Wednesday, January 18, 2012

Mitral regurgitation


Mitral regurgitation (MR) refers to the backward flow of blood from the left ventricle (LV) to the left atrium (LA), across the mitral valve (MV), during systole, due to inadequate mitral valve closure. MR may be acute or chronic.


The prevalence of chronic MR varies inversely with its severity:
  • Trivial (Physiologic) MR: is detectable with sensitive Doppler techniques in up to 70% of healthy adults.
  • Mild MR: is found in about 19% of the population.
  • Moderate MR: in about 1.9 % of the population.
  • Severe MR: in about 0.2 % of the population.
Etiology and pathology of chronic MR:

MR can arise from abnormalities of any part of the mitral valve apparatus and other structures, including;
  • MV leaflets.
  • MV annulus.
  • MV chordae tendineae.
  • MV papillary muscles.
  • LA wall.
  • LV myocardium adjacent to the papillary muscles.

The mitral valve.

The mitral valve has two papillary muscles: The anterolateral papillary muscle originates from the anterolateral LV wall and provides chordae to the anterolateral half of anterior and posterior mitral leaflets. The posteromedial papillary muscle originates from the posterior LV wall and provides chordae to the posteromedial half of both leaflets.

Mitral regurgitation may be due to:
  • A primary abnormality of the valve apparatus; or
  • Secondary to another cardiac disease.
Primary causes of chronic MR include:
  • Mitral valve prolapse.
  • Rheumatic heart disease.
  • Drugs.
  • Congenital MR.
Mitral valve prolapse (MVP) is the most common cause in developed countries.

Rheumatic heart disease is uncommon in developed countries but still common in the rest of the world.
Whether rheumatic mitral affection causes mitral stenosis (MS) or mitral regurgitation (MR) depends on physical orientation of the leaflets.

Rheumatic MR is characterized by:
  • Commissural fusion due to fibrosis & calcification.
  • Leaflet contracture.
  • Valve distortion & loss of normal coaptation of the leaflets, due to:
    • Fibrosis
    • Calcification; which extends from one leaflet to the other.
    • Secondary distortion caused by progressive LA & LV dilatation, which restricts posterior leaflet motion, dilates the mitral annulus & aggravates MR. In this manner, MR begets MR.

Drugs: prolonged use of certain drugs may result in MR e.g. the anorectic drugs: Ergotamine, Pergolide, and Cabergoline.

Congenital primary MR may be due, for example, to a valve cleft.

Secondary (functional) causes of MR include:
  • Ischemic heart disease.
  • Cardiomyopathies.
  • Collagen diseases.
  • Mitral annular calcification.
  • Congenital MR.

Ischemic heart disease:
Myocardial ischemia or infarction can cause MR by:
  • LV dilatation, with dilatation of the mitral ring.
  • Papillary muscle dysfunction, usually associated with infarction of the adjacent LV wall. Asynergic contraction of the infarct area adds to mitral leaflet distortion & MR.

Cardiomyopathies (CM):
  • Idiopathic dilated CM: MR results from:
    • Mitral annular dilatation.
    • Distortion of the orientation of the leaflets, chordae & papillary muscles.
  • Endocardial fibroelastosis: similar to dilated CM.
  • Hypertrophic CM: MR is probably caused by systolic anterior motion (SAM) of the anterior mitral leaflet, which occurs in this disease.

Collagen diseases:
Collagen diseases produce MR by restraint of the leaflets & chordae tendineae; Such as:
  • Marfan’s syndrome.
  • Ehlers Danlos syndrome.
  • Pseudo xanthoma elasticum.
  • Systemic lupus erythematosus.
  • Loffler’s endomyocardial fibrosis.
  • Osteogenesis imperfecta.
  • Scleroderma.

Mitral annular calcification:
Mitral annular calcification does not usually cause valve dysfunction, but MR may result from adhesion of the posterior leaflet to the calcific area.

