Mitral Regurgitation Topic Review

Etiology | Pathophysiology | Symptoms | Physical Examination | Diagnosis | Treatment

Introduction

The normal mitral valve permits unrestricted antegrade diastolic flow from the left atrium to the left ventricle (LV) and effectively seals off the atrium from the ventricle during LV systole, allowing atrial filling from the pulmonary veins at low pressures.

Mitral regurgitation (MR) is the term used for (abnormal) systolic retrograde flow of blood from the left ventricle to the left atrium (LA). MR occurs either due to disease involving the mitral valve apparatus, known as primary MR (or “organic” MR), or due to dilation of the mitral valve annulus associated with impaired left ventricular function, known as secondary MR (or “functional” MR). The left atrium and ventricle can adapt quite well to primary chronic mitral regurgitation, and symptoms may be delayed for years. With acute mitral regurgitation, the left ventricle cannot adequately compensate and the left atrium is relatively non-compliant and non-dilated; symptoms, usually severe, always occur.

Etiology – Mitral Regurgitation

Multiple disease processes can affect the complex mitral valve apparatus. Known causes of primary and secondary mitral regurgitation are listed below.

Primary Mitral Regurgitation

  • Myxomatous changes (Mitral valve prolapse)
  • Rheumatic heart disease (RHD)
  • Infective endocarditis
  • Collagen vascular disease
  • Papillary muscle dysfunction
  • Mitral annular calcification (MAC)
  • Spontaneous chordal rupture
  • Trauma

Secondary Mitral Regurgitation

  • Ischemic cardiomyopathy
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Left atrial dilation

Primary mitral regurgitation results from disease of, or damage, to the mitral valve apparatus itself. The mitral valve leaflets, annulus, papillary muscles and chordae tendinae must all interact properly for the mitral valve to function. Dysfunction of any of these component structures can lead to primary mitral regurgitation.

Secondary mitral regurgitation occurs when left atrial or left ventricular remodeling and dilation leads to mitral valve annular enlargement that prevents effective leaflet coaptation. There are multiple causes of left atrial or left ventricular dilation, and the first-line treatment for this type of mitral regurgitation is directed at the primary cause. For example, if a patient with heart failure (HF) and LV dilation has mitral regurgitation, initial treatment would be the institution of guideline-directed medical therapy for HF with reduced ejection fraction (see Treatment, below).

The most common cause of chronic mitral regurgitation in the United States is myxomatous change as seen in mitral valve prolapse (MVP). The middle layer of the valve leaflets become thickened, frequently causing leaflet redundancy that impairs coaptation. The chordae tendinae may also be affected, disrupting support of the mitral valve apparatus.

Rheumatic heart disease (RHD) also may cause chronic mitral regurgitation, and is common in developing countries. (Hurst’s the Heart. 2017;14th Edition;chapter 50;11a.)

Chronic inflammation of the valve leaflets results in thickening, calcification and, ultimately, dysfunction. Frequently, rheumatic mitral stenosis or aortic valve disease is also present.

Infective endocarditis involving the mitral valve leaflets leads to dysfunctional coaptation or leaflet perforation. The resulting mitral regurgitation is often acute or subacute and can cause severe symptoms. Previously diseased or prosthetic mitral valves are more commonly affected, but normal valves can also be involved.

Papillary muscle dysfunction from ischemia, infarction or rupture may occur in patients with coronary artery disease and leading to acute MR. The posterolateral papillary muscle is most commonly affected, as it usually receives its blood supply solely from branches of the posterior descending artery (PDA); the anteromedial papillary muscle usually has a dual supply by the left anterior descending artery (LAD) and the circumflex artery. Papillary muscle dysfunction resulting in mitral regurgitation usually occurs as a complication of posterior wall myocardial infarction.

Rupture of the chordae tendineae or chordal rupture associated with mitral valve prolapse can cause severe acute mitral regurgitation. Mitral annular calcification (MAC) resulting in rigidity of the mitral annulus may also lead to mitral regurgitation. Although rare, MR can be caused by penetrating trauma to the mitral valve.

