Mitral regurgitation


Most common type of heart valve insufficiency.

Mitral regurgitation is the most common valvular heart disease,affecting 2-3% of the population.

It is the most common cause of moderate-severe valvular heart disease among adults older than 55 years of age.
MR is functional in 2/3 of cases, with structurally normal valve leaflets, and regurgitation due to valve deformation caused by atrial or ventricular remodeling.
In the remaining third of cases, it is organic with structural abnormal valve, causing the regurgitation.

And individuals older than 65 years old the prevalence of moderate-severe mitral regurgitation detected on transthoracic echocardiography is 2.3%.

Its prevalence increases to about 10% in individual 75 years of age or older.

An older increasing severity of MR is associated with cardiovascular morbidity and mortality.

Even mild MR portends nearly two fold higher risk of all cause mortality compared with those without MR.

MR derives from an anatomical functional impairment of one or more components of the mitral apparatus that are necessary for normal valve function including: the left ventricle, papillary muscles, chordae tendineae, leaflets, and annulus.

The two major categories of mitral regurgitation are primary, or degenerative MR, which is most commonly caused by leaflet prolapse or flail, and secondary, or functional, MR.

Primary MR is a disease of the valve, or chordae, and secondary MR is a disease of the left ventricle or left atrium.

Its most frequent etiology is degenerating mitral valve disease leading to mitral prolapse.

Other studies suggest secondary mitral regurgitation is seen in 65% of cases, of which 60% were attributed to lieft ventricular remodeling or dysfunction and the remainder due to atrial fibrillation or flutter or idiopathic annular  dilatation.

Either from primary valve disease (degenerative) or secondary (functional) to left ventricular dysfunction, affects more than 4 million Americans, or almost one in ten people over age 75 years.

Patients affected by moderate or severe MR are generally diagnosed by echocardiography in their late 60s, most often with no or minimal symptoms.

Despite benign presentation degenerative mitral regurgitation causes mortality in excess of that expected for age and sex, with severe complications such as heart failure, atrial fibrillation, pulmonary, hypertension, or left ventricular dysfunction.

Excess mortality affects patients without these complications, proportionally to the severity of regurgitation, and to the left atrial enlargement, resulting from degenerative mitral regurgitation.

Degenerative pathology, affects the mitral valve apparatus, and is the most frequent reason for isolated mitral valve surgery.

Surgical mitral valve repair rather than  a replacement has increased survival, better preservation of left ventricular function, and reduced risk of thromboembolic events and endocarditis.

When surgical repair is performed before the occurrence of symptoms or ventricular dysfunction, life expectancy is restored, and outcomes are better than watchful, waiting.

Secondary mitral regurgitation varies is a function of left ventricular loading, heart rhythm, conduction disease, and myocardial ischemia.
Ischemic mitral regurgitation is a secondary type of mitral regurgitation that occurs after myocardial infarction.
There are high risk of illness and death from cardiovascular disease among patients with symptomatic heart failure, reduce left ventricular systolic function and moderate or greater degree of ischemic mitral regurgitation.
Secondary mitral regurgitation is associated with a lower survival than primary mitral regurgitation of a similar magnitude.
Adverse outcomes with secondary mitral regurgitation can occur with smaller regurgitant in volumes than observed with primary mitral regurgitation.
Recognition of secondary mitral regurgitation begins with the detection of the characteristic systolic murmur in the context of the patient’s history, symptoms and evidence of underlying cardiac disease.
Mitral regurgitation is categorized on the basis of normal, excessive, or restrictive leaflet mobility.
Mitral regurgitation is attributable to restricted mitral valve leaflet motion during systole in Patients  with an ischemic or nonischemic dilated cardiomyopathy.
With ischemic mitral regurgitation, the mitral valve leaflets are thickened and fibrotic with reduced lengthening.
Mitral regurgitation  occurs most often as a consequence of adverse left ventricular remodeling with papillary muscle displacement, leaflet tethering, reduced mitral valve closing forces, annular dilation , and failure of leaflet coaptation..
With atrial functional mitral regurgitation, mitral valve leaflet motion is normal and mitral regurgitation is due to left atrium and annular enlargement with insufficient leaflet lengthening, as occurs in some patients with chronic persistent atrial fibrillation.
In secondary mitral regurgitation measurements of quantitative assessment is difficult because of geometric assumptions and technical challenges and the effective regurgitant regurgitant orifice area varies among cardiology experts: from 0.2 cm² to .4 centimeters squared and from30-60 mL regurgitant volume.