Congenital MR:
Congenital MR can result from:
  • Primary mitral valve anomalies:
    • Clefts of the mitral leaflets.
    • Fenestrations.
    • Double orifice.
    • Absence of leaflets tissue.
    • Malformations of chordae & papillary muscles.
  • MR associated with other congenital heart diseases such as:
    • A–V canal defects.
    • Corrected transposition of the great arteries (TGA): In this case the left-sided tricuspid valve frequently shows Ebstein’s anomaly and is regurgitant.
    • MR may be part of the congenital polyvalvular disease.
    • Coarctation of the aorta.
    • Aortic stenosis (AS).
    • Anomalous left coronary artery from the pulmonary artery.
    • Endocardial fibroelastosis.
  • MR associated with congenital systemic diseases: e.g. Mucopolysaccharidosis.

Other causes of chronic MR:
  • Hypereosinophilic syndrome.
  • Carcinoid disease.
  • Tumors, e.g. LA myxoma.
  • Infiltrative diseases, e.g. amyloidosis, sarcoidosis.
  • Paravalvular prosthetic leak.

Causes of acute MR:
The following conditions produce acute MR by chordal and/or papillary muscle rupture, or by erosion, destruction & perforation of the leaflets:
  • Mitral valve prolapse.
  • Acute myocardial infarction.
  • Infective endocarditis.
  • Trauma.

In view of this huge list of causes of acute and chronic MR; it is really astonishing that MR does not occur more frequently than it is actually present.


Chronic MR pathophysiology:

Chronic MR creates left ventricular volume overload, with progressive LV dilatation. The dilated LV is well compliant & suited to deliver a larger stroke volume.

LV dilatation accommodates the increased end-diastolic volume trying to keep the end-diastolic pressure within normal.

According to Laplace priciple; LV wall stress = PR/2H, where P: pressure, R: radius, and H: wall thickness.
In chronic MR; LV pressure is kept normal in the compensated stage, with some increase in radius, thus wall stress incraeses, but not markedy. 

The backward flow of blood, from LV into the low-pressure LA, reduces LV afterload, since the low-pressure LA offers an easy runoff to LV, much easier than the forward flow into the much higher-pressure aorta. Thus LV systolic function looks better than it actually is, and the measured LV ejection fraction (EF) in these patients is actually over-estimated.

The regurgitant volume is determined by:
  • Regurgitant orifice area.
  • The systolic pressure gradient across the mitral valve.
  • The duration of systole.

MR increases with bigger regurgitant orifice area, higher systolic gradient, and/or longer duration of systole, and vice versa.

With progressive increase in the regurgitant volume & LV dilatation, the Frank-Starling mechanism is overcome, and LV systolic dysfunction starts, with progressive decline in EF.

When the end-diastolic dimension is ≥70 mm, the end-systolic dimension is ≥40 mm, and/or the EF is ≤0.6, systolic dysfunction is already significant, and mitral valve surgery is indicated, even if there are no symptoms related to the valve disease, to avoid the transition into an irreversible state.

Acute MR pathophysiology:

Acute MR creates:
  • Acute pressure overload on the LA & the pulmonary circulation; which often leads to acute pulmonary edema.
  • Acute volume overload on the LV; and the left ventricular end diastolic volume (LVEDV) increases due to the increased preload created by the regurgitant volume.

As in chronic MR; LV contraction is augmented due to myocardial stretch (Frank-Starling mechanism). Meanwhile; the rapid run off of blood into the LA reduces LV afterload. Stronger contraction and reduced afterload result in increased stroke volume, thus reducing the left ventricular end systolic volume (LVESV). The result is an increase of LV ejection fraction.

Because of the decrease in LV systolic volume (radius) & pressure, the systolic wall stress is actually reduced in acute MR.

Clinical manifestations of chronic MR:


Patients with isolated chronic mild, moderate, or even severe MR are asymptomatic until there is LV failure, pulmonary hypertension, or the onset of atrial fibrillation (AF).