Pathophysiology – Mitral Regurgitation

With retrograde systolic flow from the left ventricle to the left atrium, both chambers dilate in order to maintain a near-normal resting cardiac output. With primary mitral regurgitation in the absence of myocardial disease, the volume-loaded LV dilates and the ejection fraction remains normal. (Carabello BA, et al. N Engl J Med. 1997;6a.)

With hemodynamically significant MR, left atrial pressure and volume loading increases the likelihood of atrial arrhythmias. The left volume-loaded left ventricle can initially maintain forward flow maintained by the Frank-Starling principle. However, as mitral regurgitation worsens and wall stress in the left ventricle increases, left ventricular hypertrophy develops. Eventually, left ventricular pressure increases, and systolic heart failure occurs.

The ratio of the volume of blood that enters the left atrium in systole to the total stroke volume is referred to as the regurgitant fraction. Regurgitant fraction is used to estimate the severity of mitral regurgitation. As mitral regurgitation worsens, the regurgitant fraction increases.

A number of hemodynamic and anatomical factors contribute to the severity of mitral regurgitation, including afterload, left ventricular to left atrial pressure gradient, compliance of the left atrium, and the size of the mitral valve orifice during systole.

Pharmacologic afterload reduction can significantly reduce the regurgitant fraction in mitral regurgitation. With acute mitral regurgitation, reducing afterload with intra-aortic balloon pumping may be effective.

With chronic mitral regurgitation, the left atrium hypertrophies and dilates, increasing LA compliance to accommodate volume loading at near-normal pressure. In contrast, acute mitral regurgitation results in pressure and volume loading of a normal, relatively non-compliant atrium. The high left atrial and pulmonary pressures frequently lead to pulmonary edema.

Symptoms – Mitral Regurgitation

With slowly progressive chronic mitral regurgitation, patients are often asymptomatic during the initial stages. The first symptoms are usually exercise intolerance or dyspnea on exertion.

Signs of left and right heart failure occur late in disease. Left heart failure results in symptoms of limited cardiac output — exercise intolerance — and increased pulmonary pressures with shortness of breath and pulmonary congestion.

Chronic pulmonary hypertension leads to right heart failure. Right heart failure symptoms include lower extremity-dependent edema and hepatic congestion. At night, when patients are recumbent, the excess extracellular fluid redistributes centrally, causing orthopnea (the need to sit up to breathe) or paroxysmal nocturnal dyspnea (PND). Hepatic congestion may be associated with right upper quadrant abdominal pain. Other symptoms related to low cardiac output include fatigue and weakness; in extreme cases, cardiac cachexia can occur.

Patients may occasionally present with cardiac arrhythmias — most commonly atrial fibrillation. Other less common symptoms include hemoptysis, thromboembolism and symptoms of infectious endocarditis.

Acute mitral regurgitation presents with severe symptoms: syncope, acute pulmonary edema and cardiogenic shock.

Physical Examination – Mitral Regurgitation

The typical murmur of mitral regurgitation is described as a high-pitched “blowing” holosystolic murmur, best heard at the apex with the patient in the left lateral decubitus position. The radiation of the murmur depends on the nature of the mitral valve process. It usually radiates to the axilla and back — due to anterior leaflet disease — as the regurgitant jet is directed posterolaterally, striking the lateral wall of the left atrium. Less commonly, if the posterior leaflet is involved, as in papillary muscle dysfunction, the regurgitant jet is directed anteromedially and will strike the interatrial septum; this causes the murmur to radiate to the cardiac base, often mimicking the murmur of aortic stenosis, though no radiation of the murmur to the carotids will be heard.

