocity, dense Doppler envelope, and triangular jet on CW is suggestive of severe MR in the central jet, but they are not reliable in eccentric jet due to lack of alignment to Doppler signal.

4. Pulmonary Vein Flow Method

In normal conditions, the pulmonary venous flow velocity is higher in systole than in diastole. But with progressive MR, the systolic velocity gets blunted, and in severe MR, it gets reversed, which is considered a very specific sign. Sometimes, a reversal of flow selectively occurs in one over other pulmonary veins. Hence, it is recommended to assess the flow in all pulmonary veins. In the presence of elevated LA pressure and atrial fibrillation, the reversal of flow may not be prominent.

Given the advantages and disadvantages of all these quantification techniques, it is recommended to utilize as many parameters as possible during TTE/TEE for a comprehensive assessment of MR. All these methods have provided uniform applicable criteria as well as reproducibility of data for long-term follow-up.[21]

Recent advances in cardiac magnetic resonance (CMR) have enhanced the assessment of the mitral valve apparatus.[36] Several studies have shown the superiority of CMR over echocardiography for decision-making.[37] In fact, in a very recent prospective study, CMR appeared to be a better investigation than TTE for accurate assessment of etiology, mechanism, quantification of MR, and chamber dimensions, affecting decision for corrective surgical treatment.[38]

Left heart catheterization with coronary angiography and right heart catheterization for hemodynamic assessment of MR is usually done after the confirmation of significant MR with noninvasive investigations and patients being considered for surgical/transcatheter interventional treatment. With advanced noninvasive modalities, the use of contrast left ventriculography for assessment of MR has gone down. Nevertheless, MR grade of more than 3 to 4 on ventriculogram portends severe MR. Assessment of coronary anatomy for ischemic MR is very important to determine percutaneous versus surgical intervention. Recent data shows that sensitivity and specificity for the correlation between MR and magnitude of large V wave in right heart catheterization have changed but remain a reliable parameter.[39]

Treatment / Management

Due to a sudden hemodynamic decompensation, acute MR typically requires urgent surgical or percutaneous intervention.[40] Most patients with acute mitral regurgitation, as well as some patients with delayed diagnosis and treatment of chronic MR, present with decreased cardiac output, hypotension,

or cardiogenic shock with a complex challenge of hemodynamic stabilization and eventual corrective intervention. An appropriate combination of inotropic and vasopressor agents and timely intervention of mechanical support devices such as intra-aortic balloon pumps or non-surgical heart pumps are essential cornerstones along with mechanical ventilation in critical conditions.[4][41] Urgent revascularization remains the treatment of choice in the setting of acute myocardial ischemia resulting in papillary muscle dysfunction or rupture.[33]

In cases of severe MR due to acute IE, both MV replacement as well as MV repair in properly preselected patients have shown similar clinical outcomes.[42][43] Preservation of MV apparatus with repair in cases of mitral IE with MR has shown viable results.[44]

For primary chronic MR, surveillance and timely intervention are key factors for better outcomes. Early surgical intervention has shown better survival rates over conservative medical management in patients with a flail mitral leaflet.[45] Surgery is recommended for chronic severe primary MR in patients with symptoms and EF more than 30%, in asymptomatic patients with LV dilatation and EF of 30% to 60%, and patients with severe MR undergoing cardiac surgery for other indications. It is also indicated in the presence of severe primary MR with resting pulmonary hypertension, new onset of atrial fibrillation, progressive increase in LV cavity size, or decline in LV ejection fraction. Preference to mitral valve repair over replacement has been given depending on regional anatomy, the involvement of leaflets, and the chance of a successful repair.[46]

Mitral valve repair remains the preferred method of surgical correction in degenerative MR with a high success rate and less chance of recurrence or a repeat intervention.[47] Intraoperative TEE has been beneficial for anatomical evaluation and guidance of surgical repair.[48] With the use of appropriate selection criteria, the use of minimally invasive surgical techniques and avoidance of complete sternotomy has provided early recovery with excellent long-term outcomes.[49] In patients with significant degenerative MR but high-risk surgical mortality, percutaneous edge-to-edge repair with transcatheter mitral valve repair has shown to be a viable option with good safety outcomes.[50]

