Acute Mitral Regurgitation

Mitral regurgitation, in the chronic state, is commonly seen in the emergency department. Acute decompensated mitral regurgitation is less frequently encountered. An understanding of the underlying etiologies and pathophysiology of the condition is critical to direct appropriate treatment.

Acute mitral regurgitation is characterized by an increase in preload and a decrease in afterload causing an increase in end-diastolic volume (EDV) and a decrease in end-systolic volume (ESV). This leads to an increase in total stroke volume (TSV) to supranormal levels. However, forward stroke volume (FSV) is diminished because much of the TSV regurgitates as the regurgitant stroke volume (RSV). This, in turn, results in an increase in left atrial pressure (LAP). According to the Laplace principle, which states that ventricular wall stress is proportional to both ventricular pressure and radius, left ventricular wall stress in the acute phase is markedly decreased since both of these parameters are reduced.

Patients must be educated concerning the warning signs and symptoms (eg, congestive heart failure, chest pain) of mitral regurgitation, and they should be advised to see their physician early in the course of the disorder, before symptoms progress.

For patient education resources, see Heart Health Center, as well as Mitral Valve Prolapse.

Mitral regurgitation can be divided into the following three stages: acute, chronic compensated, and chronic decompensated.

Acute mitral regurgitation classically occurs with a spontaneous chordae tendineae or papillary muscle rupture secondary to myocardial infarction. Other causes include rupture of these structures due to mitral valve prolapse, endocarditis, and trauma. In this state, a sudden volume and pressure overload occurs on an unprepared left ventricle and left atrium, with an abrupt increase in left ventricular stroke work. Increased left ventricular filling pressures, combined with the reflux of blood from the left ventricle into the left atrium during systole, results in elevated left atrial pressures. This increased pressure is transmitted to the lungs, resulting in acute pulmonary edema and dyspnea.

If the patient tolerates the acute phase, the chronic compensated phase begins. The chronic compensated phase results in eccentric left ventricular hypertrophy. The combination of increased preload and hypertrophy produces increased end-diastolic volumes, which, over time, result in left ventricular muscle dysfunction. This muscle dysfunction impairs the emptying of the ventricle during systole. Therefore, regurgitant volume and left atrial pressures increase, leading to pulmonary congestion.

See the image below.

Acute rheumatic heart disease remains a significant consideration in those with mitral regurgitation who are younger than 40 years.

Mitral valve prolapse (MVP) (ie, myxomatous degeneration) accounts for approximately 45% of the cases of mitral regurgitation in the Western world. The causative agent is unknown in this condition. Myxomatous degeneration is usually a slow process, with a major complication being the rupture of the chordae tendineae. (Acute regurgitation, as mentioned earlier, can be caused by chordae tendineae rupture or papillary muscle dysfunction.) The literature now seems to suggest that MVP has become the most common cause of mitral regurgitation in the adult population.

In addition, MVP and coronary artery disease (CAD) have become major mechanisms for incompetence of the mitral valve. Ischemia is responsible for 3-25% of mitral regurgitation. The severity of regurgitation is directly proportional to the degree of left ventricular hypokinesis.

Mitral annular calcification can contribute to regurgitation. Impaired constriction of the annulus results in poor valve closure.

Left ventricular dilatation and heart failure can produce annular dilatation and poor valve closure resulting in mitral regurgitation.

Tendineae rupture can be due to endocarditis, myocardial infarction, or trauma.

Papillary muscle dysfunction usually is caused by myocardial ischemia or infarction.

Other causes include the following:

• Ehlers-Danlos syndrome

• Marfan syndrome

• Osteogenesis imperfecta

• Systemic lupus erythematosus (SLE)

United States data

Previously, chronic rheumatic heart disease was the most common cause of acquired mitral valve disease in the Western world. More recently, however, mitral valve prolapse (MVP) has become the most common cause, responsible for 45% of cases of mitral regurgitation. In the Framingham cohort, using specific echocardiographic criteria, MVP was diagnosed in 2.4% of a representative population of 3,491 subjects, a lower prevalence than had previously been reported.[1]

International data

In the developing world, rheumatic heart disease remains by far the leading cause of mitral regurgitation.

