Mitral regurgitation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S. [2] ; Lakshmi Gopalakrishnan, M.B.B.S; Mohammed A. Sbeih, M.D. [3]{{#meta: itemprop="medicalWebPageAudiences" content="patient"}}{{#meta: itemprop="medicalWebPageSpecialities" content="cardiology"}}{{#meta: itemprop="medicalWebPageInfoTypes" content="symptoms,diagnosis,treatment,causes,prognosis,complications"}} Classification Classic::Classification Atypical::Screening::

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Overview
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Differentiating Mitral Regurgitation from other Diseases
Epidemiology and Demographics
Natural History, Complications and Prognosis
Diagnosis
Stages
History and Symptoms
Physical Examination
Chest X Ray
Electrocardiogram
Echocardiography
Cardiac MRI
Cardiac Catheterization
Treatment
Overview
Acute Mitral Regurgitation Treatment
Chronic Mitral Regurgitation Treatment
Surgery
Follow Up
Case Studies
Case #1
Mitral regurgitation On the Web
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Mitral regurgitation in the news
Blogs on Mitral regurgitation
Directions to Hospitals Treating Mitral regurgitation
Risk calculators and risk factors for Mitral regurgitation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [5]; Varun Kumar, M.B.B.S. [6]; Lakshmi Gopalakrishnan, M.B.B.S. [7]; Mohammed A. Sbeih, M.D. [8]; Rim Halaby, M.D. [9]

Overview

Mitral regurgitation (MR) is a disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood. MR is the abnormal leaking of blood from the left ventricle through the mitral valve, and into the left atrium, when the left ventricle contracts. MR is the most common form of valvular heart disease. MR can be classified into either acute or chronic according to the acuity of the events leading to the valvular abnormality. Regardless of the underlying etiology of MR, a decrease in the coaptation between the leaflets of the valve commonly characterizes all cases of MR. The causes of MR depend on the acuity of the valvular abnormality and the underlying pathological mechanism. The blowing holosystolic murmur of mitral regurgitation must be distinguished from tricuspid regurgitation and a ventricular septal defect. MR is one of the most common valvular diseases in the general population, ranking first among valvular regurgitation abnormalities. The prevalence of MR of a severity equal to or worse than mild was reported in The Framingham Heart Study as 19.0% in men and 19.1% in women. The prevalence of MR increases with age. Chronic MR can be either compensated or decompensated. The natural history and prognosis of MR depend on the underlying etiology and the degree of severity of the valvular abnormality. Mild MR is associated with few if any complications. The stage of MR can be estimated based on specific criteria for the valve anatomy, valve hemodynamics, associated cardiac findings, and symptoms.

Classification

MR can be classified into either acute or chronic according to the acuity of the events leading to the valvular abnormality. Chronic MR is further classified into primary or secondary based on the presence or absence of one or more abnormalities in the structures of the valves, respectively.

Pathophysiology

Regardless of the underlying etiology of MR, a decrease in the coaptation between the leaflets of the valve commonly characterizes all cases of MR. Acute MR occurs when there is sudden disruption of one or more of the components of the mitral valve, as occurs in leaflet perforation, rupture of a chordae tendineae, or rupture of the papillary muscle. In the acute phase, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature to cause an elevation of the pulmonary capillary wedge pressure, which causes dyspnea, orthopnea, and rales. In addition, there is decreased forward stroke volume. Chronic MR can be either primary or secondary. Chronic primary MR results from chronic disruption of one or more component of the mitral valve (papillary muscles, chordae tendineae, or valve leaflets), whereas chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the mitral valve. If the chronic MR develops slowly over months to years or if the acute phase is successfully managed with medical therapy, the patient enters the chronic compensated phase of MR that can eventually deteriorate into a decompensated phase as the left ventricular systolic function worsens. The markers of MR decompensation are as follows: left ventricular end-diastolic dimension greater than 70 mm, left ventricular end-systolic dimension greater than 45 to 47 mm, and left ventricular ejection fraction (LVEF) less than 50 to 55 percent.

Causes

The causes of MR depend on the acuity of the valvular abnormality and the underlying pathological mechanism. Acute MR occurs when there is sudden disruption of one or more of the components of the mitral valve, such as leaflet perforation, rupture of a chordae tendineae, or rupture of the papillary muscle. The sudden disruption of the mitral valve can be caused by infective endocarditis, degenerative mitral valve disease, or acute ST elevation myocardial infarction. Chronic primary MR is most commonly caused by mitral valve prolapse; other causes include rheumatic fever and Marfan's syndrome. Chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the mitral valve and it can be caused by coronary artery disease (ischemic) or any disease causing left ventricular dysfunction and dilatation (functional).

Differential Diagnosis

The blowing holosystolic murmur of mitral regurgitation must be distinguished from tricuspid regurgitation and a ventricular septal defect.

Epidemiology and Demographics

MR is one of the most common valvular diseases in the general population, ranking first among valvular regurgitation abnormalities. The prevalence of MR of a severity equal to or worse than mild was reported in The Framingham Heart Study as 19.0% in men and 19.1% in women. The prevalence of MR increases with age.

Natural History, Complications, and Prognosis

The natural history of MR may follow one of two patterns, acute or chronic. Chronic MR can be either compensated or decompensated. The natural history and prognosis of MR depend on the underlying etiology and the degree of severity of the valvular abnormality. Mild MR is associated with few if any complications. However, when severe, MR may lead to development of pulmonary edema, pulmonary hypertension, and right heart failure.

Diagnosis

Stages

The stage of MR can be estimated based on specific criteria for the valve anatomy, valve hemodynamics, associated cardiac findings, and symptoms. The stages of MR are the following: at risk of MR, progressive MR, asymptomatic severe MR, and symptomatic severe MR.

