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Acute mitral regurgitation in adults

Acute mitral regurgitation in adults
Literature review current through: Jan 2024.
This topic last updated: Mar 10, 2022.

INTRODUCTION — Patients with acute mitral regurgitation (MR) are often gravely ill with significant hemodynamic abnormalities that require urgent medical and usually surgical treatment [1-3]. (Related Pathway(s): Acute decompensated heart failure: Management of patients with cardiogenic shock.)

The pathophysiology, clinical features, and management of native acute MR will be reviewed here. The changes that occur in chronic MR are discussed separately. (See "Pathophysiology and natural history of chronic mitral regurgitation" and "Clinical manifestations and diagnosis of chronic mitral regurgitation".)

ETIOLOGY — Although there are many causes of acute MR, many of which can, under other circumstances, also cause chronic MR, there are two primary categories of acute native valve MR (figure 1):

Ischemic MR – Papillary muscle rupture due to acute myocardial infarction (MI) or trauma or papillary muscle displacement due to MI or ischemia [4,5]. (See "Acute myocardial infarction: Mechanical complications" and "Chronic secondary mitral regurgitation: General management and prognosis".)

Nonischemic MR – Ruptured mitral chordae tendineae (flail leaflet) due to myxomatous disease (mitral valve prolapse) [6], infective endocarditis, blunt chest trauma [7-9], rheumatic heart disease (acute rheumatic fever [10] or chronic rheumatic mitral valve disease), or spontaneous rupture [11,12]. Acute MR has also been reported in the setting of dynamic left ventricular (LV) outflow obstruction, particularly in patients with stress cardiomyopathy [13-17]. (See "Management and prognosis of stress (takotsubo) cardiomyopathy", section on 'With left ventricular outflow tract obstruction'.)

Iatrogenic – Acute MR has been reported rarely in patients undergoing transcatheter aortic valve implantation [18] and after removal of a transaortic LV assist device [19], due to trauma to the leaflets or chords.

Different mechanisms are responsible for acute MR in prosthetic valves:

Tissue valve leaflet rupture due to endocarditis, degeneration, or calcification.

Impaired closure of mechanical valve occluders due to valve thrombosis, infection, or pannus formation. With older generation mechanical valves, there were instances of strut fracture and disk escape, but these have not been reported with currently implanted valves.

Paravalvular regurgitation due to infection or suture rupture (often related to a calcified or scarred annulus).

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

PATHOPHYSIOLOGY — The hemodynamic changes in acute MR are more severe than those in chronic MR due in part to the lack of time for the left atrium and LV to adapt to the MR [4,20]. This is in contrast to chronic MR where these adaptations have time to develop and typically preserve hemodynamic stability (figure 2). (See "Pathophysiology and natural history of chronic mitral regurgitation".)

The degree of hemodynamic deterioration in acute MR depends upon the etiology and degree of MR, which is often dramatic and rapid in onset. An important factor is left atrial compliance, which is usually normal unless the acute regurgitation is superimposed upon chronic MR. Since the normal left atrium is not compliant, the sudden and marked increase in left atrial volume in acute MR results in an abrupt elevation in pressure within the left atrium. This is immediately reflected back into the pulmonary circulation, often leading to pulmonary edema.

In addition, because the LV is not dilated and a large fraction of the blood ejected by the ventricle goes backward across the mitral valve, effective forward flow is limited. Despite a compensatory increase in heart rate, forward cardiac output falls, which can precipitate cardiogenic shock. The neurohumoral response to the reduction in cardiac output is an increase in vascular resistance, which exacerbates the regurgitation. (See "Hemodynamics of valvular disorders as measured by cardiac catheterization".)

If the degree of regurgitation is limited and left atrial compliance increases, the pressures within the left atrium and pulmonary circulation fall and hemodynamics improve. However, this does not occur in most cases because the amount of regurgitation is large and the left atrium does not accommodate well. Thus, urgent surgical intervention to repair or replace the valve is usually essential.