Sex- and age-related demographic

In those younger than 20 years, males are affected more often than females. In those older than 20 years, no sexual predilection exists. Males older than 50 years are affected more severely.

Of cases caused by prior rheumatic disease, the mean patient age is 36 ± 6 years.

The prognosis of patients with mitral regurgitation depends on the underlying etiologies and the state of the left ventricular function. The extent of left ventricular dysfunction from underlying ischemia is the primary prognostic determinant in those with regurgitation secondary to coronary artery disease (CAD).

In a 2020 report of outcomes from 1342 patients from the Society of Thoracic Surgeons (STS) national database who underwent mitral valve surgery for ischemic papillary muscle rupture, the operative mortality was 20.0%.[2] Predictors of operative mortality included mitral valve replacement, older age, lower albumin levels, the presence of cardiogenic shock, an ejection fraction below 25%, and emergent salvage status. Major morbidities included prolonged ventilation (61.8%), acute renal failure (15.4%), reoperation (10.2%), and stroke (5.2%).[2]

Morbidity/mortality

Consider the following:

• Acute pulmonary edema and cardiogenic shock often complicate the course of acute mitral regurgitation. The operative mortality in these cases approaches 80%. A patient with ruptured chordae tendineae and minimal symptoms has a much better prognosis.

• With chronic mitral regurgitation, volume overload is tolerated very well for years before symptoms of failure develop. Left atrial enlargement predisposes patients to the onset of atrial fibrillation, with subsequent complications of embolization. In addition, these patients are susceptible to endocarditis. A study of the survival of patients with chronic regurgitation using randomly selected patients revealed that 80% of the patients were alive 5 years later, and 60% were alive after 10 years.

• Most patients with mitral valve prolapse are asymptomatic. Prolapse in those older than 60 years is frequently associated with chest pain, arrhythmias, and heart failure. The prognosis of these patients is good; however, sudden death, endocarditis, and progressive regurgitation occur rarely.

• When ischemic heart disease is the mechanism for regurgitation, the extent of anatomic disease and left ventricular performance are prognostic determinants. Complicating events include sudden death and myocardial infarction.

Patients with acute mitral regurgitation secondary to infarction emergently requiring valve replacement have a 60-80% mortality if they present with severe pulmonary edema.

Complications

Major complications from chronic regurgitation include the following:

• Severe left ventricular dysfunction

• Chronic congestive heart failure

• Atrial fibrillation and its complications (eg, left atrial thrombus with embolization and stroke)

• Sudden death, ruptured chordae tendineae, and endocarditis remain infrequent complications of regurgitation secondary to long-standing mitral prolapse.

Note the following:

• The initial symptoms of dyspnea and fatigue can rapidly progress to orthopnea and paroxysmal nocturnal dyspnea.

• Patients with anginal-type pain may have underlying ischemia.

• Atypical chest pain can be associated with mitral valve prolapse (MVP) syndrome.

• In patients with MVP, palpitations and atypical chest pain are the most frequent complaints. 

• Coronary artery disease (CAD) is often accompanied by dyspnea, fatigue, orthopnea, and fluid retention. Chest pain is usually minimal in these patients.

• With underlying CAD, regurgitation usually is associated with symptoms of angina pectoris.

• Regurgitation also can develop acutely with myocardial infarction, secondary to papillary muscle rupture.

• In acute mitral regurgitation from sudden disruption of the mitral valve, the symptoms are due to acute pulmonary edema.

• When mitral regurgitation is due to left ventricular dilatation and altered valve function, patients often have chronic left-sided heart failure.

• Chronic mitral regurgitation can be tolerated for many years.

The classic murmur of mitral regurgitation is a high-pitched holosystolic murmur beginning with the first heart sound and extending to the second heart sound. The intensity usually is constant throughout systolic ejection, often radiating to the axilla. The harshness of the murmur does not correlate with the magnitude of the valvular defect. Patients with severe disease often have a third heart sound, a consequence of the increased ventricular filling volume that is ejected into the left ventricle under higher than normal pressure. Patients with mitral valve prolapse often have a mid-to-late systolic click and a late systolic murmur. These patients are usually female and often have orthostatic hypotension.

