Acute mitral regurgitation: Management

INTRODUCTION — 

Patients with acute mitral regurgitation (MR) are often gravely ill with significant hemodynamic abnormalities that require urgent medical and often surgical or transcatheter intervention [1-4].

The pathophysiology, clinical features, and management of acute native MR will be reviewed here.

The pathophysiology, clinical features, and management of chronic MR are discussed separately:

●(See "Pathophysiology and natural history of chronic mitral regurgitation".)

●(See "Clinical manifestations and diagnosis of chronic mitral regurgitation".)

●(See "Chronic primary mitral regurgitation: General management".)

●(See "Chronic primary mitral regurgitation: Indications for intervention".)

●(See "Chronic secondary mitral regurgitation: General management and prognosis".)

●(See "Chronic secondary mitral regurgitation: Intervention".)

The clinical presentation, diagnosis, and management of acute prosthetic MR are discussed separately. (See "Clinical manifestations and diagnosis of surgical aortic and mitral prosthetic valve regurgitation".)

MANAGEMENT CONSIDERATIONS — 

The approach to management of acute MR is based upon the severity of MR, severity of hemodynamic compromise, cause of MR, and associated conditions [5].

●Symptomatic patients – The discussion here focuses on management for symptomatic patients with acute severe MR who require prompt treatment to address the cause of MR.

●Patients with minimal or no symptoms – Some patients with acute moderate to severe or severe MR present with no or minimal symptoms [4]. This subacute presentation has been described primarily in patients with mitral valve prolapse with spontaneous chordal rupture [6]. These patients are managed similarly to patients with chronic primary MR. (See "Chronic primary mitral regurgitation: General management" and "Chronic primary mitral regurgitation: Indications for intervention" and "Chronic primary mitral regurgitation: Choice of intervention".)

MEDICAL STABILIZATION

Role of medical management — The role of medical management in treating acute MR depends upon the cause of MR.

●For mechanical causes of acute MR – Patients with an acute mechanical cause of acute MR such as chordal rupture with a flail leaflet (eg, as a complication of mitral valve prolapse), acute leaflet destruction (eg, as a complication of endocarditis), or papillary muscle rupture (eg, as a complication of myocardial infarction [MI]) are treated medically as a temporizing measure to treat heart failure and shock in preparation for surgical or percutaneous intervention. However, attempts at stabilization in this setting are likely to be futile. Thus, the mainstay of management for patients with an acute mechanical cause of severe MR is prompt mitral valve (surgical or transcatheter) intervention. (See 'Mitral valve intervention' below.)

●For nonmechanical causes of acute MR – Patients with a nonmechanical cause of acute MR (eg, mitral valve tethering or systolic anterior motion of the mitral valve) are treated primarily with medical management (and for patients with acute coronary syndromes, reperfusion therapy as indicated). (See 'Secondary MR' below.)

Pharmacologic therapy

General measures – If systemic blood pressure is adequate, initial medical therapy to reduce MR may include afterload reduction with intravenous nitroprusside or the use of nitroglycerin and diuretic therapy to treat pulmonary edema [7-10]. The decrease in MR severity with decreased afterload increases forward cardiac output and diminishes pulmonary congestion [11]. However, in this setting, vasodilator use is often limited by systemic hypotension, and intravenous inotropes and vasopressors (eg, norepinephrine or dopamine) may be required as temporizing measures.

●For systolic anterior motion of the mitral valve – In patients with acute MR associated with systolic anterior motion (SAM), inotropes are avoided and a beta blocker is administered, as tolerated. (See 'For systolic anterior motion (SAM) of the mitral valve' below.)

Mechanical circulatory assist devices — For patients with acute MR with cardiogenic shock, temporary stabilization may be achieved using a short-term circulatory assist device [10,12] such as intraaortic balloon counterpulsation [11] or other short-term mechanical circulatory support, such as a percutaneous transaortic left ventricular (LV) assist device (eg, Impella) [10-13]. (See "Intraaortic balloon pump counterpulsation" and "Short-term mechanical circulatory assist devices".)

Secondary MR — The management of acute MR caused by mitral valve leaflet tethering (functional or secondary MR) depends upon the cause.

Reperfusion therapy for acute coronary syndrome — In patients with acute coronary syndrome (ACS; MI or unstable angina), the presence of acute MR is associated with increased risk of heart failure and mortality [10]. For patients with ACS and acute secondary MR (associated with mitral valve tethering), standard indications for reperfusion therapy apply [14]. Observational studies have reported reduced MR in some patients with ACS undergoing percutaneous coronary intervention (eg, 32 percent), but the response is variable [10,15-18].

