Acute Mitral Regurgitation 

Updated: Dec 28, 2015
Author: Daniel DiSandro, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP 



Mitral regurgitation, in the acute and chronic decompensated states, is commonly encountered in the emergency department. An understanding of the underlying etiologies and pathophysiology of the condition is critical to direct appropriate treatment.


Mitral regurgitation can be divided into the following 3 stages: acute, chronic compensated, and chronic decompensated.

In the acute stage, which usually occurs with a spontaneous chordae tendineae or papillary muscle rupture secondary to myocardial infarction, a sudden volume overload occurs on an unprepared left ventricle and left atrium. The volume overload on the left ventricle increases left ventricular stroke work. Increased left ventricular filling pressures, combined with the transfer of blood from the left ventricle to 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.

Severe mitral regurgitation as depicted with color Severe mitral regurgitation as depicted with color Doppler echocardiography.



United States

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, being responsible for 45% of cases of mitral regurgitation. MVP has been estimated to be present in 4% of the population; however, significant regurgitation in this population only occurs in those with abnormalities of the valve.


In areas other than the Western world, rheumatic heart disease remains the leading cause of mitral regurgitation.


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).

Consider the following:

  • Acute pulmonary edema and cardiogenic shock often complicate the course of acute 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 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 the subsequent complication of embolization. In addition, these patients are susceptible to endocarditis. A study of the survival of patients with chronic regurgitation was performed using randomly selected patients. The study 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 rate if they present with severe pulmonary edema.

Major complications from chronic regurgitation include the following:

  • Severe LV 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.


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 those cases caused by prior rheumatic disease, the mean age is 36, plus or minus 6 years.




Note the following:

  • Mitral regurgitation can be tolerated for many years.

  • 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 MVP syndrome.

  • In patients with mitral valve prolapse (MVP), palpitations and atypical chest pain are the most frequent complaints. Two thirds of these patients are female, often with an underlying panic disorder.

  • With underlying coronary artery disease (CAD), regurgitation usually is associated with symptoms of angina pectoris.

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

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

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

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


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.


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)



Differential Diagnoses



Imaging Studies

Chest radiography

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

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.

Mitral regurgitation presents with acute pulmonary edema and a normal cardiac silhouette with acute mitral regurgitation that is secondary to a rupture of a valve apparatus.

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.

Transesophageal echocardiogram demonstrating prolapse of both mitral valve leaflets during systole.
Transthoracic echocardiogram demonstrating bioprosthetic mitral valve dehiscence with paravalvular regurgitation.

Other Tests


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


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


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

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 CAD.



Emergency Department Care

Acute mitral regurgitation is a specific case in which immediate intervention in the ED can make a difference.

If the etiology is myocardial infarction, infusion of thrombolytics may reestablish the 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.

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 should be controlled with digoxin or 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.

For more information, see the American College of Cardiology/American Heart Association guidelines for the management of patients with valvular heart disease.[1]


In the setting of acute regurgitation secondary to an acute myocardial infarction, a cardiologist should be involved early. Echocardiography is necessary in order to look for papillary muscle rupture. Interventional cardiology for emergency angioplasty, 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.



Medication Summary

The mainstay of treatment is preload and afterload reduction, particularly in the setting of mitral regurgitation with pulmonary edema.


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.



Further Outpatient Care

The definitive treatment of mitral regurgitation remains surgery.

The risk-benefit ratio must be examined carefully with each individual situation prior to a decision to replace the valve.

The 2 primary surgeries are mitral valve replacement and mitral valve repair.

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

Repair usually is 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 order to attempt 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.

Patients must be educated concerning the warning signs and symptoms (eg, congestive heart failure, chest pain) and 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.