History and Symptoms

Acute and decompensated MR is associated with symptoms of congestive heart failure including dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and exercise intolerance. Individuals with chronic compensated MR may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure.

Physical Examination

Chronic compensated MR causes a blowing holosystolic murmur which radiates to the left axilla. In acute severe MR, the murmur can be early systolic rather than the typical holosystolic murmur in chronic MR due to the abrupt elevation in the pressure in the left atrium and the equalization of pressures between the left atrium and the left ventricle. The intensity of the murmur decreases with valsalva maneuver and standing and becomes louder with hand grip, squatting, and leg raising. The murmur might be short or absent in severe acute MR. In addition, S1 is usually diminished and S2 is commonly widely split. The pulmonic component of the second heart sound (P2) is louder than the aortic component (A2) in the presence of severe pulmonary hypertension, thus widening the splitting of S2.

Chest X-Ray

The chest X-ray in individuals with chronic mitral regurgitation (MR) is characterized by the presence of an enlargement of the left atrium and the left ventricle. In acute MR, pulmonary edema is present and the heart is not enlarged.

Electrocardiogram

In severe cases of chronic MR, signs of left ventricular hypertrophy with strain, left atrial enlargement, and pulmonary hypertension may be observed on the resting electrocardiogram (ECG). Chronic mitral regurgitation is associated with an increased risk for atrial fibrillation. The ECG may reveal findings of coronary artery disease or other cardiac conditions that might have led to MR.

Echocardiography

Transthoracic echocardiography (TTE) should be performed in a patient with suspected MR to confirm the diagnosis and to establish the baseline severity of disease. It should then be performed to monitor the course of disease over time. Color doppler flow on the TTE will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole. Echocardiographic features that suggest severe MR include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.

Cardiac MRI

Cardiac magnetic resonance (CMR) may be beneficial to evaluate the structure and function of the left atrium and left ventricle as well as the severity of the mitral regurgitation when echocardiography findings are inconclusive.

Cardiac Catheterization

Cardiac catheterization is useful to evaluate mitral regurgitation when the results of the non-invasive testing are insufficient. In addition, cardiac catheterization might be performed when there is lack of consistency between the clinical findings and the results of the non-invasive testing in order to rule out cardiac etiologies or pulmonary hypertension as the cause of the patient's symptoms. Coronary angiography should be considered prior to mitral valve surgery among patients with risk factors of coronary artery disease among whom the underlying etiology of mitral regurgitation is suspected to be of ischemic origin.

Treatment

Treatment Overview

Vasodilator therapy with ACE inhibitors and hydralazine is the foundation of medical therapy; once the patient becomes symptomatic, mitral valve surgery is the definitive therapy. This chapter reviews general treatment measures for the patient with mitral regurgitation.

Acute Mitral Regurgitation Treatment

Surgery is the main treatment of symptomatic acute severe primary MR and it should be performed urgently without any delay. Although some patients with moderate acute MR develop some compensatory mechanisms, surgery remains the treatment of choice for the majority of patients with acute MR. Medical therapy with vasodilators might be needed to decrease the afterload and thereby decrease the regurgitant fraction until surgery can be performed. Prior to the surgical procedure, an intra-aortic balloon pump or percutaneous circulatory assist device might also be used to stabilize the patient.

Chronic Mitral Regurgitation Treatment

The distinction between primary and secondary MR is of the utmost importance when determining the appropriate treatment strategies for patients with chronic MR. Primary and secondary MR have different underlying pathophysiology and, therefore, have different indications for surgery and medical therapy. Surgery is generally the treatment of choice among patients with chronic primary MR and left ventricular systolic dysfunction; nevertheless, medical therapy is warranted when surgery is delayed or not planned. The cornerstone of the treatment of patients with chronic secondary MR with decreased ejection fraction is the standard regimen for the treatment of heart failure, which includes one or more of the following: beta blockers, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, or aldosterone antagonists. Mitral valve surgery is indicated in some circumstances among patients with chronic severe secondary MR, particularly those undergoing coronary artery bypass graft or patients with NYHA class III/IV heart failure symptoms.

Follow Up

Regular follow up is recommended among patients with asymptomatic MR and preserved left ventricular ejection fraction.

References

Pathophysiology

https://https://www.youtube.com/watch?v=nY4aaBezu9o%7C350}}

Resident Survival Guide

Mitral Regurgitation Microchapters
Home
Patient Information
Overview
Classification
Pathophysiology
Causes
Differentiating Mitral Regurgitation from other Diseases
Epidemiology and Demographics
Natural History, Complications and Prognosis
Diagnosis
Stages
History and Symptoms
Physical Examination
Chest X Ray
Electrocardiogram
Echocardiography
Cardiac MRI
Cardiac Catheterization
Treatment
Overview
Acute Mitral Regurgitation Treatment
Chronic Mitral Regurgitation Treatment
Surgery
Follow Up
Case Studies
Case #1
Mitral regurgitation On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Mitral regurgitation All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA onMitral regurgitation
CDC on Mitral regurgitation
Mitral regurgitation in the news
Blogs on Mitral regurgitation
Directions to Hospitals Treating Mitral regurgitation
Risk calculators and risk factors for Mitral regurgitation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [10]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S., Lakshmi Gopalakrishnan, M.B.B.S., Mohammed A. Sbeih, M.D. [11], Rim Halaby, M.D. [12]