For functional MR, the role of surgery is still not very clear, as MR is just one part of the LV disease spectrum, and addressing MR without adequate attention to underlying myocardial disease has not provided therapeutic success.[51] Standard guideline-directed medical therapy (GDMT) for CHF is the first-line treatment, and in the case of ischemic MR, revascularization of underlying coronary artery disease is recommended.[46] Cardiac resynchronization therapy (CRT) for symptomatic MR who fulfills the criteria has shown significant improvement in the quality of life with a survival benefit.[52] Coronary artery bypass surgery (CABG) with mitral annuloplasty for functional MR has shown symptomatic improvement in the early period but failed to show long-term positive outcomes as compared to CABG alone, stressing the importance of addressing underlying LV pathology.[53] As per the current guidelines, restrictive mitral valve annuloplasty with surgical coronary revascularization remains the preferred treatment for ischemic MR.[54] Surgical correction of chronic secondary MR has been deemed reasonable if the patient is undergoing cardiac surgery for other indications or in symptomatic patients despite optimal GDMT.[46]

For evaluation of patients being considered for MV replacement, several factors need to be considered for the choice of metallic versus bioprosthetic valves, such as age, MV anatomy, patients' preference, available surgical expertise, risk of bleeding on long term anticoagulation, access to healthcare, and monitoring of anticoagulation.[46]

Several echocardiographic parameters have been described as predictors of recurrence of ischemic MR after MV repair.[22] The COAPT Trial has successfully shown that the transcatheter repair of the mitral valve is a reasonable choice of treatment in patients with symptomatic congestive heart failure and moderate-to-severe/severe functional MR, with a reduction in both morbidity and mortality.[55] On the other hand, the MITRA-FR trial showed no significant benefit of this technique in another group of similar patients with functional MR.[56] However, there were several differences between study populations in terms of patient selection criteria, the severity of MR, baseline LV geometry, and symptomatology. The importance of the safety profile of the device as well as the patient population before intervention remains pivotal.[57]

While transcatheter repair has been established as a standard of treatment for severe MR, percutaneous replacement of mitral valve with a bioprosthetic valve for inoperable cases of MR is still under the process of rigorous research and trials with its inherent challenges.[58] 

Differential Diagnosis

• Acute coronary syndrome
• Severe aortic stenosis
• Infective endocarditis
• Cardiogenic shock
• Exacerbation of chronic systolic, diastolic, or combined CHF
• Ventricular septal defect
• Pulmonary embolism
• Blunt chest trauma
• Carcinoid syndrome
• Unstable supraventricular or ventricular arrhythmia

Staging

Stages of chronic primary mitral regurgitation can be categorized as follows with consideration of hemodynamics, valvular anatomy with echocardiographic features, and symptoms which are typically present only in stage D, i.e., severe symptomatic MR.[59]

A. At risk of MR - mild MVP, mild leaflet thickening, normal coaptation- no MR or small central jet (20% of LA), vena contracta less than 0.3 cm

B. Progressive MR - severe MVP, rheumatic changes as leaflet thickening and loss of central coaptation, history of IE- central MR jet (20% to 40% of LA), mild LA enlargement, normal LV size, and function, normal pulmonary pressure.