Patients with coronary artery disease can have the above mentioned murmur any time during systole, accompanied by an atrial gallop.

In acute mitral regurgitation, the examination usually is consistent with acute pulmonary edema and left ventricular failure. The heart size usually is normal, but an audible systolic thrill is often present. The murmur often is harsh. It may be heard over the back of the neck, vertebra, and/or sacrum and may radiate to the axilla, back, and left sternal border.

Importantly, nearly one third of patients with acute severe mitral regurgitation following myocardial infarction may present without a clinically appreciable murmur.[3]

Chest radiography

The cardiac silhouette often is normal in patients with mitral valve prolapse (MVP).

Acute mitral regurgitation presents with acute pulmonary edema and, often, a normal cardiac silhouette if it is secondary to a rupture of a valve apparatus.

With chronic mitral regurgitation, left ventricular and left atrial enlargement are present. The left atrium can be large enough that it produces elevation of the left mainstem bronchus.

Occasionally, the double density sign can be seen along the right heart border, which is produced by the shadow of the wall of the dilated left atrium.

The heart size of patients with coronary artery disease (CAD) can range from normal to significant dilatation of the left ventricle and left atrium.

Two-dimensional echocardiography

Evidence of posterior motion of valve leaflets during mid-systole is present in patients with mitral valve prolapse.

Annular calcifications may be seen in patients with coronary artery disease. In addition, evidence of posterior or inferior wall motion abnormalities may be observed.

With acute mitral regurgitation, the ruptured chordae tendineae or papillary muscle, as well as perforated interventricular septum, can be visualized. The left atrium and ventricle are generally of normal size.

Transesophageal echocardiography provides a better estimate of the severity of damage.

See the videos below.

Electrocardiography (ECG)

Chronic mitral regurgitation

Atrial fibrillation is often present secondary to a dilated left atrium. The ECG shows evidence of left ventricular hypertrophy and left atrial enlargement.

Coronary artery disease

Evidence of inferior and posterior Q waves may be present, indicating prior infarction.

Mitral valve prolapse

Patients most commonly have ST- and T-wave changes, with T-wave inversions in the inferior leads. ECG may reveal an underlying arrhythmia (eg, sinus arrhythmia, sinus arrest, atrial fibrillation, premature ventricular contractions [PVCs]).

Acute mitral regurgitation

The ECG may reveal evidence of an acute myocardial infarction, more commonly inferior or posterior.

Cardiac catheterization

Angiography is considered to be the criterion standard in the assessment of the severity of the disease.

Mitral regurgitation is graded on a scale from 0 (none), 1 (mild), 2 (moderate), 3 (moderately severe), to 4 (severe).

The severity is based on the opacity of the left atrium.

The regurgitant volume can be calculated based on information from the catheterization.

In addition, this test will identify those with underlying coronary artery disease.

The definitive treatment of mitral regurgitation remains surgery, of which the two primary surgeries are mitral valve replacement and mitral valve repair. The risk-benefit ratio must be examined carefully with each individual situation prior to a decision to replace the valve.

If mitral regurgitation is treated early enough, mitral valve repair is the optimal choice (lower risk of infectious endocarditis and better postoperative left ventricular function).

Repair is usually available only to those whose condition has a nonrheumatic, noninfectious, and nonischemic cause; therefore, candidates for mitral valve repair are few.

Valve replacement should not be undertaken in asymptomatic patients.

Early recognition of even minimal symptoms is crucial in attempting to preserve as much left ventricular function as possible.

Chordal transection during replacement surgery results in some impairment of left ventricle function; thus, the more left ventricular function prior to surgery, the better the outcome.

See also the Guidelines section for management and intervention recommendations from the American College of Cardiology/American Heart Association (ACC/AHA) (2014, 2017),[4, 5]  American Association for Thoracic Surgery (2016),[6]  and, European Society of Cardiology/European Association for Cardio-Thoracic Surgery (ESC/EACTS) (2017).[7]

Acute mitral regurgitation is a specific case in which immediate intervention in the emergency department can make a difference. However, early involvement of cardiology and cardiac surgery teams is essential.

If the etiology is myocardial infarction, and immediate percutaneous coronary intervention (PCI) is not available, infusion of thrombolytics may reestablish blood flow to the papillary muscle, possibly restoring function.