Overview

Regardless of the underlying etiology of mitral regurgitation (MR), a decrease in the coaptation between the leaflets of the valve commonly characterizes all cases of MR. Acute MR occurs when there is sudden disruption of one or more of the components of the mitral valve, as occurs in leaflet perforation, rupture of a chordae tendineae, or rupture of the papillary muscle. In the acute phase, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature to cause an elevation of the pulmonary capillary wedge pressure which causes dyspnea, orthopnea, and rales. In addition, there is decreased forward stroke volume. Chronic MR can be either primary or secondary. Chronic primary MR results from chronic disruption of one or more component of the mitral valve (papillary muscles, chordae tendineae, or valve leaflets), whereas chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the mitral valve. If the chronic MR develops slowly over months to years or if the acute phase is successfully managed with medical therapy, the patient enters the chronic compensated phase of MR that can eventually deteriorate into a decompensated phase as the left ventricular systolic function worsens. The markers of MR decompensation are as follows: left ventricular end-diastolic dimension greater than 70 mm, left ventricular end-systolic dimension greater than 45 to 47 mm, and left ventricular ejection fraction (LVEF) less than 50 to 55 percent.

Anatomy

• The mitral valve is composed of the valve leaflets, the mitral valve annulus (which forms a ring around the valve leaflets), the papillary muscles (which tether the valve leaflets to the left ventricle, preventing them from prolapsing into the left atrium), and the chordae tendineae (which connect the valve leaflets to the papillary muscles).
• A dysfunction of any of these portions of the mitral valve apparatus can cause MR.
• The mitral annulus changes in shape and size during the cardiac cycle. It is smaller at the end of atrial systole due to the contraction of the left atrium around it, like a sphincter.
• This reduction in annulus size at the end of atrial systole may be important for the proper coapting of the leaflets of the mitral valve when the left ventricle contracts and pumps blood.

Mechanical Basis of Mitral Regurgitation

The mechanical basis underlying MR includes the following:

• Anterior mitral leaflet prolapse
• Posterior mitral leaflet prolapse
• Bileaflet prolapse
• Restricted mitral leaflets
• Apical tethering
• Papillary muscle rupture
• Ischemic papillary muscle rupture
• Mitral leaflet perforation
• Rupture or tear of the chordae tendineae
• Dilation of the mitral annulus
• "Functional MR" due to dilation of the heart itself

Shown below is an image depicting the abnormal flow of blood from the left ventricle, through the mitral valve, and into the left atrium during systole.

Mitral regurgitation (schematic drawing)
During systole, contraction of the left ventricle causes abnormal backflow (arrow) into the left atrium.
1 Mitral valve
2 Left Ventricle
3 Left Atrium
4 Aorta

Factors Affecting the Regurgitant Volume

The volume of the regurgitant flow determines the severity of MR. The factors that affect the regurgitant volume are:

• The effective regurgitant orifice (principle factor)
• The gradient of pressure between the left ventricle and the left atrium (principle factor)
• The compliance of the left atrium
• The left ventricular function
• The duration of systole
• Left ventricular afterload

Pathophysiology of Acute Mitral Regurgitation

• Acute MR occurs when there is sudden disruption of one or more of the components of the mitral valve, such as leaflet perforation, rupture of a chordae tendineae, or rupture of the papillary muscle.
• The sudden disruption of the mitral valve may occur in the context of infective endocarditis, degenerative mitral valve disease, or acute ST elevation myocardial infarction.
• In the acute setting, the total stroke volume (i.e. the forward plus the regurgitant volume) is increased, but the forward cardiac output into the aorta is decreased because a proportion of the blood is going backward into the left atrium.
• Consequently, acute MR causes a sudden volume overload of both the left atrium and the left ventricle. As a result, pulmonary congestion and hypoxia occur following the elevation of the pressure in the left atrium.

Shown below is an image depicting the pressures in the left atrium, left ventricle, and aorta in acute MR.

Pathophysiology of Chronic Mitral Regurgitation

Chronic Primary Mitral Regurgitation

Chronic primary MR results from chronic disruption of one or more component of the mitral valve (papillary muscles, chordae, and valve leaflets). This may occur among patients with:

• Mitral valve prolapse
  • Myxomatous degeneration (young patients)
  • Fibroelastic deficiency disease (old patients)
• Infective endocarditis
• Connective tissue disease
• Rheumatic heart disease
• Radiation heart disease

Chronic Compensated Phase

• If the MR develops slowly over months to years or if the acute phase is successfully managed with medical therapy, the patient enters the chronic compensated phase of MR.
• In this phase, the left ventricle develops eccentric hypertrophy to reduce the wall stress associated with the rise in total stroke volume (i.e. the forward plus the regurgitant volume) .
• The eccentric hypertrophy and the increased diastolic volume combine to increase the total stroke volume to levels well above normal, so that the forward stroke volume (forward cardiac output) is maintained.
• In the left atrium, the chronic volume overload causes left atrial enlargement, allowing the filling pressure in the left atrium to decrease.
• This dilation of the left atrium reduces the pulmonary capillary wedge pressure, and is associated with an improvement in the signs (e.e. rales) and symptoms (dyspnea, PND, and orthopnea) of pulmonary congestion.
• These compensatory changes in the left ventricle and left atrium maintain the forward cardiac output of the left ventricle, and minimize the signs and symptoms of pulmonary congestion that occur in the acute phase of the disease.
• Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerance.
• In the compensated stage; the left ventricular (LV) end-diastolic dimension is less than 60 mm, and the end-systolic dimension is less than 40 mm on echocardiography.