CLINICAL MANIFESTATIONS — Acute MR usually presents as a cardiac emergency with the sudden onset and rapid progression of pulmonary edema, hypotension, and signs and symptoms of cardiogenic shock. In some cases, the pulmonary hypertension leads to acute right-sided heart failure (HF). In clinical practice, acute MR may not be recognized at presentation because the clinical history mimics an acute pulmonary process (such as infection or acute respiratory distress syndrome) [21] and the physical examination findings often are subtle. Physicians should include acute valve regurgitation in the differential diagnosis of any patient presenting with pulmonary decompensation and consider echocardiography early in the disease course to exclude or confirm this possibility.

The presentation may not be as dramatic if acute MR is superimposed upon chronic MR or the patient is younger and physically fit. Such patients may present subacutely in the office or clinic, rather than in the Emergency Department. They may note increasing shortness of breath, dyspnea on exertion, fatigue, and weakness with little or no overt HF.

Physical examination — The patient with acute MR is often in pulmonary edema and there is evidence of poor tissue perfusion with peripheral vasoconstriction, pallor, and diaphoresis. The arterial pulse is often rapid and of low amplitude or thready due to the reduction in forward stroke volume. When there is an associated increase in right-sided pressure, the neck veins become distended; they may also become pulsatile with a marked "v" wave if the elevated right ventricular pressure leads to tricuspid regurgitation. (See "Examination of the arterial pulse" and "Examination of the jugular venous pulse".)

The cardiac apical impulse is hyperdynamic but is usually normal in location because LV size is normal. If, however, acute regurgitation is superimposed upon chronic MR, the cardiac impulse may be displaced due to the underlying LV enlargement. There may be a hyperdynamic precordium with a right ventricular lift due to the acute increase in pressure within this chamber and the development of tricuspid regurgitation.

Cardiac auscultation — The murmur of acute MR may be early systolic, midsystolic, or holosystolic. However, since the pressure within the left atrium markedly increases during ventricular systole and the pressure gradient between the left atrium and ventricle diminishes or disappears by the end of systole, the systolic murmur is often soft, low-pitched, and decrescendo, often ending well before A2. (See "Auscultation of cardiac murmurs in adults" and "Auscultation of heart sounds".)

When present, the murmur is often best heard along the left sternal border and base of the heart, generally without a thrill, and may radiate to the back. It can be confused with an acute ventricular septal defect which, like acute MR, is a complication of an acute MI.

An S3 filling sound is commonly heard but may be difficult to appreciate if tachycardia is present. With the development of pulmonary hypertension, P2 is increased in intensity and the murmurs of pulmonary and tricuspid regurgitation may be appreciated. (See "Auscultation of heart sounds".)

Silent MR — Approximately 50 percent of patients with moderate to severe acute ischemic MR have no audible murmur, particularly those with acute ischemic MR [22-27]. As an example, a community-based series of 773 patients who underwent echocardiography within 30 days of an MI found that 89 had moderate to severe MR; 28 of these patients (31 percent) had no murmur [22].

The presumed mechanism of silent MR is a relatively low systolic pressure gradient between the LV and left atrium due to the combination of a low systemic blood pressure and elevated left atrial pressure. In addition, acoustic transmission of the murmur may be obscured by obesity and respiratory distress. Thus, the absence of a systolic murmur does not reliably exclude the diagnosis of acute severe MR.

TESTING — Testing in patients with acute MR consists of an electrocardiogram, chest radiograph, echocardiography, and, in some patients, coronary angiography.

Electrocardiogram — There are generally no electrocardiographic abnormalities specifically associated with acute MR. There may, however, be changes that reflect the etiology, such as an acute MI, LV hypertrophy, or P-mitrale reflecting underlying chronic MR.