C. Asymptomatic severe MR - severe MVP, flail leaflet, rheumatic changes as leaflet thickening and loss of central coaptation, history of IE, radiation-induced thickened leaflets - moderate/severe LA enlargement, LV dilation, pulmonary hypertension (pulmonary artery systolic pressure PASP greater than 50 mmHg), central MR jet (greater than 40% of LA), holosystolic eccentric MR jet, vena contracta ≥0.7 cm, regurgitant volume (RV) ≥60 mL, Regurgitant fraction (RF) ≥50%, ERO ≥0.40 cm

•  C1: LVEF >60% and LVESD <40 mm
•  C2: LVEF ≤60% and LVESD ≥40 mm

(LVEF= LV Ejection Fraction, LVESD= LV End Systolic Dimension)

D. Severe symptomatic MR- severe MVP, flail leaflet, rheumatic changes with leaflet thickening & loss of central coaptation, history of IE, radiation-induced thickened leaflets- moderate/severe LA enlargement, LV dilation, pulmonary hypertension, central MR jet (greater than 40% of LA), holosystolic eccentric MR jet, vena contracta ≥0.7 cm, RV ≥60 mL, RF ≥50%, ERO ≥0.40 cm. Symptoms- impaired exercise tolerance, dyspnea on exertion.

Similarly, stages of chronic secondary MR can be briefly summarized with valve hemodynamics and anatomy as follows; in all the categories, symptoms from coronary artery disease or CHF may be present, but only in the last category symptoms can be attributed to underlying MR.[51]

A. At risk of MR- Normal valve apparatus in a patient with known coronary artery disease- No MR jet or small central jet (<20% of LA), Vena contracta <0.3 cm

B. Progressive MR- Regional wall motion abnormality (RWMA), LV dilation, annular dilatation, mild tethering of leaflets, mild loss of central coaptation- ERO <0.40 cm, RV <60 mL, RF <50%

C. Asymptomatic severe MR- RWMA, annular dilation, severe tethering of leaflets, severe loss of central coaptation- ERO ≥0.40 cm RV ≥60 mL, RF <50%

D. Symptomatic severe MR- RWMA, annular dilation, severe tethering of leaflets, severe loss of central coaptation- ERO ≥0.40 cm RV ≥60 mL, RF <50%. 

Prognosis

Prognosis, in terms of mortality and morbidity, is highly variable. The presence of moderate to severe MR in patients with asymptomatic mitral valve prolapse (MVP) is a significant prognostic factor in long-term cardiovascular health and mortality.[60] Also, the presence of severe MR with LV systolic dysfunction is known to have a poor outcome.[61] On the other hand, in patients with myocardial infarction, the presence of significant MR has been independently associated with the risk of heart failure and death.[10] In the absence of symptoms, LV dysfunction has been a key factor for consideration for surgery because the so-called 'normal' EF is actually low in severe MR due to significant retrograde flow to LA. This low EF can cause significant impairment in recovery after surgical correction. Patients should be referred for MV surgery, and once EF declines below 60%. Consideration for MV repair vs. replacement depends on valvular anatomy such as calcification, annular dilatation, the involvement of the prolapsed segment, and surgical expertise. Intraoperative TEE has been very beneficial for decision-making regarding repair versus replacement.[21][62] Current ACC/AHA guidelines recommend surgery for asymptomatic MR if there is evidence of LV dysfunction.[63] Prognosis remains very good with very low rates of reoperation (<1%) for both MV repair and replacement when surgery is performed in high volume centers.[64] A large multicenter study showed that after balancing and matching characteristics in each group, MV repair was superior to MV replacement with lower rates of postoperative mortality, early and long term survival over 2 decades, postoperative complications, and fewer chances of reoperation.[65] For patients with high perioperative risk, referral for percutaneous intervention should be done when the valve anatomy is adequately assessed for the feasibility of transcatheter mitral valve repair, and careful preselection of patients should be done to optimize the outcome. The landmark trials, MITRA-FR and COAPT, have shown contrasting outcomes with variable success rates, but the results have provided a comprehensive insight for screening the patient population while investigating the exact role of MR in LV dysfunction with symptomatology and prediction of outcomes after transcatheter mitral valve repair.[66]

Complications

Complications of MR itself include progressive CHF with or without symptoms, LV dysfunction, development of atrial fibrillation, and subsequent risk of thromboembolism, right ventricular dysfunction, pulmonary hypertension, infective endocarditis. Early complications from the surgery or percutaneous intervention for MR include bleeding, infection at the local incision site, dehiscence of prosthetic material and infective endocarditis, stroke, atrial fibrillation, cardiac tamponade, and death. Late complications after the surgery include the redevelopment of MR requiring repeat surgery, symptomatic CHF, LA/LV enlargement and dysfunction, arrhythmias, and death.[65]