Chronic Decompensated Phase

• An individual may remain in the compensated phase of MR for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of MR.
• It is currently unclear what causes an individual to enter the decompensated phase of this disease. However, the decompensated phase is characterized by calcium overload within the cardiac myocytes.
• In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of MR, and the stroke volume of the left ventricle begins to decrease. The reduced stroke volume causes a decrease in the forward cardiac output and an increase in the end-systolic volume.
• The increased left ventricular end-systolic volume in turn causes increased left ventricular end diastolic pressures and increased pulmonary capillary wedge pressures.
• As the wedge pressure rises, the patient may develop symptoms of congestive heart failure such as dyspnea, PND and orthopnea and signs of congestive heart failure including rales.
• With the rise in wall stress that accompanies the rise in pressure and volume in the left ventricle, the left ventricle begins to dilate during this phase.
• This causes a dilatation of the mitral valveannulus, which may further worsen the degree of MR. While the ejection fraction is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase of MR, it may still be in the normal range (i.e: > 50 percent), and may not decrease until late in the disease course.
• A decreased ejection fraction in an individual with MR and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase.
• The decompensated stage defined on the basis of decompensated ventricular function. At this stage; the patients are at risk for a poor results of valve replacement.
• It is helpful to classify the stage of the patient's disease so as to recognize signs that may indicate that the patient is transitioning into the decompensated phase of the disease.
• The goal is to perform mitral valve surgery before the patient transitions into the decompensated phase.
• Once the patient transitions into the decompensated phase, (left ventricular enlargement and a low left ventricular ejection fraction) there may not be recovery of left ventricular function following operative repair or replacement of the mitral valve.

Markers of Decompensated Ventricular Function in Mitral Regurgitaiton

1. Left ventricular end-diastolic dimension greater than 70 mm
2. Left ventricular end-systolic dimension greater than 45 to 47 mm
3. Left ventricular ejection fraction (LVEF) less than 50 to 55 percent

Chronic Secondary Mitral Regurgitation

Chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the mitral valve. Chronic secondary MR may occur in the setting of:

• • Coronary artery disease (ischemic), or
  • Any disease causing left ventricular dysfunction and dilatation (functional)

• In secondary MR, the left ventricular dysfunction precedes the valvular abnormality.
• MR may be the result of an enlargement in the annular component of the mitral valve secondary to the dilatation of the left ventricle and/or the displacement of the papillary muscle following remodeling of the left ventricle.
• Ischemic heart disease causes mitral regurgitation by the combination of ischemic dysfunction of the papillary muscles, the abnormal motion of the underlying wall, and the dilatation of the left ventricle that is present in ischemic heart disease, with the subsequent displacement of the papillary muscles and the dilatation of the mitral valve annulus.
• Secondary mitral regurgitation due to the dilatation of the left ventricle is caused by stretching of the mitral valve annulus and displacement of the papillary muscles.
• This dilatation of the left ventricle can be due to any cause of dilated cardiomyopathy, including aortic insufficiency, nonischemic dilated cardiomyopathy and noncompaction cardiomyopathy.
• It is also called functional mitral regurgitation, because the papillary muscles, chordae, and valve leaflets are usually normal.
• When MR is present, the regurgitant flow into the left atrium increases the pressure in this chamber which compensates by dilatation leading to an increase in the preload.
• In addition, the decrease in the afterload causes a series of adaptation in the left ventricle in order to increase the stroke volume.
• The left ventricle adaptation mechanisms to increase the stroke volume include an increment in the preload and the ventricular wall tension.
• The long term overload on the left ventricle contributes to its further dilatation, which by itself leads to a worsening of the MR and subsequent deterioration of the heart failure.

Summary Chart Distinguishing Acute and Chronic Mitral Regurgitation

Comparison of acute and chronic mitral regurgitation

	Acute mitral regurgitation	Chronic mitral regurgitation
Electrocardiogram	Normal unless there are findings related to the etiology of the MR, such as STEMI	P mitrale, atrial fibrillation, left ventricular hypertrophy
Heart size	Normal	Cardiomegaly, left atrial enlargement
Systolic murmur	Heard at the base, radiates to the neck, spine, or top of head	Heard at the apex, radiates to the axilla
Apical thrill	May be absent	Present
Jugular venous distension	Present	Absent

References

Template:WikiDoc Sources

Epidemiology and Demographics

Resident Survival Guide

Mitral Regurgitation Microchapters
Home
Patient Information
Overview
Classification
Pathophysiology
Causes
Differentiating Mitral Regurgitation from other Diseases
Epidemiology and Demographics
Natural History, Complications and Prognosis
Diagnosis
Stages
History and Symptoms
Physical Examination
Chest X Ray
Electrocardiogram
Echocardiography
Cardiac MRI
Cardiac Catheterization
Treatment
Overview
Acute Mitral Regurgitation Treatment
Chronic Mitral Regurgitation Treatment
Surgery
Follow Up
Case Studies
Case #1
Mitral regurgitation On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Mitral regurgitation All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA onMitral regurgitation
CDC on Mitral regurgitation
Mitral regurgitation in the news
Blogs on Mitral regurgitation
Directions to Hospitals Treating Mitral regurgitation
Risk calculators and risk factors for Mitral regurgitation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [13]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S., Lakshmi Gopalakrishnan, M.B.B.S., Rim Halaby, M.D. [14]

Overview

Mitral regurgitation (MR) is one of the most common valvular diseases in the general population, ranking first among valvular regurgitation abnormailities. The prevalence of MR of a severity equal to or more than mild was reported in The Framingham Heart Study as 19.0% in men and 19.1% in women. The prevalence of MR increases with age.

Prevalence

• The Framingham Heart Study, a prospective epidemiologic study, evaluated the prevalence and severity of MR and other valvular diseases by color Doppler examinations in 1,696 men and 1,893 women.
• The study revealed that MR is the most common valvular regurgitation in the general population, followed by tricuspid regurgitation and then aortic regurgitation.
• The prevalence of MR (with a severity ranging from trace to ≥ moderate regurgitation) was 87.7% in men and 91.5% in women.
• When trace regurgitation is excluded, the prevalence of MR of a severity ≥ mild was 19.0% in men and 19.1% in women.
• The elevated prevalence of trace regurgitation can be a normal finding related to an artifact or an anatomic characteristic of the closure of the mitral valve.