Chest radiograph — The chest radiograph usually shows a normal size cardiac silhouette and signs of pulmonary edema. Signs of interstitial and alveolar edema are most commonly symmetric. Occasionally (9 percent in one study), the pulmonary edema is unilateral, typically limited to the right upper lobe [28,29].

Echocardiography — The echocardiogram, including Doppler studies, should establish the diagnosis, mechanism, and etiology of acute MR. (See "Echocardiographic evaluation of the mitral valve" and "Transesophageal echocardiography in the evaluation of mitral valve disease".)

With transthoracic echocardiography:

Left atrial size may be normal and LV size may be normal.

However, enlarged LV and left atrium may be present if chronic MR has been present prior to the acute event.

Systolic function is normal or hyperdynamic.

A reduced forward stroke volume shortens the duration of an open aortic valve.

Other findings are related to the etiology of acute MR (figure 1):

There will be evidence of a flail mitral leaflet when the etiology is papillary muscle or chordal rupture. With papillary muscle rupture, the ruptured head is seen in the LV and usually prolapses back into the left atrium (movie 1 and movie 2). Chordal rupture with rheumatic disease more often affects the anterior leaflet, while chordal rupture with myxomatous disease more often involves the posterior leaflet [11].

Vegetations on the leaflets may be seen in patients with endocarditis.

The severity of regurgitation is evaluated with Doppler studies. (See "Echocardiographic evaluation of the mitral valve", section on 'Determination of severity'.)

Transthoracic echocardiography can underestimate the severity of MR due to inadequate imaging of the color flow jet. Thus, when transthoracic echocardiography is nondiagnostic in patients with suspected acute native valve MR (eg, acute HF with a hyperdynamic LV), transesophageal echocardiography provides improved images of the mitral valve and assessment of regurgitant severity [30]. For prosthetic mitral valves, transesophageal imaging is almost always necessary.

Exercise echocardiography — Most patients with acute severe MR have hemodynamic compromise and exercise testing is not appropriate. However, in patients with ischemic MR, regurgitation that is not severe at rest may become severe with exercise. Detecting significant MR under these circumstances may require exercise echocardiography.

The mechanism of worsening MR with exercise may be papillary muscle displacement (previously known as papillary muscle dysfunction) or alterations in papillary muscle orientation due to hypokinesis of the underlying LV wall. However, worsening of MR with exercise can occur in the absence of detectable ischemia, as evidenced by the absence of chest pain or typical electrocardiographic or echocardiographic findings [31]. Such patients can present with acute pulmonary edema and have a worse prognosis. These issues are discussed in detail separately. (See "Clinical manifestations and diagnosis of chronic mitral regurgitation", section on 'Stress testing'.)

Cardiac catheterization — In selected patients with acute MR who are hemodynamically stable, coronary angiography may be warranted before surgical intervention to detect significant coronary obstruction. Although data supporting efficacy are limited, these lesions are usually revascularized at the time of mitral valve surgery since concurrent bypass surgery typically adds little morbidity or mortality to the procedure.

We agree with the 2020 American College of Cardiology/American Heart Association valvular heart disease recommendations for coronary angiography prior to valve surgery [30]:

Coronary angiography was recommended before elective valve surgery in patients who have angina, objective evidence of ischemia, chronic severe secondary MR, decreased LV systolic function, history of coronary artery disease, or coronary risk factors (including males >40 years old and postmenopausal females).

In selected patients with a low to intermediate pretest probability of coronary artery disease (CAD), contrast-enhanced coronary computed tomography angiography is reasonable to exclude the presence of significant obstructive CAD.

If cardiac catheterization is performed for an acute coronary syndrome complicated by MR, contrast angiography of the LV is generally avoided because of the contrast load in an already compromised patient. Furthermore, ventricular angiography is rarely needed with the availability of transthoracic and transesophageal echocardiography.

Surgery without coronary angiography may be reasonable in patients undergoing emergency surgery for acute valve regurgitation or infective endocarditis (or for disease of the aortic sinuses or ascending aorta).