Postoperative and Rehabilitation Care

Routine postoperative care with immediate critical care monitoring and subsequent inpatient recovery should be done as per the institutional protocols. Rehabilitative services should be introduced as early as possible for expedited recovery. A postoperative echocardiogram is recommended before discharge and at follow-up on a regular basis.[67] Exercise training with cardiac rehabilitative services, management of anticoagulation for prosthetic valve, antibiotic prophylaxis for infective endocarditis, and outpatient follow-up with cardiology services at regular intervals is recommended as per the guidelines.[68] 

Consultations

When the diagnosis of MR is suspected based on symptoms, physical examination, and/or investigation, the patient should be referred to a cardiologist. Based on the severity of MR with structural changes seen on echocardiogram and symptoms, cardiovascular physicians can recommend medical treatment versus surgical intervention. In the latter case, a thorough discussion with the heart valve team, preferably in the experienced center, should be carried out to determine the most appropriate therapeutic approach.[59]

Deterrence and Patient Education

Mitral regurgitation (MR) or mitral valve insufficiency is a very common heart valve disorder. It is defined as the leaking of blood flow from the left ventricle (LV) to the left atrium (LA). Most patients do not have any symptoms, but with the progression of leakiness, they can have shortness of breath, chest pain, exercise intolerance, leg swelling, and many more. Patients should seek medical attention in case of any of these symptoms. Investigations including EKG, echocardiogram, chest x-ray, and advanced tests of imaging can confirm the diagnosis. After confirmation of the diagnosis of clinically significant MR, routine surveillance and regular follow-up should be done under cardiology services. Depending on etiology, symptomatology, results of investigations, and team discussions, the patient should be guided for medical treatment and/or surgical treatment, including open-heart surgery or transcatheter intervention.[46][59] Several factors, including etiology of MR, age and demographics, comorbidities, baseline functional status, LV size, and EF, need to be taken into account before making recommendations for treatment. If deemed suitable for surgical intervention, thorough counseling about the risks and benefits of surgery should be done.[67] 

Enhancing Healthcare Team Outcomes

MR remains a very common global valvular heart disease with a rising patient population due to a rapid increase in the aging population.[2] But as mentioned above, it is still highly underdiagnosed and hence, undertreated disease.[Level 1] Healthcare providers need to have an integrated approach for screening, diagnosis, referral, evaluation, and treatment strategies. A comprehensive interprofessional team inclusive of a cardiologist, cardiothoracic surgeon, echocardiographer, cardiac anesthesiologist, pharmacists, nurses have been proven to enhance outcomes and hence recommended. [Level 3-4][69][70]

MV surgery is recommended in symptomatic, severe, primary MR without significant impairment of LV function (LVEF>30%)[Level 1] and with impaired LV function as well (LVEF <30%). [Level 2] In asymptomatic, severe primary MR, with normal EF >60% and normal LV cavity size (LVESD <40 mm), MV surgery is recommended [level 2], with preference to MV repair over replacement when the likelihood of successful repair is high (>95%) and expected mortality is low (<1%). [Level 2] Presence of LV cavity dilatation (LVESD >40 mm) or intermediate decline in systolic function (LVEF=30% to 60%) in asymptomatic severe MR is considered class I recommendation for MV surgery.[Level 1] New-onset atrial fibrillation or the development of pulmonary hypertension (PASP>50mmHg) are also indications for MV surgery.[Level 2] In patients with severe symptomatic secondary MR despite optimal treatment of CAD, HF, and CRT, MV repair can be considered for symptomatic improvement. [Level 2] In symptomatic severe MR with prohibitive surgical risk, a transcatheter repair is recommended when MV anatomy is favorable and patients have a reasonable life expectancy otherwise.[46] [Level 2]