In patients with rheumatic MR, symptoms may not appear except two decades after the initial attack of rheumatic carditis.

In the natural history of MR, the first symptoms to appear are usually those due to low cardiac output; particularly easy fatigue, due to backward flow of blood to the extent of reducing forward aortic flow.

Next are pulmonary congestive manifestations, due to LV systolic failure; with dyspnea, orthopnea and paroxysmal nocturnal dyspnea. At this stage, myocardial dysfunction might have become already irreversible due to the long standing MR.

In exceptional cases, irreversible LV systolic dysfunction occurs in the absence of symptoms. Thus; some of the asymptomatic patients with chronic MR will really need mitral valve surgery, when one or more of the indices of significant LV systolic dysfunction mentioned above are fulfilled. This fact clearly illustrates the crucial need for clinical & echocardiographic regular follow up of all patients with MR.

Other symptoms include: thromboembolism, hemoptysis, and right-sided heart failure, but these symptoms are less common than in MS.

There is a high risk for infective endocarditis, with its clinical manifestations & complications, in patients with moderate to severe MR.

Symptoms related to the etiology of MR may be present, e.g. symptoms of ischemic heart disease (IHD), MVP …etc.

Physical examination:

Arterial pulse is usually brisk in upstroke, when the ejection fraction is normal, and usually falls-off rapidly, giving the impression of bounding pulse, but the pulse volume is usually normal.

Sings of LV dilatation & volume overload: with hyperdynamic apical impulse that is displaced outward & downward.

A systolic expansion impulse along the lower left sternal border may be palpable, due to excess filling of the enlarged LA, which pushes the heart anteriorly.

Systolic thrill at the apex is usually detected in patients with significant MR.

Diminished intensity of the first heart sound (S1); reflecting failure of the mitral leaflets to close properly. When the initial mitral valve closure is uninterrupted, S1 intensity is often normal; as occurs in MR secondary to MVP or papillary muscle dysfunction.

Wide splitting of the second heart sound (S2) may occur, due to shortened LV ejection time & early aortic component (A2).

If pulmonary artery hypertension is present, the pulmonary component of the second heart sound (P2) will be accentuated and delayed, thus further widening the splitting of S2.

Third heart sound (S3) is present in hemodynamically significant MR, due to an augmented flow rate across the mitral valve orifice into a dilated left ventricle.

If S3 is accompanied by a harsh systolic murmur; LV systolic function is usually preserved. On the other hand, an S3 accompanied by a soft systolic murmur usually indicates depressed LV systolic function.

Fourth heart sound (S4) is rare, unless there is associated IHD with high left ventricular end diastolic pressure (LVEDP).

Mid systolic click may be heard if MR is due to MVP.

MR specific murmur;
  • In most cases, the murmur is pan systolic high-pitched and blowing, best heard at the apex, and radiated to the left axilla.
  • It may be only mid-to-late systolic when MR is due to MVP or papillary muscle dysfunction.
  • It may radiate to the back when very loud, or if the anterior leaflet is predominantly affected. 
  • It may radiate anteriorly to the sternum when the posterior leaflet is predominantly affected. In these cases it may be heard well at the cardiac base, and could be confused with the murmur of aortic stenosis (AS), but it does not radiate to the carotid arteries.
  • Late systolic accentuation of the murmur may be found in cases with MVP or IHD with papillary muscle dysfunction.
  • In most patients with primary MR; there is good correlation between the loudness of the murmur & the severity of MR, but this correlation is weak in patients with functional MR.
  • Usually there is little variation of the murmur of MR with respiration.

Mid-diastolic apical rumble may be heard if MR is significant, due to excess flow across the mitral valve (Relative stenosis).

Signs of right-sided congestive heart failure will be detected in long standing severe cases with CHF and pulmonary hypertension.