The mainstay of medical treatment in most other cases of mitral regurgitation is afterload reduction. Afterload reduction decreases the impedance to left ventricular ejection and, as a result, decreases the regurgitant volume. Administering arterial vasodilators (eg, sodium nitroprusside) may reduce aortic impedance to help raise aortic outflow while decreasing regurgitation.[8] However, the use of these agents may be limited in the setting of cardiac output and hypotension; in such cases, afterload reduction and decreased regurgitant flow may be achieved with aortic balloon counterpulsation while augmenting mean arterial blood pressure. Most often, urgent mitral valve repair is required for restoration of normal circulation.[8]

The treatment of pulmonary edema should include oxygen, diuretics, nitrates, and early intubation if respiratory failure results.

These individuals can benefit from afterload reduction with nitroprusside, even in the setting of a normal blood pressure.

Do not attempt to alleviate tachycardia with beta-blockers. Mild-to-moderate tachycardia is beneficial in these patients because it allows less time for the heart to have backfill, which lowers regurgitant volume.

Rapid atrial fibrillation secondary to chronic mitral regurgitation may be controlled with diltiazem or, less commonly, digoxin. Patients with severe heart failure or hypotension should not be treated with diltiazem.

The physician should consider cardioversion in refractory or unstable patients. If cardioversion is effective, however, the restored sinus rhythm usually is transient due to the left atrium being severely dilated.

In the setting of acute mitral regurgitation secondary to an acute myocardial infarction, a cardiologist should be involved early. Point-of-care ultrasonography (POCUS) may reveal a hyperdynamic left ventricle or wall motion abnormalities; however, standard echocardiography is typically necessary to identify papillary muscle rupture. Interventional cardiology for emergent cardiac catheterization and intervention, as an alternative to thrombolysis, should be obtained as per protocol in institutions with such capability.

For highly suspicious cases, a cardiothoracic surgeon should be notified as soon as possible, even before echocardiography is performed. This will allow the surgical team to mobilize. Placement of an intraaortic balloon pump or a percutaneous left ventricular assist device may stabilize a patient prior to surgery.

Guidelines are available from the following organizations for mitral valve regurgitation:

• American College of Cardiology/American Heart Association (ACC/AHA) (2014, 2017) ^{[4, 5]}
• American Association for Thoracic Surgery (2016) ^[6]
• European Society of Cardiology/European Association for Cardio-Thoracic Surgery (ESC/EACTS) (2017) ^[7]

In 2014 and 2017, the American Heart Association and American College of Cardiology (AHA/ACC) released revisions and focused updates, respectively, to their 2008 guidelines for management of patients with valvular heart disease (VHD).[4, 5]

The recommendations did not include acute mitral regurgitation (MR) but provided guidance for chronic primary and secondary MR.[4, 5]  

Chronic primary MR

The guidelines note that when assessing chronic MR, it is important to distinguish between chronic primary (degenerative) MR and chronic secondary (functional) MR, as these conditions have more differences than similarities.[4, 5]  Note the following about chronic primary MR[4] :

• Valve incompetence is due to pathology of  one or more of the valve components (leaflets, chordae tendineae, papillary muscles, annulus). Systolic regurgitation of blood from the left ventricle (LV) to the left atrium (LA) ensues.
• In developed nations, mitral valve prolapse is the most common etiology.
• Younger patients: Severe myxomatous degeneration with gross redundancy of anterior and posterior leaflets and the chordal apparatus (Barlow valve)
• Older patients: Fibroelastic deficiency disease, wherein lack of connective tissue results in chordal rupture.

Diagnosis and follow-up

◊ Class I recommendations

Transthoracic echocardiography (TTE) is indicated for baseline evaluation of LV size and function, right ventricular (RV) function and LA size, pulmonary artery pressure, and the mechanism and severity of primarly MR (stages A to D) in any patient  with suspected chronic primary MR (level of evidence [LOE]: B).

Cardiac magnetic resonance imaging (CMRI) is indicated in patients with chronic primary MR to assess LV and RV volumes, function, or MR severity and when these issues are not satisfactorily addressed by TTE (LOE: B).