Dynamic maneuvers help distinguish the murmur of mitral regurgitation from other murmurs. The intensity of the mitral regurgitation murmur does not increase with inspiration, differentiating it from the murmur of tricuspid regurgitation. Increasing afterload by handgrip or transient arterial occlusion (TAO) will increase the murmur of mitral regurgitation. Any condition that increases left ventricular volume will also increase the mitral regurgitation murmur; this includes prolonged diastole after a premature ventricular contraction or a long pause, as can occur in atrial fibrillation. Conversely, decreasing LV volume by the Valsalva maneuver will also decrease the murmur of mitral regurgitation.

The murmur of acute mitral regurgitation is early systolic, terminating in early to mid-systole — not holosystolic as in chronic mitral regurgitation because the left atrial pressure rises rapidly in systole reducing retrograde flow.

An S3 heart sound is common in severe mitral regurgitation due to volume loading of the LV during early diastole; an S4 heart sound is less common. The S1 may be diminished due incomplete mitral valve closure. A widened split S2 heart sound may be present as the A2 occurs early, with reduced forward stroke volume. The P2 is usually not affected in severe mitral regurgitation.

A narrow pulse pressure is often seen in severe mitral regurgitation. The point of maximal intensity (PMI) may be displaced laterally if left ventricular dilation and heart failure are present. Signs of left heart failure, including pulmonary rales, may be present, along with indications of right heart failure, including distension of the jugular veins and lower extremity pitting edema.

Diagnosis – Mitral Regurgitation

The electrocardiogram changes in mitral regurgitation are non-specific. Broadening of the P wave, indicating LA enlargement, occurs due to the increased time required for propagation of electrical activity throughout the enlarged left atrium. Changes consistent with left ventricular hypertrophy may also be present. Less commonly, signs of pulmonary hypertension, such as right ventricular hypertrophy or right bundle branch block, may be seen.

The chest X-ray changes with chronic mitral regurgitation are also non-specific. Cardiomegaly is the most common finding. Left atrial enlargement, indicated by a “double density” or “straightening” of the left heart border, may be seen. Signs of congestive heart failure may be present in severe or acute mitral regurgitation. Calcification of the mitral annulus is frequently present but is also non-specific.

Transthoracic echocardiography (TTE) is the preferred modality in the diagnosis of acute MR as well as primary and secondary chronic MR. (Otto CM, et al. Circulation. 2020;49a, 53a). Echocardiography can accurately determine not only the presence of mitral regurgitation, but also the severity and usually the etiology, based on imaging of the mitral valve apparatus. For example, mitral valve prolapse can be identified, or a vegetation indicating infective endocarditis may be seen.

Two classification systems for chronic mitral regurgitation that fully or partially rely on echocardiography are currently in widespread use: the ASE grading system and the ACC/AHA staging system.

The ASE grading system classifies chronic MR into three categories: mild, moderate and severe; or four grades: grade I (mild MR), grade II (moderate MR), grade III (moderate-to-severe MR) and grade IV (severe MR). This system is based on echocardiographic findings alone, and considers: (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;30a(table 8), 31a.)

  1. structural parameters (mitral leaflet anatomy, LV size and LA size)
  2. qualitative Doppler parameters (color flow jet area, flow convergence and continuous wave Doppler jet)
  3. semiquantitative parameters (vena contracta width, pulmonary vein flow and mitral inflow)
  4. quantitative parameters (regurgitant volume, regurgitant fraction and effective regurgitant orifice area [EROA])

The most informative (semi)quantitative echocardiographic parameters are discussed below.

The vena contracta is the narrowest portion of the regurgitant flow that occurs at or immediately after (downstream of) the regurgitant orifice (in the case of MR, the mitral valve). (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;7a.) A vena contracta width (VCW) of less than 0.3 cm characterizes mild MR, while a VCW between 0.3 and 0.7 cm indicates moderate MR, and that of 0.7 cm or above severe MR. (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;30a(table 8).)

Regurgitant jet area is obtained on the color Doppler and expressed as a percentage of left atrial area. While useful in eliminating MR, it is not considered an informative quantitative parameter in the ASE classification system, although a jet area of 50% of the LA and higher indicates severe MR. (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;22a, 30a(table 8).) Regurgitant jet area is an important parameter in the ACC/AHA staging system (see below).