Dynamic auscultation in patients with chronic MR:

Dynamic auscultation is not usually used nowadays in clinical practice, because its interpretation is often difficult and may not be reproducible, and these maneuvers have rarely been validated. The best tool for evaluation of cardiac murmurs is echocardiography.

The murmur of MR may become louder with:
  • Increased preload with increased LV volume, as occurs in:
    • leg raising.
    • lying down.
  • Increased afterload, as occurs in:
    • Squatting.
    • Isometric hand grip.
    • Phenylephrine infusion.

On the other hand, there is a decrease in intensity of the murmur with:
  • Reduced preload, as occurs in:
    • Standing.
    • Valsalva maneuver.
  • Reduced afterload, as occurs in:
    • Amyl nitrate inhalation.

In patients with MVP; the disparity between the redundant mitral valve and the mitral annulus increases with smaller LV volume, thus aggravating MVP & MR. On the other hand; this disparity decreases with larger LV volume.

Thus; decreased preload or afterload, with decreased LV volume, may produce earlier systolic click, and longer but still fainter systolic murmur. On the other hand; increased preload or afterload may cause a delayed systolic click and shorter murmur, but its intensity is often louder.

Clinical manifestations of acute MR:

Acute MR almost always presents with acute heart failure & acute pulmonary edema.
Exceptionally; the acute phase may be well tolerated, with gradual transition into a sub-acute followed by a chronic state.
Normal heart size is usually found in the acute phase.
The systolic thrill may radiate to the base of the heart in presence of posterior leaflet prolapse.
The systolic murmur of MR is usually heard only in early & mid systole, because in late systole the regurgitant V-Wave in LA peaks rapidly & reduces the systolic gradient between LV & LA, thus reducing MR, and the murmur disappears. The murmur may radiate widely, to the axilla, back of the neck, and sacrum.
S3 & S4 are common.

Electrocardiogram in patients with chronic MR:

One or more of the following may be found:
  • LA enlargement similar to that seen in mitral stenosis.
  • LV hypertrophy.
  • RV hypertrophy, in late cases with pulmonary arterial hypertension.
  • Arrhythmia; e.g. AF.
  • Changes related to the etiology of MR, e.g. ischemia and/or infarction pattern in cases of IHD, loss of precordial R-waves in infiltrative cardiomyopathy, and non-specific ST-T changes in MVP.

Chest x-ray:

One or more of the following may be present:
  • Cardiomegaly; with LV configuration. LV size, however, does not correlate with the degree of MR.
  • LA enlargement. Again; LA size, however, does not correlate with the elevation of LA pressure.
  • RA & RV enlargement, with dilated central pulmonary arteries; in the presence of pulmonary hypertension.
  • Pulmonary congestion; in the presence of congestive heart failure (CHF).
  • Pulmonary edema with normal heart size is the usual finding in patients with acute MR.
  • Mitral annular calcification may be detected.
  • Thoracic cage abnormalities may be seen in patients with MVP.
Acute pulmonary edema in a 28-year-old woman with previously undiagnosed combined mitral stenosis and regurgitation who had just given birth to a full-term neonate. Frontal chest radiograph shows massive pulmonary edema with a bias for the perihilar and lower lung regions. The cardiac silhouette is moderately enlarged. Dilation of the main and central pulmonary arteries and cephalization of pulmonary vascular flow are evident. Note the splaying of the angle of tracheal bifurcation, a finding that is indicative of marked left atrial enlargement (arrow).
LA (black arrow) & LV (red arrow) enlargement, with hilar congestion.


Echocardiography is essential for establishing:
  • The diagnosis of the presence of MR.
  • Severity of MR.
  • Etiology of MR.
  • LA size, and exclusion of LA thrombus.
  • LV size and systolic function.
  • Pulmonary artery pressures.

Trans-Esophageal Echocardiography (TEE) is recommended if Trans-Thoracic Echocardiography (TTE) image quality is suboptimal.