Age

• The prevalence of MR increases with age. MR is one of the most common valvular heart disease in the elderly.
• Shown below are tables depicting the prevalence of MR by age and severity in men and women according the results of the Framingham Heart Study.

Severity of MR	Prevalence of MR by age in men
	26-29	40-49	50-59	60-69	70-83
No MR (%)	14.4	13.3	11.3	12.7	9.0
Trace (%)	76.7	72.9	74.6	60.3	51.7
Mild (%)	8.9	13.5	12.5	24.6	28.1
Moderate or severe (%)	0	0.3	1.6	2.4	11.2

Severity of MR	Prevalence of MR by age in women
	26-29	40-49	50-59	60-69	70-83
No MR (%)	14.0	8.6	9.0	7.2	5.6
Trace (%)	76.3	75	74	66.5	70.8
Mild (%)	9.7	15.5	16	24	23.6
Moderate or severe (%)	0	0.9	1	2.3	0

Gender

• Overall, mitral regurgitation affects both males and females equally. However, there are some minor differences when age is considered.

References

Causes

Resident Survival Guide

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Mitral Regurgitation Microchapters
Home
Patient Information
Overview
Classification
Pathophysiology
Causes
Differentiating Mitral Regurgitation from other Diseases
Epidemiology and Demographics
Natural History, Complications and Prognosis
Diagnosis
Stages
History and Symptoms
Physical Examination
Chest X Ray
Electrocardiogram
Echocardiography
Cardiac MRI
Cardiac Catheterization
Treatment
Overview
Acute Mitral Regurgitation Treatment
Chronic Mitral Regurgitation Treatment
Surgery
Follow Up
Case Studies
Case #1
Mitral regurgitation On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Mitral regurgitation All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA onMitral regurgitation
CDC on Mitral regurgitation
Mitral regurgitation in the news
Blogs on Mitral regurgitation
Directions to Hospitals Treating Mitral regurgitation
Risk calculators and risk factors for Mitral regurgitation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [15]; Associate Editor(s)-in-Chief: Mohammed A. Sbeih, M.D. [16]; Cafer Zorkun, M.D., Ph.D. [17]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.; Mugilan Poongkunran M.B.B.S [18]

Overview

The causes of mitral regurgitation (MR) depend on the acuity of the valvular abnormality and the underlying pathological mechanism. Acute MR occurs when there is sudden disruption of one or more of the components of the mitral valve, such as leaflet perforation, rupture of a chordae tendineae, or rupture of the papillary muscle. The sudden disruption of the mitral valve can be caused by infective endocarditis, degenerative mitral valve disease, or acute ST elevation myocardial infarction. Chronic primary MR is most commonly caused by mitral valve prolapse; other causes include rheumatic fever and Marfan's syndrome. Chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the mitral valve and it can be caused by coronary artery disease (ischemic) or any disease causing left ventricular dysfunction and dilatation (functional).

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Acute coronary syndrome
• Blunt or penetrating chest trauma
• Infective endocarditis
• Myocardial rupture
• NSTEMI
• Papillary muscle rupture
• STEMI
• Temporal arteritis

Common Causes

Acute Mitral Regurgitation

• Acute coronary syndrome
• Papillary muscle rupture
• Infective endocarditis
• Blunt or penetrating chest trauma

Chronic Mitral Regurgitation

Primary Mitral Regurgitation

• Developed World: Mitral valve prolapse (MVP)
• Developing World: Rheumatic heart disease

Secondary Mitral Regurgitation

• Ischemic heart disease
• Dilated left ventricle (due to any cause of dilated cardiomyopathy, including aortic insufficiency, nonischemic dilated cardiomyopathy and noncompaction cardiomyopathy)