TREATMENT — Acute MR is a medical and surgical emergency, as the patient typically presents in acute pulmonary edema or cardiogenic shock. In most cases, the definitive treatment is prompt surgical intervention. However, medical therapy may be needed to support the patient while the diagnosis is made and in the interval until surgery can be performed.

Medical stabilization — The primary goal of medical therapy in acute MR is to stabilize the patient in preparation for surgery. Intravenous nitroprusside can reduce MR, by reducing systemic vascular resistance [32-34]. The decrease in MR severity increases forward cardiac output and diminishes pulmonary congestion [30]. Vasodilator use is often limited by systemic hypotension.

Intraaortic balloon counterpulsation has been used as a temporizing measure prior to emergency valve surgery in patients with acute MR [30]. Temporary stabilization may also be achieved using a short-term circulatory assist device [35] (see "Intraaortic balloon pump counterpulsation" and "Short-term mechanical circulatory assist devices"). From a physiologic point of view, a percutaneous transaortic LV assist device (such as an Impella device) should improve forward cardiac output in patients with acute MR and there have been case reports suggesting this approach may provide clinical benefit in supporting hemodynamics until surgical correction of MR can be performed.

Surgery — The exact timing and risk of surgical intervention depend upon whether MR is nonischemic (chordal rupture). Older studies showed a very high risk of surgery for patients with acute MR, with mortality rates as high as 50 percent [36-39]. In a later multicenter study of surgery for acute severe MR in 279 patients, overall 30-day mortality was 23 percent, but 15-year survival was 67 percent [40]. All 279 patients were hemodynamically unstable before surgery. Valve repair was performed in 27 percent, with valve replacement in the remainder. The cause of regurgitation was ischemic in 45 percent, myxomatous mitral valve disease in 26 percent, and endocarditis in 28 percent. Multivariate predictors of 30-day mortality were acute MI, acute endocarditis, shock, LV dysfunction, and coronary disease.

Chordal rupture — Prompt mitral valve surgery is recommended for symptomatic acute severe nonischemic MR [30,41].

Acute MR caused by chordal rupture often can be treated early with mitral valve repair [42,43]. Compared with valve replacement, mitral valve repair is associated with a lower operative mortality, preservation of LV function, and better long-term survival. In addition, the risks of a prosthetic valve and anticoagulation are avoided.

Management of patients with flail leaflet with chronic MR is discussed separately. (See "Chronic primary mitral regurgitation: Indications for intervention".)

Infective endocarditis — Early surgical intervention is indicated in patients with acute MR due to infective endocarditis that results in HF, as recommended in the 2020 American College of Cardiology/American Heart Association (ACC/AHA) valve disease guidelines [30] and the 2015 AHA infective endocarditis scientific statement [44]. Similarly, the European Society of Cardiology guidelines for infective endocarditis recommend emergency surgery for acute MR due to endocarditis if HF or echocardiographic signs of poor hemodynamic tolerance are present [45]. (See "Surgery for left-sided native valve infective endocarditis".)

Urgent surgery is recommended if there is persistent HF or echocardiographic signs of hemodynamic compromise, including pulmonary hypertension and early mitral valve closure. Elective surgery is appropriate for acute severe regurgitation due to endocarditis, even in the absence of HF. In a propensity-matched study of early versus late surgery for endocarditis, the absolute risk reduction in mortality with surgery was 5.9 percent [46]. Subgroups benefiting most from early surgery included those with paravalvular abscess, systemic embolism, and infection with Staph aureus.

Valve repair is preferred but is not always possible depending upon the extent of tissue destruction [30]. The efficacy of mitral valve repair can be illustrated in the following observations:

In a review of 53 patients with MR due to endocarditis, the valve could be repaired in 40 percent with an operative mortality of 0 percent; in contrast, the operative mortality was 13 percent in those who required valve replacement [47].