●In patients with ST-elevation MI, reperfusion strategy is based upon the clinical presentation, timing, and availability of percutaneous coronary intervention (algorithm 1). (See "Overview of the acute management of ST-elevation myocardial infarction" and "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy".)

●In patients presenting with non-ST-elevation ACS (MI or unstable angina), acute heart failure and/or worsening MR is an indication for primary percutaneous coronary intervention given the risk of adverse outcomes. Management of non-ST-elevation ACS is discussed separately. (See "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Non-ST-elevation acute coronary syndromes: Selecting a management strategy".)

Supportive care for stress cardiomyopathy — Mitral valve tethering is one of the mechanisms for acute MR in patients with stress (takotsubo) cardiomyopathy. Since stress cardiomyopathy with associated acute MR due to mitral valve tethering is generally a transient disorder, management is largely supportive, as discussed separately. (See "Management and prognosis of stress (takotsubo) cardiomyopathy", section on 'Management'.)

For systolic anterior motion (SAM) of the mitral valve — In patients with acute MR caused by SAM, inotropes are avoided. Treatment with beta blockers (if tolerated) may resolve associated LV outflow obstruction.

●With hypertrophic cardiomyopathy – In patients with hypertrophic cardiomyopathy (HCM) with SAM, LV outflow tract obstruction, and MR, careful assessment of mitral valve anatomy and MR jet characteristics is required to determine if MR is caused by SAM and/or other etiologies (eg, mitral valve prolapse). Management of LV outflow tract obstruction and MR caused by SAM in patients with HCM is discussed separately. (See "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Approach to therapy'.)

●After mitral valve repair – SAM of the mitral valve is a complication identified in some patients early after mitral valve repair. Management includes volume repletion, avoidance of inotropes, and beta blocker therapy as tolerated. Patients with severe persistent SAM are treated with immediate tailored surgical revision of the mitral valve repair. (See "Anesthesia for patients with mitral regurgitation", section on 'Postbypass TEE assessment'.)

●With stress cardiomyopathy – Management for patients with stress cardiomyopathy with LV outflow obstruction and SAM causing acute MR is supportive, as discussed separately. (See "Management and prognosis of stress (takotsubo) cardiomyopathy", section on 'With left ventricular outflow tract obstruction'.)

●Other causes – Acute MR caused by SAM has been identified in patients without HCM or the above conditions, particularly in perioperative settings. Supportive management includes volume repletion (as needed), avoidance of inotropes and use of beta blocker therapy as tolerated. (See "Anesthesia for patients with mitral regurgitation", section on 'Key goals and issues'.)

MITRAL VALVE INTERVENTION

Choice of intervention

For an acute mechanical cause — Symptomatic patients with acute severe MR with an acute mechanical cause (eg, papillary muscle rupture in the setting of MI, chordal rupture with a flail leaflet segment in the setting of mitral valve prolapse, or with leaflet destruction due to endocarditis) require prompt valve intervention [11,19-24]. Symptomatic patients with persistent severe MR after percutaneous coronary intervention for ACS are also treated with mitral valve surgery.

●For surgical candidates – For most patients with a mechanical cause of acute mitral regurgitation (eg, valve destruction caused by endocarditis, chordae tendonae rupture, papillary muscle rupture, or valve destruction caused by endocarditis), urgent mitral valve surgery is the treatment of choice, with valve repair (if feasible) generally preferred to valve replacement [10].

•Infective endocarditis – The timing of valve surgery, antibiotic therapy, and choice of procedure for patients with infective endocarditis and acute MR is discussed separately. (See "Surgery for left-sided native valve infective endocarditis".)

•Chordae tendonae rupture – Mitral valve repair for ruptured chordae involves use of artificial chordae (expanded polytetrafluoroethylene [PTFE] sutures) to replace ruptured chordae. Recurrent MR after repair is most commonly caused by progressive mitral valve disease or incomplete repair. Rupture of artificial chordae is a rare cause of recurrent MR [25]. In an early study of 131 patients (mean age 57) with ruptured chordae tendinae, mitral valve repair was associated with higher 5 year survival than mitral valve replacement (92 versus 72 percent) [26]. In addition, the risks of a prosthetic valve and anticoagulation are avoided with mitral valve repair.

•Papillary muscle rupture – As discussed separately, mitral valve repair is feasible at experienced centers only if there is no papillary muscle necrosis, so mitral valve replacement is commonly required. (See "Acute myocardial infarction: Mechanical complications", section on 'Management'.)