Regurgitant volume (RVol) per beat, which can be calculated as the difference between the stroke volume though the affected valve and stroke volume through a competent valve (among other methods), is a measure of volume overload severity. [(Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;9a.) In mild (grade I) MR, RVol is less than 30 mL/beat, while it is 30-44 mL/beat in moderate (grade II) MR, 45-59 mL/beat in moderate-to-severe (grade III) MR, and 60 mL//beat and higher in severe (grade IV) MR. (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;30a(table 8).)

Regurgitant fraction (RF) is the ratio of the regurgitant volume and the forward stroke volume expressed as a percentage. (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;9a.) to ASE classification, a regurgitant fraction of less than 30% indicates mild MR (grade I), 30% to 39% indicates mild-to-moderate MR (grade II), 40% to 49% indicates moderate-to-severe MR (grade III), and 50% or greater indicates severe MR (grade IV). (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;30a(table 8).)

Effective regurgitant orifice area (EROA) is considered a fundamental measure of lesion severity. (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;9a.)

An EROA of less than 0.20 cm2 indicates mild (grade I) MR. Moderate (grade II) MR is characterized by an EROA of 0.20-0.29 cm2, and moderate-to-severe (grade III) disease by an EROA of 0.30-0.39 cm2. An EROA of 0.40 cm2 or higher indicates severe (grade IV) MR. (Zoghbi WA, et al. J Am Soc Echocardiogr. 2017;30a(table 8).)

Chronic MR is also classified according to the staging system developed by the ACC and the AHA, which divides the disease into four distinct categories (Stages A, B, C and D) on the basis of valve anatomy, valve hemodynamics, LV or LA enlargement, and the presence or absence of symptoms. (Otto CM, et al. Circulation;2020;50a, 57a(table 17, e121; table 18, e128).) There is a separate staging scheme for primary and secondary MR.

In chronic primary MR:

Stage A (at risk of) primary MR comprises conditions characterized by mild mitral valve prolapse and mild valve thickening. Coaptation is normal, and there is either no regurgitant jet or it is small (< 20% LA area). The vena contracta is small — below 0.3 cm. No symptoms are present. (Otto CM, et al. Circulation;2020;50a(table 17, e121).)

Stage B (progressive) primary MR is anatomically characterized by moderate to severe mitral valve prolapse, rheumatic valve changes with leaflet restriction and prior infective endocarditis. Hemodynamically, a central regurgitant jet of 20-40% LA area or a late systolic eccentric jet, a VCW below 0.7 cm, a regurgitant volume of less than 60 mL, a regurgitant fraction below 50% and an EROA of less than 0.40 cm2 characterize Stage B chronic primary MR. Stage B primary MR comprises angiographic grade 1+ and 2+ MR. There is mild LA enlargement, but no LV enlargement, and pulmonary pressure is normal. Like in Stage A and C primary MR, symptoms are absent (Otto CM, et al. Circulation;2020;50a(table 17, e121).)

Stage C (asymptomatic severe) primary MR is defined by severe mitral valve prolapse with loss of coaptation (or flail leaflet), rheumatic changes that restrict leaflet motion and cause loss of central coaptation, prior infective endocarditis or leaflet thickening with radiation heart disease. Hemodynamic characteristics of Stage C primary MR include a central regurgitant jet greater than 40% LA area or a holosystolic eccentric jet, a VCW of 0.7 cm or greater, a regurgitant volume of 60 mL or greater, a regurgitant fraction of 50% or above, and an EROA of 0.40 cm2 or larger. The severe hemodynamics result in moderate or severe LA enlargement and LV enlargement and pulmonary hypertension may be present (either at rest or during exercise). Angiographic grades 3+ and 4+ fall into Stage C primary MR. On the basis of LV dysfunction, Stage C primary MR is further subdivided into Stage C1 (characterized by a left ventricular ejection fraction [LVEF] above 60% and a left ventricular end-systolic dimension [LVESD] below 40 mm) and Stage C2 (characterized by a LVEF of 60% or less and a LVESD of 40 mm or greater). However, like in Stage A and B primary MR, no symptoms are present. (Otto CM, et al. Circulation;2020;50a(table 17, e121).)