Causes by Organ System

Cardiovascular	Acute coronary syndrome, aortic insufficiency, atrial septal defect (ostium primum), carcinoid syndrome, cardiac myxoma, cardiac tumors, congenital heart disease, congestive heart failure, coronary artery disease, dilated cardiomyopathy, endocardial cushion defect, endocarditis, endomyocardial fibrosis, hypertrophic cardiomyopathy, hypertensive heart disease, infective endocarditis, ischemic heart disease, Kawasaki disease, left ventricle dialation, mitral annular calcification, mitral valve prolapse, myocardial rupture, myocarditis, NSTEMI, papillary muscle rupture, rheumatic heart disease, STEMI, Takotsubo cardiomyopathy
Chemical / poisoning	No underlying causes.
Dermatologic	Psoriatic arthropathy
Drug Side Effect	3,4-Methylenedioxymethamphetamine, cabergoline, dexfenfluramine, ergotamine, fenfluramine, fluoxetine, methysergide, paroxetine, pergolide, phentermine, sertraline
Ear Nose Throat	No underlying causes.
Endocrine	No underlying causes.
Environmental	No underlying causes.
Gastroenterologic	No underlying causes.
Genetic	Barth syndrome, Becker muscular dystrophy, Cohen syndrome, Duchenne muscular dystrophy, Emery-Dreifuss muscular dystrophy, Fabry disease, familial hypertrophic cardiomyopathy, Friedreich ataxia, Marfan's syndrome, myotonic dystrophy, osteogenesis imperfecta, polycystic kidney disease, Pompe's disease, pseudoxanthoma elasticum, Turner syndrome, X-linked dilated cardiomyopathy
Hematologic	Antiphospholipid syndrome
Iatrogenic	Balloon valvuloplasty of the mitral valve, cardiac catheterization, cardiopulmonary resuscitation, cathether ablation for arrhythmias, heart surgery, pacemaker syndrome, percutaneous coronary intervention, postpericardiotomy syndrome, prosthetic valve dysfunction
Infectious Disease	Chagas disease, cytomegalovirus, diphtheria, ECHO virus, infective endocarditis, Lyme disease, myocarditis, pneumococcus, rheumatic fever,coxsackie B virus, rickettsial disease, staphylococcus, streptococcus
Musculoskeletal / Ortho	Ankylosing spondylitis, Becker muscular dystrophy, Duchenne muscular dystrophy, Ehlers-Danlos syndrome, Emery-Dreifuss muscular dystrophy, Marfan's syndrome, osteogenesis imperfecta, psoriatic arthropathy, rheumatoid arthritis
Neurologic	Friedreich ataxia
Nutritional / Metabolic	Barth syndrome, Fabry disease, Pompe's disease
Obstetric/Gynecologic	Peripartum cardiomyopathy
Oncologic	Carcinoid syndrome, cardiac myxoma, cardiac tumors
Opthalmologic	No underlying causes.
Overdose / Toxicity	No underlying causes.
Psychiatric	Takotsubo cardiomyopathy
Pulmonary	No underlying causes.
Renal / Electrolyte	End stage renal disease, polycystic kidney disease
Rheum / Immune / Allergy	Ankylosing spondylitis, Behçet's disease, Ehlers-Danlos syndrome, Marfan's syndrome, osteogenesis imperfecta, polychondritis, rheumatic heart disease, rheumatoid arthritis, Sjögren's syndrome, systemic lupus erythematosus, temporal arteritis
Sexual	No underlying causes.
Trauma	Blunt or penetrating chest trauma
Urologic	No underlying causes.
Miscellaneous	Alcoholism, athletes, functional mitral regurgitation

Causes in Alphabetical Order

• 3,4-methylenedioxymethamphetamine
• Acute coronary syndrome
• Alcoholism
• Ankylosing spondylitis
• Antiphospholipid syndrome
• Aortic insufficiency
• Athletes
• Atrial septal defect (Ostium primum)
• Balloon valvuloplasty of the mitral valve
• Barth syndrome
• Becker muscular dystrophy
• Behçet's disease
• Blunt or penetrating chest trauma
• Cabergoline
• Carcinoid syndrome
• Cardiac catheterization
• Cardiac myxoma
• Cardiac tumor
• Cardiopulmonary resuscitation
• Cathether ablation for arrhythmias
• Chagas disease
• Cohen syndrome
• Congenital heart disease
• Congestive heart disease
• Coxsackie B virus
• Cytomegalovirus
• Dexfenfluramine
• Dilated cardiomyopathy
• Diphtheria
• Duchenne muscular dystrophy

• ECHO virus
• Ehlers-Danlos syndrome
• Emery-Dreifuss muscular dystrophy
• Endocardial cushion defect
• Endocarditis
• Endomyocardial fibrosis
• Ergotamine
• Fabry disease
• Familial hypertrophic cardiomyopathy
• Fenfluramine
• Fluoxetine
• Friedreich ataxia
• Functional mitral regurgitation
• Heart surgery
• Heart tumors
• Hypertensive heart disease
• Hypertrophic cardiomyopathy
• Infective endocarditis
• Ischemic heart disease
• Kawasaki disease
• Left ventricle dialation
• Marfan's syndrome
• Methysergide
• Mitral valve prolapse
• Myocardial rupture
• Myocarditis
• Myotonic dystrophy
• NSTEMI
• Lyme disease
• Osteogenesis imperfecta

• Pacemaker syndrome
• Papillary muscle rupture
• Paroxetine
• Percutaneous coronary intervention
• Pergolide
• Peripartum cardiomyopathy
• Phentermine
• Pneumococcus
• Polychondritis
• Polycystic kidney disease
• Pompe's disease
• Postpericardiotomy syndrome
• Prosthetic valve dysfunction
• Pseudoxanthoma elasticum
• Psoriatic arthropathy
• Rheumatic heart disease
• Rheumatoid arthritis
• Rickettsial disease
• Sertraline
• Sjögren's syndrome
• Staphylococcus
• STEMI
• Streptococcus
• Syphilis
• Systemic lupus erythematosus (SLE)
• Takotsubo cardiomyopathy
• Temporal arteritis
• Turner syndrome
• X-linked dilated cardiomyopathy

References

Differential Diagnosis

Resident Survival Guide

File:Critical Pathways.gif

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [19]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [20]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.; Mohammed A. Sbeih, M.D. [21]; Yamuna Kondapally, M.B.B.S[22]

Overview

The blowing holosystolic murmur of mitral regurgitation must be distinguished from tricuspid regurgitation and a ventricular septal defect.

Differentiating Mitral regurgitation from other Diseases

Differentiating Mitral regurgitation from Tricuspid Regurgitation and Ventricular Septal Defects

Physical Examination

All the three cardiac conditions have holosystolic murmur on auscultation. But they can be differentiated by characteristics of the murmur detailed below:

Mitral Regurgitation	Tricuspid Regurgitation	VSD
The murmur in mitral regurgitation is high pitched and best heard at the apex with diaphragm of the stethoscope with patient in the lateral decubitus position. Left ventricular function can be assessed by determining the apical impulse. A normal or hyperdynamic apical impulse suggests good ejection fraction and primary mitral regurgitation. A displaced and sustained apical impulse suggests decreased ejection fraction and chronic and severe mitral regurgitation.	Can be best heard over the fourth intercostal area at left sternal border. The intensity can be accentuated following inspiration (Carvallo's sign) due to increased regurgitant flow in right ventricular volume. Tricuspid regurgitation is most often secondary to pulmonary hypertension. Primary tricuspid regurgitation is less common and can be due to bacterial endocarditis following IV drug use, Ebstein's anomaly, carcinoid disease, or prior right ventricular infarction.	The holosystolic murmur can be best heard over the left third and fourth intercostal spaces and along the sternal border. When the shunt becomes reversed ("Eisenmenger's syndrome"), the murmur may be absent and S2 can become markedly accentuated and single.