●For high or prohibitive surgical risk – For selected symptomatic patients with acute MR with high or prohibitive surgical risk with favorable mitral valve anatomy, we suggest mitral transcatheter edge-to-edge repair (TEER). However, mitral TEER is contraindicated in patients with acute MR with active infective endocarditis given the presence of infected valve tissue and vegetation.

For persistent acute secondary MR — For patients with persistent symptomatic acute severe MR despite medical management and reperfusion therapy (if indicated) (see 'Reperfusion therapy for acute coronary syndrome' above), we suggest TEER. This approach is similar to that for chronic secondary MR. (See "Chronic secondary mitral regurgitation: Intervention", section on 'Indications for mitral valve intervention'.)

Intervention outcomes — Intervention outcomes vary among etiologies of acute MR.

Surgical outcomes — Among hemodynamically unstable patients with acute severe MR, operative and longer-term mortality rates are higher for patients with acute MI or endocarditis than for those with myxomatous mitral valve disease, as illustrated by the following study.

In a multicenter study of surgery for acute severe MR in 279 hemodynamically unstable patients, the cause of regurgitation was acute MI in 45 percent (nearly all with papillary muscle rupture or mitral valve tethering/LV remodeling), myxomatous mitral valve disease in 26 percent (the majority with chordal rupture), and infective endocarditis in 28 percent (most with leaflet perforation or chordal rupture) [27]. Overall 30-day mortality was 23 percent and 15-year mortality was 33 percent. Survival after surgical intervention at 15 years was higher in patients with myxomatous valve disease (75±9 percent) and those with endocarditis (77±10 percent) compared with those with acute MI (39±11 percent). Valve repair was performed in 27 percent, with valve replacement in the remainder. Multivariate predictors of 30-day mortality were acute MI, acute endocarditis, shock, LV dysfunction, and coronary disease.

TEER outcomes — Outcomes following TEER for management of acute MR vary among etiologies of acute MR, as illustrated by the following studies:

●Cardiogenic shock – A meta-analysis included 24 observational studies with a total of 5428 patients (mean age 71) with severe MR, cardiogenic shock, and a high surgical risk score (mean Society of Thoracic Surgery score 15.2±8.9) treated with TEER [28]. Device success (defined as MR reduction of at least two grades) was achieved in 86 percent and MR was ≤2+ in 89 percent. The mean mortality rate at 30 days was 14 percent. Among the subgroup of patients with acute MI, the 30-day mortality rate was 20 percent. Among patients without acute MI, the 30-day mortality rate was 13 percent.

The largest study included in the above meta-analysis was a registry study including 3797 patients (mean age 73 years, mean Society of Thoracic Surgery score [mitral valve repair] 14.9±15.3 percent) with severe MR and cardiogenic shock who underwent TEER [29]. The etiology of MR was degenerative (mitral valve prolapse) in 53.4 percent and functional (secondary) in 27.4 percent. Device success was achieved in 85.6 percent of patients overall (83.7 percent in patients with degenerative MR and 87.2 percent in patients with secondary MR). Device success was associated with a lower one-year mortality rate (34.6 versus 55.5 percent; adjusted hazard ratio [HR] 0.49, 95% CI 0.41-0.59) and lower composite of mortality or heart failure admission (29.6 versus 45.2 percent; adjusted HR 0.51, 95% CI 0.42-0.62). However, long-term outcome data are not available.

●For papillary muscle or acute secondary MR – In a registry study including 176 patients with severe MR post-MI managed with TEER, the patients with papillary muscle rupture (compared with the patients with acute secondary MR) had higher in-hospital mortality rates (adjusted odds ratio [OR] 3.05, 95% CI 1.15-8.12), higher 30-day mortality rates (unadjusted OR 3.99, 95% CI 1.42-11.26) and a higher rate of conversion to surgical mitral valve replacement (22 versus 3 percent; unadjusted OR 8.17, 95% CI 2.15-30.96) [30].

Comparative data — Available data are not adequate to compare outcomes with surgical, transcatheter, and medical approaches in patients with acute MR.

In a retrospective international registry of patients with severe MR after acute MI, the 205 patients who underwent intervention (surgical mitral intervention in 106 and mitral TEER in 99) had lower in-hospital and one-year mortality (11 versus 27 percent and 16 versus 35 percent compared with 266 patients treated medically [adjusted HR 0.28, 95% CI 0.18-0.46]) [31]. In-hospital and one-year mortality rates were higher with surgical mitral valve replacement or repair compared with mitral TEER (16 versus 6 percent and 31 versus 17 percent; adjusted HR 3.75, 95% CI 1.55-9.07), but long-term outcome data are not available.