Intraoperative transesophageal echocardiography (TEE) is indicated to establish the anatomic basis for chronic primary MR (stages C and D) and to guide repair (LOE: B).

Esophageal echocardiography is indicated for evaluation of patients with chronic primary MR (stages B to D) in whom noninvasive imaging provides nondiagnostic information about the MR severity, MR mechanism, and/or LV functional status (LOE: C).

◊ Class IIa recommendations

Exercise hemodynamics with either Doppler echocardiography or cardiac catheterization is reasonable in symptomatic patients with chronic primary MR where there is a discrepancy between symptoms and the severity of MR at rest (stages B and C) (LOE: B).

Exercise treadmill testing can be useful in patients with chronic primary MR to establish symptom status and exercise tolerance (stages B and C) (LOE: C).

Medical therapy

◊ Class IIa recommendations

Medical therapy for systolic dysfunction is reasonable in symptomatic patients with chronic primary MR (stage D) and LV ejection fraction (EF) less than 60% in whom surgery is not contemplated (LOE: B).

◊ Class III: No benefit

Vasodilator therapy is not indicated for normotensive, asymptomatic patients with chronic primary MR (stages B and C1) and normal systolic LV function (LOE: B).

Intervention

◊ Class I recommendations

Mitral valve surgery is recommended for symptomatic patients with chronic severe primary MR (stage D) and LVEF greater than 30% (LOE: B).

Mitral valve surgery is recommended for asymptomatic patients with chronic severe primary MR and LV dysfunction (LVEF 30% to 60% and/or LV end-systolic diameter [ESD] ≥40 mm, stage C2) (LOE: B)

Mitral valve repair is preferred to mitral valve replacement (MVR) when surgical treatment is indicated for patients with chronic severe primary MR limited to the posterior leaflet (LOE: B).

Mitral valve repair is preferred to MVR when surgical treatment is indicated for patients with chronic severe primary MR involving the anterior leaflet or both leaflets when a successful and durable repair can be accomplished (LOE: B)

Concomitant mitral valve repair or MVR is indicated in patients with chronic severe primary MR undergoing cardiac surgery for other indications (LOE: B)

◊ Class IIa recommendations

Mitral valve repair is reasonable in asymptomatic patients with chronic severe primary MR (stage C1) with preserved LV function (LVEF >60% and LVESD < 40 mm) in whom the likelihood of a successful and durable repair without residual MR is greater than 95% with an expected mortality rate of less than 1% when performed at a Heart Valve Center of Excellence (LOE: B).

Mitral valve repair is reasonable for asymptomatic patients with chronic severe primary MR (stage C1) and preserved LV function  (LVEF >60% and LVESD < 40 mm) with a progressive increase in LV size or decrease in ejection fraction on serial imaging studies (LOE: C-limited data).

Mitral valve repair is reasonable for asymptomatic patients with chronic severe nonrheumatic primary MR (stage C1) and preserved LV function (LVEF >60% and LVESD < 40 mm) in whom there is a high likelihood of a successful and durable repair with 1) new onset of atrial fibrillation [AF] or 2) resting pulmonary hypertension (pulmonary artery systolic arterial pressure >50 mm Hg) (LOE: B).

Concomitant mitral valve repair is reasonable in patients with chronic moderate primary MR (stage B) when undergoing cardiac surgery for other indications (LOE: C).

◊ Class IIb recommendations

Mitral valve surgery may be considered in symptomatic patients with chronic severe primary MR and an LVEF of up to 30% (stage D) (LOE: C).

Mitral valve repair may be considered in patients with rheumatic mitral valve disease when surgical treatment is indicated if a durable and successful repair is likely or when the reliability of long-term anticoagulation management is questionable (LOE: B).

Transcatheter mitral valve repair may be considered for severely symptomatic patients (New York Heart Association [NYHA] class III to IV) with chronic severe primary MR (stage D) who have favorable anatomy for the repair procedure and a reasonable life expectancy but who have a prohibitive surgical risk because of severe comorbidities and remain severely symptomatic despite optimal guideline-directed medical therapy (GDMT) for heart failure (HF) (LOE: B).

