Mitral Regurgitation

Introduction
Background

Mitral regurgitation (MR) is defined as an abnormal reversal of blood flow from the left ventricle to the left atrium. It is caused by disruption in any part of the mitral valve apparatus, which comprises the mitral annulus, the leaflets (a large anterior [aortic] leaflet and a small posterior [mural] leaflet), the chordae tendineae, and the papillary muscles (anteromedial and posterolateral). The most common etiologies of MR include mitral valve prolapse (MVP), rheumatic heart disease, infective endocarditis, annular calcification, cardiomyopathy and ischemic heart disease. The pathophysiology, clinical manifestations and management of MR differ with the chronicity of the disease and the etiology.
Pathophysiology


MR can be caused by organic disease (eg, rheumatic fever, ruptured chordae tendineae, myxomatous degeneration, leaflet perforation) or a functional abnormality (ie, a normal valve may regurgitate [leak] because of mitral annular dilatation, focal myocardial dysfunction, or both). Congenital MR is rare but is commonly associated with myxomatous mitral valve disease. Alternatively, it can be associated with cleft of the mitral valve, as occurs in persons with Down syndrome, or a ostium primum atrial septal defect.

Acute mitral regurgitation

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

Chronic compensated mitral regurgitation

In chronic compensated MR, the left atrium (LA) and ventricle have sufficient time to dilate and accommodate the regurgitant volume. Thus LA pressure is often normal or only minimally elevated. Because of the left ventricular dilatation via the process of eccentric hypertrophy, TSV and FSV are maintained. Wall stress may be normal to slightly increased as the radius of the LV cavity increases but the end-diastolic LV pressure remains normal. As the LV progressively enlarges, the mitral annulus may stretch and prevent the mitral valve leaflets from coapting properly during systole, thus worsening the MR and LV dilatation.

Chronic decompensated mitral regurgitation

In the chronic decompensated phase, muscle dysfunction has developed, impairing both TSV and FSV (although ejection fraction still may be normal). This results in a higher ESV and EDV, which in turn causes a elevation of LV and LA pressure, ultimately leading to pulmonary edema and, if left untreated, cardiogenic shock.

Frequency
United States

Acute and chronic MR affect approximately 5 in 10,000 people. Mitral valve disease is the second most common valvular lesion, preceded only by aortic stenosis. Myxomatous degeneration has replaced rheumatic heart disease as the leading cause of mitral valvular abnormalities. Mitral valve prolapse has been estimated to be present in 4% of the normal population. With the aid of color Doppler echocardiography, mild MR can be detected in as many as 20% of middle-aged and older adults. MR is independently associated with female sex, lower body mass index, advanced age, renal dysfunction, prior myocardial infarction, prior mitral stenosis, and prior mitral valve prolapse. It is not related to dyslipidemia or diabetes.
International

In areas other than the Western world, rheumatic heart disease is the leading cause of MR.
Clinical
History


Acute mitral regurgitation


When associated with coronary artery disease and acute myocardial infarction (typically, inferior myocardial infarction, which may lead to papillary muscle dysfunction), significant acute mitral regurgitation (MR) is accompanied by symptoms of impaired LV function, such as dyspnea, fatigue, and orthopnea. In these cases, pulmonary edema is often the initial manifestation because of rapid volume overload on the left atrium and the pulmonary venous system.


Chronic mitral regurgitation
Often results from a primary defect of the mitral valve apparatus with subsequent progressive enlargement of the left atrium and ventricle. In this state, patients may remain asymptomatic for years.
Patients may have normal exercise tolerance until systolic dysfunction of the LV develops, at which point they may experience symptoms of a reduced forward cardiac output (ie, fatigue, dyspnea on exertion, or shortness of breath).
With time, patients may feel chest palpitations if atrial fibrillation develops as a result of chronic atrial dilatation. For related information, see Medscape's Atrial Fibrillation Resource Center.
Patients with LV enlargement and more severe disease eventually progress to symptomatic congestive heart failure with pulmonary congestion and edema. At this stage of LV dilatation, the myocardial dysfunction often becomes irreversible. For related information, see Medscape's Heart Failure Resource Center.

Physical

Palpation

Brisk carotid upstroke and hyperdynamic cardiac impulse
Prominent LV filling wave may be present

Auscultation
S 1 may be diminished in acute MR and chronic severe MR with defective valve leaflets.
Wide splitting of S 2 may occur due to early closure of the aortic valve.
S 3 may be present due to LV dysfunction or as a result of increased blood flow across the mitral valve.
P 2 may be accentuated if pulmonary hypertension is present.
Murmur
Quality
Usually high-pitched, blowing
Location
Usually best heard over the apex
Usually radiates to the left axilla or subscapular region
Posterior leaflet dysfunction causes murmur to radiate to the sternum or aortic area
Anterior leaflet dysfunction causes murmur to radiate to the back or top of the head
Duration
Usually holosystolic
May be confined to early systole in acute MR
May be confined to late systole in MVP or papillary muscle dysfunction
S 1 will probably be normal in these cases since initial closure of mitral valve cusps is unimpeded.
A midsystolic click preceding murmur is suggestive of MVP.
Intensity
Little correlation exists between intensity of murmur and severity of MR.
Intensity may be diminished in severe MR caused by LV dysfunction, acute myocardial infarction, or periprosthetic valve regurgitation.

Causes

Acute mitral regurgitation

Coronary artery disease (ischemia or acute myocardial infarction)
Papillary muscle dysfunction
The posteromedial papillary muscle is supplied by the terminal branch of the posterior descending artery and is more vulnerable to ischemic insult than the anterolateral papillary muscle, which is usually supplied by both the left anterior descending and circumflex arteries.
Transient ischemia may result in transient MR associated with angina.
Myocardial infarction or severe prolonged ischemia produces irreversible papillary muscle dysfunction and scarring.
Chordae tendineae dysfunction or rupture
Infectious endocarditis
Abscess formation
Vegetations
Rupture of chordae tendineae
Leaflet perforation
Status post valvular surgery
Trauma
Percutaneous valvuloplasty
Suture interruption
Tumors (most commonly atrial myxoma)
Myxomatous degeneration
Mitral valve prolapse
Ehlers-Danlos syndrome
Marfan syndrome
Systemic lupus erythematosus (Libman-Sacks lesion)
Acute rheumatic fever (Carey Coombs murmur)
Acute global left ventricular dysfunction
Prosthetic mitral valve dysfunction

Chronic mitral regurgitation
Rheumatic heart disease
Systemic lupus erythematosus
Scleroderma
Myxomatous degeneration
Mitral valve prolapse
Ehlers-Danlos syndrome
Marfan syndrome
Calcification of mitral valve annulus
Infective endocarditis (can affect normal, abnormal, or prosthetic mitral valves)
Ruptured chordae tendineae
Trauma
Mitral valve prolapse
Endocarditis
Spontaneous
Rupture or dysfunction of papillary muscles
Coronary artery disease (see causes for acute MR)
Dilation of mitral valve annulus and/or left ventricular cavity (functional MR)
Dilated cardiomyopathies
Aneurysmal dilation of the left ventricle
Hypertrophic cardiomyopathy
Perivalvular prosthetic leak
Congenital
Mitral valve clefts
Mitral valve fenestrations
Parachute mitral valve abnormality
Drug-related
Ergotamine, methysergide, pergolide, anorexiant medications

http://emedicine.medscape.com/article/155618-overview