Similar outcomes were noted in a series of 78 patients with endocarditis and MR: Valve repair was feasible in 81 percent and operative mortality was only 3 percent [48]. However, 60 percent of patients had healed endocarditis and may therefore have been at lower risk than patients with active infection.

In a meta-analysis of 24 studies of surgery for endocarditis, a total of 470 (39 percent) patients underwent valve repair and 724 (61 percent) underwent valve replacement. Valve repair was associated with a lower early (2.3 versus 14.4 percent) and long-term (7.8 versus 40.5 percent) mortality, lower rates of early and later reoperation, and lower rates of recurrent endocarditis (1.8 versus 7.3 percent) [49].

Ischemic MR — In patients with acute ischemic MR, treatment depends upon the exact etiology of valve dysfunction [50,51]:

Myocardial ischemia – Among patients with acute MR due to myocardial ischemia, percutaneous revascularization may lead to resolution of the MR [52-55]. In these patients, medical therapy and an intraaortic balloon pump may be used during the acute episode, with weaning of these modalities as myocardial function improves. (See "Chronic secondary mitral regurgitation: General management and prognosis".)

Papillary muscle rupture – In contrast, surgical intervention is needed with papillary muscle rupture [36-39,56,57]. (See "Acute myocardial infarction: Mechanical complications", section on 'Papillary muscle rupture'.)

Partial papillary muscle rupture – Echocardiography can distinguish partial papillary muscle rupture from complete papillary muscle rupture. The prognosis for patients with partial papillary muscle rupture depends upon the extent of myocardial damage and severity of MR. With partial papillary muscle rupture, some surgeons prefer to stabilize the patient and delay surgery for six to eight weeks after MI when possible to avoid operating on the necrotic myocardial tissue. However, many patients cannot be stabilized, and acute intervention must be considered.

In the Society of Thoracic Surgeons database, a total of 1342 patients underwent mitral valve surgery for papillary muscle rupture between 2011 and 2018 [58]. Mitral valve replacement was performed in 79.8 percent, with emergency surgery in 52 percent of cases and concurrent coronary bypass grafting in 59.3 percent. An intraaortic balloon pump was used for patient stabilization preoperatively in 56.9 percent, with a transaortic axial flow support device (Impella) in 4.1 percent and extracorporeal membrane oxygenation in 3.1 percent. Overall operative mortality was 20 percent. Complications included prolonged ventilation (61.8 percent), acute renal failure (15.4 percent), reoperation (10.2 percent), and stroke (5.2 percent). Predictors of mortality included mitral valve replacement (versus repair), older age, cardiogenic shock, an LV ejection fraction <25 percent, and emergency surgery.

Smaller observational studies have evaluated longer term outcomes after papillary muscle rupture. In a study of 54 patients undergoing surgery for papillary muscle rupture between 1980 and 2000, 10-year survival was only 35 percent and 10-year survival free of HF was only 23 percent [59]. These patients had a mean age of 70±8 years, were predominantly male (74 percent), and 91 percent presented with cardiogenic shock, pulmonary edema, or cardiac arrest. It is likely that the underlying cause of papillary muscle rupture (eg, coronary artery disease) is the primary factor in these poor long-term outcomes.

Transcatheter edge-to-edge repair — Case reports describe mitral transcatheter edge-to-edge repair (TEER), but surgical intervention is recommended when possible.

In a systematic review of mitral TEER with a total of 141 patients with cardiogenic shock and significant MR, in-hospital mortality was 15.6 percent, 90-day mortality was 29.5 percent, and one-year mortality was 42.6 percent, emphasizing the poor outcomes with this clinical presentation [60]. There were lower rates of adverse events in the 89 percent of patients who had a successful mitral TEER procedure, compared with those who had an unsuccessful procedure and residual MR greater than 2+ in severity. However, evidence for the benefit of mitral TEER over surgical intervention is lacking; surgical intervention remains the most appropriate option in most patients. (See "Transcatheter edge-to-edge mitral repair".)