Stage D (symptomatic severe) primary MR is distinguished from Stage C primary MR by the presence of symptoms: decreased exercise tolerance and exertional dyspnea. This stage is otherwise characterized by the same anatomic features, hemodynamic severity, and functional consequences as Stage C primary MR, except that pulmonary hypertension is typically present. (Otto CM, et al. Circulation;2020;50a(table 17, e121).)

In chronic secondary MR:

Stage A (at risk of) secondary MR comprises cases where the mitral valve is anatomically normal in the presence of coronary artery disease (CAD) or cardiopathy. Valve hemodynamics are the same as in Stage A primary MR. The primary myocardial pathology may result in LV dilation and dysfunction, with regional wall motion abnormalities. (Otto CM, et al. Circulation;2020;57a(table 18, e128).)

Stage B (progressive) secondary MR is characterized by regional wall motion abnormalities with mild tethering of mitral leaflets, or by annular dilation with mild loss of central coaptation. Regurgitant volume, regurgitant fraction, and EROA are the same as in Stage B primary MR. Associated cardiac findings include LV dilation and dysfunction caused by the primary myocardial pathology. (Otto CM, et al. Circulation;2020;57a(table 18, e128).)

Stage C (asymptomatic severe) secondary MR is typified by regional wall motion abnormalities and/or LV dilation with severe tethering of mitral leaflets, or by annular dilation with severe loss of central coaptation of the mitral leaflets. Hemodynamically, it is defined by the same RVol, RF and EROA values as Stage C primary MR. Associated cardiac findings are the same as in Stage B secondary MR. (Otto CM, et al. Circulation;2020;57a(table 18, e128).) While symptoms attributable to coronary ischemia or heart failure may be present in Stage A through C secondary MR, they will abate in response to revascularization and appropriate medical therapy. (Otto CM, et al. Circulation;2020;57a(table 18, e128).)

Stage D (symptomatic severe) secondary MR is identical to Stage C secondary MR, except for the presence of symptoms that persist even after revascularization and optimal medical therapy, including symptoms of heart failure, decreased exercise tolerance and exertional dyspnea. (Otto CM, et al. Circulation;2020;57a(table 18, e128).)

Due to the accuracy and non-invasive nature of echocardiography, cardiac catheterization is often not needed to diagnose or grade mitral regurgitation severity. Coronary angiography is indicated prior to surgical mitral valve repair or replacement to determine if concurrent coronary artery disease, possibly requiring concomitant bypass grafting, is present.

Findings on catheterization include opacification of the left atrium during left ventriculography due to retrograde flow of contrast. The angiographic severity is graded on a scale of 1+ to 4+; a score of 1+ is considered mild (contrast material flows back into the LA but clears on each beat) and a score of 4+ severe (contrast material regurgitates all the way into the pulmonary veins). (Apostolakis EE, et al. J Cardiothorac Surg. 2009;2a) Additionally, pulmonary capillary wedge pressure tracings usually identify a large “V” wave, indicating the presence of mitral regurgitation.

Note that a large V wave is not specific for mitral regurgitation unless it is significantly larger than the A wave (ie, 100-200% larger).

Treatment – Mitral Regurgitation

Appropriate treatment of mitral regurgitation requires an accurate diagnosis and should be based on the natural history of the underlying disease process.

Recent studies of percutaneous mitral valve repair have fundamentally altered the management of secondary mitral regurgitation based on the concept of proportionate and disproportionate mitral regurgitation. (Otto CM, et al. Circulation;2020;55d-e(e126).) The data indicate that patients with disproportionate MR have larger effective regurgitant orifice areas and lower LV volumes benefit from (percutaneous) valve repair, whereas those with proportionate MR do not.