Echocardiography

The above three cardiac conditions can also be differentiated more definitively using echocardiography where the echogenicity of blood flow across the defective valves or septum can be visualized and the severity can be quantified.

Mitral regurgitation must be differentiated from the following:

Diseases	History	Symptoms	Physical Examination	Murmur	Diagnosis				Other Findings
					ECG	CXR	Echocardiogram	Cardiac Catheterization
Mitral Stenosis	Age ( Mitral annular calcification in older patients) Rheumatic fever Endocarditis	Dyspnea on exertion Paroxysmal nocturnal dyspnea Orthopnea New onset atrial fibrillation	Mitral facies Heart murmur Jugular vein distension Apical impulse displaced laterally or not palpable Diastolic thrill at the apex Signs of heart failure in severe cases	Diastolic murmur Low pitched Opening snap followed by decrescendo-crescendo rumbling murmur Best heard with the bell of the stethoscope at apex at end-expiration in left lateral decubitus position Intensity increases after a valsalva maneuver, after exercise and after increased after load (eg., squatting, isometric hand grip)	P mitrale Atrial fibrillation: No P waves and irregularly irregular rhythm Right axis deviation Right ventricular hypertropy: Dominant R wave in V1 and V2	Straightening of the left border of the heart suggestive of enlargement of the left atrium Double right heart border (Enlarged left atrium and normal right atrium) Prominent left atrial appendage Splaying of subcarinal angle (>120 degrees) Calcification of mitral valve Kerley B lines	Reduced valve leaflet mobility Valve calcification Doming of mitral valve Valve thickening Enlargement of left atrium	Right heart catheterization: Pulmonary capillary wedge pressure (left atrial pressure) Left heart catheterization: Pressures in left ventricle Determines the gradient between the left and right atrium during ventricular diastole (marker of the severity of mitral stenosis)	Hemoptysis (heart failure) Ortner's syndrome
Mitral Regurgitation	CAD MI Rheumatic fever Endocarditis Mitral valve prolapse Cardiomyopathy Radiation therapy Trauma	Palpitations Symptoms of heart failure in severe cases	Palpation Brisk carotid upstroke and hyperdymanic carotid impulse on palpation Apical impulse is displaced to left S3 and a palpable thrill Auscultation Murmur	Holosystolic murmur High pitched, blowing Radiates to axilla Best heard with the diaphragm of the stethoscope at apex in left lateral decubitus position Intensity increases with hand grip or squatting Decrease in intensity on standing or valsalva maneuver	P mitrale in lead II Increased QRS voltage Right axis deviation Atrial fibrillation	Acute MR Kerley B lines No enlargement of cardiac silhouette Chronic MR Enlarged cardiac silhouette Straightening of left heart border Splaying of subcarinal angle Calcification of mitral annulus Double right heart border	Enlargement of left atrium and ventricle Identify valve abnormality Valve calcification Severity of regurgitation	Grading of MR is done with left ventriculography	Decompensated and acute MR may lead to heart failure
Atrial septal defect	Frequent respiratory or lung infections Dyspnea Tiring when feeding (Infants) Shortness of breath on exertion Palpitations Swelling of feet	Shortness of breath Fatigue Failure to thrive Swelling of feet and abdomen (Right heart failure) Palpitations Respiratory infections	Inspection Precordial bulge Precordial lift Palpation Right ventricular impulse Pulmonary artery pulsations Thrill Auscultation Murmur	Midsystolic (ejection systolic) murmur Widely split, fixed S2 Upper left sternal border	Normal Prolonged PR interval Right bundle branch block ECG findings varies according to the underlying type of ASD	Increased pulmonary markings Cardiomegaly Triangular appearance of heart Schimitar sign	Gold standard test for diagnosis of atrial septal defect (for more information click Atrial septal defect echocardiography)	Defect size Pulmonary venous return Pulmonary vascular resistance Pulmonary artery hypertension	Asymptomatic until later part of their life May be associated with migraine with aura
Left Atrial Myxoma	Dyspnea Orthopnea Pulmonary edema Hyperpigmentation of skin and endocrine activity Cerebral embolism	Symptoms may mimic mitral stenosis	Skin Signs of an embolic phenomenon Raynaud's phenomenon Swelling Clubbing Auscultation: Lung: Fine crepitations Heart: Characteristic "tumor plop"	Early diastolic sound as "tumor plop" Low frequency diastolic murmur may be heard if the tumor obstructing mitral valve	Often normal	Often normal Rare findings: cardiomegaly Left atrial enlargement tumor calcification etc.,	Initial and most useful diagnostic study For more information click Myxoma echocardiography or ultrasound	Useful to detect vascular supply of the tumor by the coronary arteries	Associated with Carney complex (genetic predisposition)
Prosthetic Valve Obstruction	History of valve replacement Systemic embolism	Shortness of breath Fatigue	Ausculation Muffling of murmur	Muffling or disappearance of prosthetic sounds Appearance of new regurgitant or obstructive murmur			Degree of stenosis Assess thrombus size and location Differentiate between thrombus, pannus and vegetations		Causes: Thrombus Pannus formation
Cor Triatriatum	Dyspnea on exertion Recent onset of congestive heart failure	Dsypnea on exertion Orthopnea Tachypnea Palpitations Growth failure	Auscultation Murmur Other findings Signs of heart failure	Diastolic murmur with loud P2 No opening snap or a loud S1	Non specific but may have Right axis deviation Right atrial enlargement Right ventricular hypertrophy	Normal cardiac silhouette Hemodynamic changes similar to mitral stenosis (non specific findings)	Direct visualization of membrane through the atrium +/- visualization of accessory chamber	Normal left ventricular hemodynamic profile with a trans atrial gradient	Types Cor triatriatum sinistrum Cor triatriatum dextrum
Congenital Mitral Stenosis	Respiratory distress shortly after birth Recurrent severe pulmonary infections Other associated congenital cardiovascular anamolies Atrial fibrillation	Infants: Exhaustion and sweating on feeding Rapid breathing Failure to thrive Pulmonary infections Chronic cough Older patients: Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Peripheral edema Fatigue	Auscultation Murmur Other findings Signs of heart failure	Mild-Moderate Loud S1 Loud P2 Low frequency diastolic murmur best heard at the apex Severe Soft S1 Loud pulmonic component of S2 with minimal respiratory splitting of S2 Holodiastolic murmur with presystolic accentuation best heard at the apex Early diastolic murmur of pulmonic valve regurgitation	Sharp P waves in leads I and II Inversion of P wave in lead III Marked Q waves in leads II and III	Left atrial dilation Moderate enlargement of right heart Pulmonary venous congestion Esophageal compression	Reduced valve leaflet mobility Left atrial size Severity of mitral stenosis		Very rare condition
Supravalvular Ring Mitral Stenosis	Other associated congenital heart defects Fatigue Frequent respiratory infections Failure to thrive Poor feeding Precocious congestive heart failure	Shortness of breath Tachypnea Dyspnea Nocturnal cough Heamoptysis Syncope	Auscultation: Lungs: Fine, crepitant rales and rhonchi or wheezes may be present Heart: Murmur	An apical mid diastolic murmur with presystolic accentuation No opening snap The murmur is more prominent if associated with VSD or PDA		Left atrial and ventricular enlargement Alveolar edema	Supramitral ring: Associated with normal mitral valve apparatus Intramitral ring: Hypomobility of the posterior leaflet Reduced interpapillary muscle distance Reduced chordal length Dominant papillary muscle Hypoplastic mitral annulus (Difficult to visualize membrane <1mm in size)	Persistently elevated pulmonary venous pressures Increased pulmonary artery pressure	Types Supramitral Intramitral It is attached between the opening of the atrial appendage and the mitral annulus which helps in differentiating with Cor triatriatum sinister. Intramitral type is associated with shone complex