TEER is an evolving technology. In a registry of 93 patients (mean age 70 years) with acute MR following MI, 30-day mortally was not statistically significantly different after mitral TEER in the 50 patients with cardiogenic shock compared with those without cardiogenic shock (10 versus 2.3 percent). There also was no difference between those with and without cardiogenic shock in procedure success (90 versus 93 percent) or the combined endpoint of mortality or reintervention at a median follow-up of seven months (28 versus 25.6 percent) [61]. However, there was no surgical comparison group.

Mitral TEER is not appropriate in patients with acute MR due to active endocarditis due to the presence of infected valve tissue. In patients with myxomatous mitral valve disease and spontaneous chordal rupture, surgical intervention with mitral valve repair is preferred, although mitral TEER may be considered in patients with high or prohibitive surgical risk.

We agree with the 2020 ACC/AHA valve guidelines recommendation for severely symptomatic patients (New York Heart Association class III or IV) with primary severe MR and high or prohibitive surgical risk; in this setting TEER is reasonable if mitral valve anatomy is favorable for the repair procedure and patient life expectancy is at least one year.

Management of chronic ischemic MR is discussed separately. (See "Chronic secondary mitral regurgitation: General management and prognosis".)

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".)

SUMMARY AND RECOMMENDATIONS

There are two primary categories of causes of acute native valve mitral regurgitation (MR) (see 'Etiology' above):

Ischemic MR – Papillary muscle rupture due to acute myocardial infarction (MI), or papillary muscle displacement due to MI or ischemia. (See "Acute myocardial infarction: Mechanical complications" and "Chronic secondary mitral regurgitation: General management and prognosis".)

Nonischemic MR – Ruptured mitral chordae tendineae (flail leaflet) due to myxomatous disease (mitral valve prolapse), infective endocarditis, trauma, rheumatic heart disease (acute rheumatic fever or chronic rheumatic mitral valve disease), or spontaneous rupture. Acute MR has also been reported in the setting of dynamic left ventricular (LV) outflow obstruction, particularly in patients with stress cardiomyopathy. (See "Management and prognosis of stress (takotsubo) cardiomyopathy", section on 'With left ventricular outflow tract obstruction'.)

Acute MR is often misdiagnosed as a primary pulmonary process or as heart failure (HF) due to LV dysfunction. Echocardiography is diagnostic and a high level of clinical awareness is needed. (See 'Clinical manifestations' above.)

Approximately 50 percent of patients with moderate to severe acute ischemic MR have no audible murmur. (See 'Silent MR' above.)

Immediate therapy of acute MR includes urgent surgical consultation. Most patients with primary acute severe MR require urgent mitral valve surgery. Despite a high operative mortality, the outcome is even worse with medical therapy. (See 'Treatment' above.)

The primary goal of medical therapy in acute MR is to stabilize the patient in preparation for surgery. Vasodilator therapy with nitroprusside and/or placement of an intraaortic balloon pump (or other ventricular assist device) may be helpful while awaiting surgical intervention. (See 'Medical stabilization' above.)

Chordal rupture often can be treated early with mitral valve repair. (See 'Chordal rupture' above.)

Early surgical intervention is indicated in patients with acute MR due to endocarditis that results in HF. (See 'Infective endocarditis' above.)

In patients with acute ischemic MR, treatment depends upon the exact etiology of valve dysfunction (see 'Ischemic MR' above):

Among patients with acute MR due to myocardial ischemia, percutaneous revascularization may lead to resolution of the MR. In these patients, medical therapy and an intraaortic balloon pump may be used during the acute episode with weaning of these modalities as myocardial function improves.

Surgical intervention is needed to treat papillary muscle rupture. Case reports describe performing a transcatheter mitral edge-to-edge repair in high-risk patients as a bridge to surgery, but surgical intervention is recommended when possible.

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Topic 8170 Version 24.0

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