With primary mitral regurgitation, due to the potential complications of prosthetic valves, mitral valve repair is the surgical intervention of choice. When echocardiographic data indicate that mitral valve repair is feasible, a lower threshold for surgery may be considered. Rheumatic mitral valve disease is less amenable to repair than degenerative mitral valve disease. Therefore, repair should be attempted only in patients with less advanced rheumatic mitral valve disease or those who are not candidates for a mechanical prosthesis because of anticoagulation management concerns. (Otto CM, et al. Circulation;2020;55d-e(e126).)

Mitral valve replacement decreases symptoms of mitral regurgitation; however, data are lacking regarding a survival benefit compared with the natural history of chronic mitral regurgitation. Conversely, mitral valve repair has been shown to reduce both symptoms and long-term mortality. According to the ACC/AHA Guidelines, for cases of isolated primary MR limited to less than one-half of the posterior leaflet, mitral valve replacement should not be performed (class 3 recommendation: harm) unless an attempt at mitral valve repair has been unsuccessful. (Otto CM, et al. Circulation;2020;55f(e126).)

Mitral transcatheter end-to-end repair (TEER) is a non-surgical intervention in which the anterior and posterior leaflet are clipped together at one or more locations (such as with MitraClip, Abbott). Because comparative studies have demonstrated superior outcomes with mitral valve surgery, TEER should be reserved only for patients with a prohibitive surgical risk.

The actual timing of surgical intervention is a difficult decision and must take into account multiple factors; these include the feasibility of mitral valve repair vs. replacement, stage of mitral regurgitation, left ventricular systolic function, presence or absence of atrial fibrillation, clinical judgement and patient preference.

According to the 2020 ACC/AHA Guidelines, mitral valve surgery (repair preferred to replacement), performed at a primary or comprehensive valve center (CVC), is indicated (class 1 recommendation) for: (Otto CM, et al. Circulation;2020;54a(figure 8, e125.)

  • Patients with Stage C2 or Stage D degenerative primary MR, in whom successful and durable surgical outcome is possible

TEER is reasonable (class 2a recommendation) for: (Otto CM, et al. Circulation;2020;54a(figure 8, e125.)

  • Patients with Stage C2 and Stage D primary MR who have a high or prohibitive surgical risk, whose anatomy is favorable to a transcatheter approach and whose life expectancy is greater than 1 year

Mitral valve repair, performed at a primary or CVC, is reasonable (class 2a recommendation) for: (Otto CM, et al. Circulation;2020;54a(figure 8, e125.)

  • Patients with Stage C1 primary MR, whose expected surgical mortality risk is below 1% and whose likelihood of successful and durable repair is greater than 95%

Mitral valve repair or replacement may be considered (class 2b recommendation) for: (Otto CM, et al. Circulation;2020;54a(figure 8, e125.)

  • Patients with Stage C1 primary MR, whose expected surgical mortality risk is above 1%, whose likelihood of successful and durable repair/replacement is lower than 95%, and who showed a progressive increase in LV size or decrease in LVEF on 3 or more studies
  • Mitral valve repair, performed at a CVC, may be considered (class 2b recommendation) for: (Otto CM, et al. Circulation;2020;54a(figure 8, e125.)
  • Patients with Stage C2 or Stage D rheumatic primary MR, in whom successful and durable repair is possible
  • Since chronic secondary MR is only one component of a multifaceted cardiac pathology, the optimal treatment strategy is not always apparent. (Otto CM, et al. Circulation;2020;55g(e126).)
  • The 2020 ACC/AHA Guidelines recommend (class 1) guideline-directed medical therapy (GDMT) supervised by a heart failure specialist for all patients with secondary MR. (Otto CM, et al. Circulation;2020;59a(figure 9, e130).)