Echocardiographic assessment of the severity of MR:

Accurate estimation of the severity of MR is of prime importance; since surgery is indicated only for severe MR.

Doppler and color flow Doppler can be used to evaluate the severity of MR, by measuring and calculating:
  • Vena contracta: the narrowest segment of the jet on color flow imaging.
  • Regurgitant volume.
  • Regurgitant fraction.
  • Regurgitant orifice area.
The following findings are consistent with severe MR, in the average-size adult patient:
  • Vena contracta width ≥0.7 cm.
  • Regurgitant orifice area ≥0.40 cm2.
  • Regurgitant volume ≥60 ml.
  • Regurgitant fraction ≥50%.
  • Regurgitant jet area >40% of LA area.
  • Systolic reversal of flow in a pulmonary vein.

These values are based on an average adult size and may need to be adjusted for body size in small or large patients. Unfortunately, however, there is no specific formula for this adjustment.

In the presence of more than one of these findings, severe MR is diagnosed with more certainty.

Although severe chronic MR may be asymptomatic, it is almost always associated with a clear evidence of LA and/or LV enlargement.

Parasternal short axis (SAX) view: showing the mitral valve ring and leaflets; with its fish-mouth appearance while opened.

In parasternal long axis view the jet can be either directed toward or away from the probe, then its color can be yellow-red (toward the probe) or green-blue (away from the probe).
In apical 4 or 2 chamber views, MR will appear as a blue-green systolic jet going away from the probe.
Apical four chamber view showing LV (left ventricle), RV (right ventricle), RA (right atrium), LA (left atrium) and AML (anterior mitral leaflet) with a small mitral regurgitation (MR) jet into LA. MR jet is seen as a mosaic (multi colour) area within the left atrium within the color flow mapping. Mosaic color is due to aliasing as the MR jet velocity is much above the aliasing velocity of the system. Severity of the mitral regurgitation can be assessed by the extent to which the jet extends into the left atrium. Other measures are the area of the jet, especially in comparison with the area of the left atrium. The larger the ratio, the more severe the mitral regurgitation. AML is seen in the closed position between the LA and LV indicating that it is a systolic frame.
Echocardiographic image in parasternal long axis (PLAX) view illustrating a combination of mitral stenosis and regurgitation. Right half shows the two dimensional image while the left half shows superimposed colour Doppler (color flow mapping) image. The bluish mosaic coloured jet within the Doppler sample volume is suggestive of mild mitral regurgitation. RV: right ventricle; LV: left ventricle; Ao: aorta; LV: left ventricle; LA: left atrium; AML: anterior mitral leaflet; PML: posterior mitral leaflet. The left atrium is dilated, when compared to the aorta, both of which are usually of equal size in this view in normals. Left ventricular size is normal. The anterior mitral leaflet is seen doming into the left ventricle in diastole. The posterior mitral leaflet is pulled along with it due to commissural fusion, causing the paradoxical anterior motion in diastole. Normally the anterior leaflet moves anteriorly and posterior leaflet moves posteriorly while opening in ventricular diastole, allowing free flow of blood from the left atrium to the left ventricle. Both doming of the anterior mitral leaflet and paradoxical anterior motion of the posterior mitral leaflet are characteristic echocardiographic features of rheumatic mitral stenosis.
Baseline transthoracic echocardiography showing a moderate organic mitral regurgitation due to the previous thoracic radiotherapy. (A) Parasternal long-axis view showing the thickening of aorto-mitral aponevrosis highly suggestive of radiation-associated valvular disease. (B) Four-chamber view showing a moderate mitral regurgitation using Colour Doppler. (C) Vena contracta was 4.5 mm. (D) Flow convergence of the regurgitant jet: the effective regurgitant orifice was 0.17 cm2 and the regurgitant volume 37 ml.

Magnetic Resonance Imaging (MRI):

MRI may be useful in selected patients with MR, if echocardiographic imaging is inadequate, or there is a discrepancy between clinical findings and echocardiography.
MRI enables accurate quantitation of LV volumes and ejection fraction.