◊ Class III: Harm

MVR should not be performed for the treatment of isolated severe primary MR limited to less than one half of the posterior leaflet unless mitral valve repair has been attempted and was unsuccessful (LOE: B).

Chronic secondary MR

Diagnosis and follow-up

◊ Class I recommendations

TTE is useful to establish the etiology of chronic secondary MR (stages B to D) and the extent and location of wall motion abnormalities, and to assess global LV function, MR severity, and magnitude of pulmonary hypertension (LOE: C).

Noninvasive imaging (stress nuclear/positron emission tomography, CMRI, or stress echocardiography), cardiac computed tomography (CT) angiography, or cardiac catheterization, including coronary arteriography, is useful to establish the etiology of chronic secondary MR (stages B to D) and/or to assess myocardial viability, which in turn may influence management of functional MR (LOE: C).

Medical therapy

◊ Class I recommendations

Patients with chronic secondary MR (stages B to D) and HF with reduced LVEF should receive standard GDMT therapy for HF, including angiotensin-converting enzyme inhibitors (ACEIs), angiotensin-receptor blockers (ARBs), beta blockers, and/or aldosterone antagonists as indicated (LOE: A).

Cardiac resynchronization therapy (CRT) with biventricular pacing is recommended for symptomatic patients with chronic severe secondary MR (stages B to D) who meet the indications for device therapy (LOE: A).

Intervention

◊ Class IIa recommendations

Mitral valve surgery is reasonable for patients with chronic severe secondary MR (stages C and D) who are undergoing CABG or aortic valve replacement (AVR) (LOE: C).

It is reasonable to choose chordal-sparing MVR over downsized annuloplasty repair if operation is considered for severely symptomatic patients  (NYHA class III-IV) with chronic severe ischemic MR (stage D) and persistent symptoms despite GDMT for HF (LOE: B-randomized trial data).

◊ Class IIb recommendations

Mitral valve repair or replacement may be considered for severely symptomatic patients (NYHA class III-IV) with chronic severe secondary MR (stage D) who have persistent symptoms despite optimal GDMT for HF (LOE: B).

In patients with chronic, moderate, ischemic MR (state B) undergoing CABG, the usefulness of mitral valve repair is uncertain (LOE: B-randomized trial data).

Mitral valve repair may be considered for patients with chronic moderate secondary MR (stage B) who are undergoing other cardiac surgery. (LOE: C).

In 2016, the American Association for Thoracic Surgery (AATS) released updates to their 2015 consensus guidelines for ischemic mitral valve regurgitation (IMR).[6]

Moderate ischemic MR

In patients with moderate IMR undergoing coronary artery bypass grafting (CABG), mitral valve repair with an undersized complete rigid annuloplasty ring may be considered.

Severe ischemic MR

Mitral valve replacement is reasonable in patients with severe IMR who remain symptomatic despite guideline-directed medical and cardiac device therapy, and who have a basal aneurysm/dyskinesis, significant leaflet tethering, and/or severe left ventricle dilation (left ventricular end diastolic diameter [LVEDD] >6.5 cm).

Mitral valve repair with an undersized complete rigid annuloplasty ring may be considered in patients with severe IMR who remain symptomatic despite guideline-directed medical and cardiac device therapy and who do not have a basal aneurysm/dyskinesis, significant leaflet tethering, or severe left ventricle enlargement.

Mitral valve replacement versus repair

Mitral valve repair for IMR is performed with complete preservation of both anterior and posterior leaflet chords.

Mitral valve repair for IMR is performed with a small, undersized, complete rigid annuloplasty ring.

The European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) released their guidelines for the management of valvular heart disease in 2017.[7] Their recommendations for intervention in mitral regurgitation (MR) are outlined below.

Severe primary MR

Class I recommendations

Mitral valve repair should be the preferred technique when the results are expected to be durable (level of evidence [LOE]: C).

Surgery is indicated in symptomatic patients whose left ventricular (LV) ejection fraction (EF) are over 30%, as well as in asymptomatic patients with LV dysfunction (LV end-systolic diameter [ESD] ≥45 mm and/or LVEF ≤60%) (both LOE: B).