Beyond that, the Guidelines state that:

  • TEER is reasonable (class 2a recommendation) in patients with Stage D secondary MR who have persistent symptoms (NYHA Functional Class II-IV) while on
  • GDMT, and who have: 1) anatomy favorable to a transcatheter approach; 2) LVEF between 20% and 50%; 3) LVESD ≤ 70 mm; and 4) pulmonary artery systolic pressure ≤ 70 mm Hg. (Otto CM, et al. Circulation;2020;58a(e129, 7.3.4).)
  • These criteria are consistent with the enrollment criteria in the COAPT trial, which demonstrated the superiority of TEER over continued GDMT in patients with chronic secondary mitral regurgitation who experienced persistent symptoms despite optimization of GDMT. (Otto CM, et al. Circulation;2020;58b-c(e129).)
  • Mitral valve surgery is reasonable (class 2a recommendation) in patients with Stage C and D secondary MR when coronary artery bypass grafting is undertaken to treat myocardial ischemia (Otto CM, et al. Circulation;2020;58a(e129, 7.3.4).)
  • Mitral valve surgery may be considered (class 2b recommendation) in patients with Stage D secondary MR from atrial annular dilation (with a LVEF of 50% or higher) who have severe persistent symptoms (NYHA Functional Class III-IV) while on GDMT and therapy for associated atrial fibrillation or another condition (Otto CM, et al. Circulation;2020;58a(e129, 7.3.4).)
  • Mitral valve surgery may be considered (class 2b recommendation) in patients with Stage D secondary MR related to LV systolic dysfunction (LVEF below 50%) who have severe persistent symptoms (NYHA Functional Class III-IV) while on GDMT (Otto CM, et al. Circulation;2020;58a(e129, 7.3.4).)
  • Chordal-sparing mitral valve replacement may be reasonable over downsized annuloplasty repair in patients with Stage D secondary MR who are undergoing mitral valve surgery because of severe persistent symptoms (NYHA Functional Class III-IV) (Otto CM, et al. Circulation;2020;58a(e129, 7.3.4).)

For non-surgical candidates, vasodilators can be utilized with some improvement in symptoms and progression of mitral regurgitation. For acute decompensated heart failure due to chronic mitral regurgitation, nitroprusside is the drug of choice. ACE inhibitors and nitrates have no effect on cardiac index and may actually increase the regurgitant fraction — especially in patients with mitral regurgitation from mitral valve prolapse.

Vasodilator therapy is generally not indicated for asymptomatic patients with chronic mitral regurgitation due to lack of data showing benefit and the possibility of masking symptoms that may indicate a need for surgical intervention. However, when another indication such as hypertension or diabetes arises, the use of vasodilators including ACE inhibitors or angiotensin receptor blockers is accepted.

Symptomatic patients who are not surgical candidates have been shown to benefit from therapy with vasodilators. ACE inhibitors with nitrates is considered the combination of choice in patients with mitral regurgitation from ischemic heart disease or dilated cardiomyopathy. In patients with mitral regurgitation from mitral valve prolapse, however, reducing only preload actually increases regurgitation (see Mitral Valve Prolapse Topic Review); thus, the recommended treatment combination is beta-blockers with diuretics. Finally, patients with mitral regurgitation from rheumatic heart disease benefit the most from reduction in systolic blood pressure, as reduction of preload will not decrease the orifice of mitral regurgitation; beta-blockers, diuretics and hydralazine should be used in these individuals.

Use of digoxin for heart failure in general is common and considered reasonable in patients with symptomatic mitral regurgitation who are not surgical candidates.

Oral anticoagulation is indicated for patients with atrial fibrillation associated with mitral regurgitation, or if significant mitral stenosis is also present. The role of anticoagulation in patients with chronic mitral regurgitation in normal sinus rhythm with enlarged left atrium (> 5.5 cm) is controversial.

Antibiotic prophylaxis before surgical or dental procedures is no longer indicated for patients with mitral regurgitation to reduce the risk for bacterial endocarditis, unless a prosthetic valve is present.

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