A randomized controlled trial of mitral TEER compared with medical therapy in patients with severe MR and inotrope-dependent cardiogenic shock is in progress [32].

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient education" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Mitral regurgitation (The Basics)")

●Beyond the Basics topic (see "Patient education: Mitral regurgitation (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Management considerations – The approach to management of acute mitral regurgitation (MR) is based upon the patient's symptoms and hemodynamic status, the severity of MR and the cause of MR. (See 'Management considerations' above.)

●Role of medical therapy

•For patients with a mechanical cause of acute MR – The goal of medical therapy in this setting is to stabilize the patient to the extent possible in preparation for prompt mitral valve intervention (for patients with disruption of the mitral valve apparatus) and/or other care (eg, percutaneous coronary intervention as indicated for patients with acute coronary syndrome [ACS]).

Supportive medical care includes vasodilator therapy with nitroprusside or nitroglycerin (as tolerated). However, vasodilator use is often limited by systemic hypotension and intravenous inotropes and vasopressors (eg, norepinephrine or dopamine) and/or mechanical circulatory support (eg, intraaortic balloon pump or other left ventricular [LV] assist device) may be required as temporizing measures. (See 'Medical stabilization' above.)

•For patients with acute MR and systolic anterior motion (SAM) of the mitral valve – In this setting, acute MR is managed by supportive therapy including volume repletion (as needed), avoiding inotropes and treatment with beta blocker therapy as tolerated. (See 'For systolic anterior motion (SAM) of the mitral valve' above.)

-With hypertrophic cardiomyopathy (HCM) – In patients with HCM with SAM, careful assessment of mitral valve anatomy and MR jet characteristics is required to determine if MR is caused by SAM and/or other etiologies (eg, mitral valve prolapse). Management of LV outflow tract obstruction and MR caused by SAM in patients with HCM is discussed separately. (See "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Approach to therapy'.)

-With stress cardiomyopathy – Management for patients with stress cardiomyopathy with LV outflow obstruction and SAM causing acute MR is supportive, as discussed separately. (See "Management and prognosis of stress (takotsubo) cardiomyopathy", section on 'With left ventricular outflow tract obstruction'.)

-Following mitral valve repair – MR with SAM immediately after mitral valve repair is initially treated with supportive therapy. Patients with severe persistent severe SAM are treated with immediate tailored surgical revision of the mitral valve repair. (See "Anesthesia for patients with mitral regurgitation", section on 'Postbypass TEE assessment'.)

-Other causes – Acute MR caused by SAM without the above causes is treated with supportive therapy.

•Management of acute coronary syndrome – For patients with ACS (including ST-elevation myocardial infarction [MI] or non-ST-elevation ACS) with acute severe secondary MR, standard indications for reperfusion apply. (See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy" and "Non-ST-elevation acute coronary syndromes: Selecting a management strategy", section on 'Choice of revascularization strategy'.)

Percutaneous coronary intervention may improve acute MR in patients with ACS, but the response is variable.

●Role of mitral valve intervention

•For patients with a mechanical cause of acute MR – Symptomatic patients with acute severe MR and disruption of the mitral valve apparatus (papillary muscle rupture, chordal rupture, or valve destruction/perforation) require prompt mitral valve intervention.

-For surgical candidates – For most patients with hemodynamic instability from a mechanical cause of acute MR (severe or moderately severe), urgent mitral valve surgery is the treatment of choice, with valve repair generally preferred to valve replacement.

-For high or prohibitive surgical risk – For selected symptomatic patients with acute severe or moderately severe MR with high or prohibitive surgical risk with favorable mitral valve anatomy, transcatheter edge-to-edge repair (TEER) is an alternative option. However, mitral TEER is contraindicated in patients with acute MR with active infective endocarditis given the presence of infected valve tissue.

•For patients with persistent acute secondary MR – For patients with persistent symptomatic acute secondary MR despite medical management (and any indicated reperfusion therapy), we suggest TEER rather than surgical intervention or ongoing medical therapy alone (Grade 2C). This suggestion is based upon limited data on TEER for acute secondary MR and indirect data on TEER in patients with chronic secondary MR, as discussed separately. (See 'Choice of intervention' above and "Chronic secondary mitral regurgitation: Intervention", section on 'Indications for mitral valve intervention'.)