Class IIa recommendations

Consider surgery in asymptomatic patients with preserved LV function (LVEF >60%) and the following:

• LVESD < 45 mm, and atrial fibrillation secondary to MR or pulmonary hypertension (systolic pulmonary pressure at rest >50 mm Hg) (LOE: B)
• LVESD of 40-44 mm, when durable repair is likely, surgical risk is low, and the repair is performed in a heart valve center, and in the presence of at least flail leaflet or significant left atrial (LA) dilatation (volume index ≥60 mL/m ² [body surface area BSA]) in sinus rhythm (LOE: C).

Consider mitral valve repair in symptomatic patients with LV dysfunction (LVEF < 30% and/or LVESD > 55 mm) refractory to medical management in the setting of a high likelihood of successful repair and low comorbidity (LOE: C).

Class IIb recommendations (all LOE: C)

Mitral valve repair may be considered in symptomatic patients with severe LV dysfunction (LVEF < 30% and/or LVESD > 55 mm) refractory to medical management in the setting of a low likelihood of successful repair and low comorbidity.

Percutaneous edge-to-edge procedure may be considered in patients with symptomatic severe primary MR who fulfill the echocardiographic eligibility criteria and who the heart team judge to be inoperable or at high surgical risk, avoiding futility.

Chronic secondary MR

Class I recommendation

Surgery is indicated in patients with severe secondary MR undergoing coronary artery bypass grafting (CABG) and LVEF above 30% (LOE: C).

Class IIa recommendation

Consider surgery in symptomatic patients with severe secondary MR, LVEF below 30% but with an option for revascularization and evidence of myocardial viability (LOE: C).

Class IIb recommendations (all LOE: C)

When revascularization is not indicated, surgery may be considered in patients with severe secondary MR and LVEF above 30% who remain symptomatic despite optimal medical management (including cardiac resynchronization therapy [CRT] if indicated) and have a low surgical risk.

When revascularization is not indicated and surgical risk is not low, a percutaneous edge-to-edge procedure may be considered in patients with severe secondary MR and LVEF over 30% who remain symptomatic despite optimal medical management (including CRT if indicated) and who have a suitable valve morphology as shown on echocardiography, avoiding futility.

In patients with severe secondary MR and LVEF below 30% who remain symptomatic despite optimal medical management (including CRT if indicated) and who have no option for revascularization, the heart team may consider a percutaneous edge-to-edge procedure or valve surgery after careful evaluation for ventricular assist device (VAD) or heart transplant based on individual patient characteristics.

The mainstay of treatment is preload and afterload reduction, particularly in the setting of mitral regurgitation with pulmonary edema. Nitrates and diuretics reduce filling pressures, and inotropics and an intraaortic balloon pump are useful in the setting of hypotension and hemodynamic instability.[7]

In the setting of chronic mitral regurgitation with good ventricular function, no evidence supports the prophylactic use of vasodilators, including angiotensin-converting enzyme inhibitors (ACEIs).[7] However, consider ACEIs in patients who develop heart failure but who are not surgical candidates or whose symptoms persist postoperatively. Beta-blockers and spironolactone are also appropriate agents.[7]

Class Summary

These agents are used to reduce preload and the left ventricular volume.

Furosemide (Lasix)

An excellent preload reducer. Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Dose must be individualized. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until a satisfactory effect is achieved.

Class Summary

These agents are useful in preload reduction and as antianginal agents.

Nitroglycerin topical (Nitro-Bid)

Causes relaxation of the vascular smooth muscle via stimulation of intracellular, cyclic guanosine monophosphate production, which causes a decrease in blood pressure.

Nitroprusside (Nipride, Nitropress)

DOC for afterload reduction. Has an effect on afterload reduction but also some effect on preload; produces vasodilation and increases inotropic activity of the heart. In addition, reduces peripheral resistance by directly acting on arteriolar and venous smooth muscle.

Class Summary

These agents are used for the control of atrial fibrillation in the setting of chronic mitral regurgitation.

Digoxin (Lanoxin)

DOC in rate control of atrial fibrillation. Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system.

Diltiazem (Cardizem)

Useful as second line of therapy in rate control of atrial fibrillation and chronic mitral regurgitation. During the depolarization, it inhibits the calcium ion from entering the slow channels or the voltage-sensitive areas of the vascular smooth muscle and myocardium.