MRI quantitation of the severity of MR:
  • Calculation of the difference between LV stroke volume and ascending aortic forward flow.
  • Planimetry of the regurgitant orifice.

Cardiac catheterization:

Nowadays; cardiac catheterization is no more needed in most patients with chronic MR.

Indications for cardiac catheterization in MR:
  • For definition of coronary anatomy:
    • Patients >40 years of age.
    • Patients with angina pectoris.
    • Patients with major cardiovascular risk factors, namely: diabetes mellitus, hypertension, Dyslipidemia and smoking.
  • If echocardiographic imaging is inadequate, or there is a discrepancy between clinical findings and echocardiography.
  • Other associated cardiac disease that indicates the need for cardiac catheterization.
  • Patients with acute MR in whom the etiology of MR cannot be accurately defined by non-invasive tests.
  • In infants & children with complex congenital anomaly associated with MR.

Quantitation of the severity of MR by cardiac catheterization:
  • Grade I/IV: When the dye is injected into the LV, the LA partially opacifies & completely clears with each cardiac cycle.
  • Grade II/IV: When the dye is injected into the LV, the LA completely opacifies after several cardiac cycles, but never attains the same opacity like the LV.
  • Grade III/IV: When the dye is injected into the LV, the LA completely opacifies after several cardiac cycles, and attains the same opacity like the LV.
  • Grade IV/IV: When the dye is injected into the LV, the LA completely opacifies within one cardiac cycle attaining the same opacity like the LV.

Management of chronic mitral regurgitation:

Medical management:
  • Vasodilators in asymptomatic patients with moderate-to-severe MR, e.g. angiotensin converting enzyme (ACE) inhibitors, are controversial, but may help delay the need for surgery, by reducing the afterload, thus encouraging forward flow into the aorta & reducing backward regurgitation into the left atrium.
  • Symptomatic heart failure patients need treatment with ACE inhibitors, diuretics, β-blockers, digitalis…etc.
  • Treatment of arrhythmia, accordingly.
  • Antibiotic prophylaxis against infective endocarditis whenever indicated.

Indications for surgery:
  • Symptomatic patients with congestive heart failure (NYHA class II, III or IV) with an ejection fraction >30%.
    • When the EF is ≤30%, LV systolic dysfunction is already irreversible and the surgical mortality is unacceptable.
  • Asymptomatic patients with:
    • LV Ejection fraction ≤60 %.
    • LV end systolic dimension ≥40 mm.
    • Pulmonary artery systolic pressure ≥50 mmHg.

Surgical procedures:
  • Mitral valve repair is the procedure of choice, whenever possible.
  • When valve repair is not possible; mitral valve replacement is done.

Percutaneous procedures:

The following percutaneous procedures might help:
  • Coronary sinus ring; to push the mitral annulus anteriorly and reduce MR.
  • Mitral valve clip; fastening the middle scallops of both mitral leaflets, thus creating a double-orifice mitral valve and reducing MR.
  • Cardiac Re-synchronization Therapy may help in patients with severe congestive heart failure (NYHA class III or IV) despite optimal medical therapy, who have a wide QRS complex >120 msec.

Management of acute MR:

Acute MR is usually a medical emergency. Most patients need urgent surgery with either mitral valve repair or replacement as the case implies.

Intravenous vasodilator therapy with sodium nitrprusside is often needed to control acute pulmonary edema.

Intraaortic balloon couterpulsation is needed in many patients for heomynamic support, as well as intrvenous inotropic support, to tide the ptient over until surgery is carried out as early as possible.

Some patients with hypoxic respiratory failure may require mechnical ventilation.

The indications for cardiac catheterization are the same as in chronic MR.

If cardiac catheterization is indicated, the patient may be taken to the catheterization laboratory with the intraaortic balloon in place and the ventilator connected, and transferred directley from there to the operting room.


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