References

Natural History, Complications & Prognosis

Natural History

Resident Survival Guide

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [23]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [24]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.; Mohammed A. Sbeih, M.D. [25]

Overview

The natural history of mitral regurgitation (MR) may follow one of two patterns, acute or chronic. Chronic MR can be either compensated or decompensated. The natural history and prognosis of MR depend on the underlying etiology and the degree of severity of the valvular abnormality. Mild MR is associated with few if any complications. However, when severe, MR may lead to development of pulmonary edema, pulmonary hypertension, and right heart failure.

Natural History

The natural history of MR may follow one of two patterns, acute or chronic. In acute MR, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature leading to sudden onset of dyspnea, PND, orthopnea and rales. Chronic MR can be either compensated or decompensated. During the chronic compensated phase of MR, compensatory changes in the left ventricle and left atrium maintain the forward cardiac output of the left ventricle, and minimize the signs and symptoms of pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerance. An individual may remain in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation. Once the patient transitions into the decompensated phase, there may not be recovery of left ventricular funtion following operative repair or replacement of the mitral valve. The decompensated stage is defined on the basis of a decompensated ventricular function. At this stage, the patients are at risk for a poor results of valve replacement.

Complications

Mild MR is associated with few if any complications. However, when severe, MR may lead to development of (in alphabetical order):

• Atrial fibrillation
• Cardiogenic Shock
• Endocarditis
• Pulmonary edema
• Pulmonary hypertension
• Right heart failure
• Thromboembolism-Stroke

Prognosis

Patients with asymptomatic chronic severe MR have a high likelihood of developing symptoms or left ventricular dysfunction over the course of 6 to 10 years. The incidence of sudden death in asymptomatic patients with normal left ventricular function varies widely among studies.

The prognosis is poor in patients with severe symptomatic MR with an estimated eight year survival rate of only 33% in the absence of surgical intervention. Heart failure and sudden death due to ventricular arrhythmia are common causes of death.

Among subjects with severe MR due to a flail posterior mitral leaflet, 90% of patients are either dead or require mitral valve surgery by 10 years with a mortality rate of 6% to 7% per year. However, the risk of death is higher in those patients with a left ventricular ejection fraction <60% or with NYHA functional class III–IV symptoms.

Severe symptoms are associated with a poor outcome after mitral valve repair or replacement. Postoperative survival rates in patients with NYHA functional class III–IV symptoms at 5 and 10 years are 73 ± 3% and 48 ± 4% respectively, compared to 5 and 10 years survival rates of 90 ± 2% and 76 ± 5% respectively among patients with NYHA functional class I/II symptoms before surgery.

In a long-term retrospective study, 198 patients with an effective orifice area >40 mm² had a risk of cardiac death of 4% per year during a mean follow-up period of 2.7 years.

Acute MR with cardiogenic shock is associated with an operative mortality of 80%.

References

Complications

Prognosis

Mitral regurgitation prognosis

Diagnosis

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Treatment

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