Prevalence is age-dependent, with greater than 6% of those aged greater than 65 years affected.

Primary mitral regurgitation occurs when there are intrinsic abnormalities of the mitral valve apparatus.

Most common cause of primary mitral regurgitation is degenerative mitral valve disease in which there is myxomatous degeneration of the mitral valve leaflets, and elongation and redundance in chordal apparatus.

Other causes of primary mitral stenosis include: rheumatic disease, drug-induced mitral disease, healed infective endocarditis, and mitral regurgitation associated with systemic illness.

In secondary mitral regurgitation, regional or global left ventricular dysfunction leads to enlargement of the left ventricular chamber and mitral annulus, apical and lateral migration of the papillary muscles, leaflet tethering, and reduced closing forces of the mitral valve.

In secondary mitral regurgitation the mitral valve leaflets and chordate are structurally normal, and the regurgitation results from alterations in left ventricular geometry and function.

In secondary mitral regurgitation the valve leaflets are normal but unable to coapt completely owing to distortion of the supporting apparatus resulting from ischemic or dilated cardiomyopathy.

Severe secondary mitral insufficiency is a predictor of poor clinical outcomes in patients with heart failure and reduce left ventricular ejection fraction.

Ischemic mitral regurgitation is a subset of secondary mitral regurgitation caused by coronary artery disease that may be acute such as with papillary muscle ischemia or rupture, or may be chronic as occurs after myocardial infarction.

In patients with coronary artery disease, moderate severe chronic ischemic mitral regurgitation affects approximately 12% of individuals.

Some degree of mitral regurgitation is found in almost 20% of men and women over the age of 55 years by echocardiogram examination.

Two dimensional and Doppler echocardiography are the major tools to assess patients presenting with mitral regurgitation.

Two dimensional and Doppler echocardiography can establish feasibility of the valve repair by analyzing the morphology and the pathoanatomic abnormalities of the valve.

A progressive process.

It has an incidence of approximately 2% of the population.

Ischemic mitral regurgitation effects 1.6-2,800,000 patients in US.

Affects males and females equally.

The mitral valve is present between the two chambers of the left heart, and mittral regurgitation occurs when the mitral valve does not close properly.

Impaired mitral valve closure causes blood to flow backward, leak, into the upper heart chamber when the left lower heart chamber contracts.

Thickened redundant leaflets will prolapse back into the left atrium causing malcoaptation of leaflet edges and subsequent regurgitation.

Ruptured of chordal structures is not uncommon in patients with mitral regurgitation, especially in older men, which cause a further increase in the severity of mitral regurgitation because of unsupported segments of the mitral valve leaflets.

Regurgitation refers to leaking from a valve that does not close all the way.

Diseases that weaken or damage the valve or the heart tissue around the valve cause mitral regurgitation.

Patients with severe primary with mitral regurgitation have an excess mortality rate of 6.3% per year compared with the expected survival rate.

Severe primary mitral regurgitation is associated with a high morbidity and 10 year history incidence of atrial fibrillation of 30% and heart failure 36-63%.

90% of patients with severe mitral regurgitation will have died or undergone surgical repair because of mitral regurgitation symptoms in 10 years of follow up.

Sudden death may occur with severe mitral regurgitation and is responsible for about 25% of deaths in patients on medical therapy.

May lead to congestive heart failure.

Ischemic MR is a consequence of adverse ventricular remodeling after myocardial infarction.

Ischemic MR associated with enlargement of the left ventricular chamber and mitral annulus, apical and lateral migration of papillary muscles and leaflet tethering, and reduced closing forces.

The above changes lead to malcoadaptation of leaflets and variable degrees of mitral regurgitation that fluctuates as a function of volume status, heart rhythm, afterload, and ischemia.

In ischemic mitral regurgitation valve leaflets are normal, and the disease occurs in the myocardium rather than in the valve itself.

The treatment functional ischemic mitral regurgitation is therefore different from primary degenerative mitral regurgitation.

MR places a volume load on heart with increased preload and reduces afterload.

Associated with enlarged LV and an increased ejecion fraction.

With time the stress of left ventricular volume overload weakens it, and ejection fraction drops and end systolic volume rises.

May begin acutely with myocardial infarction.

Persistent regurgitation can become a chronic process.

Commonly caused by mitral valve prolapse, although in most cases patients do not develop severe mitral regurgitation.

One out of three cases of chronic mitral regurgitation are caused by rheumatic heart disease.

Congenital mitral regurgitation is most often part of a more complex heart defect or syndrome.

Common causes include: Coronary artery disease, myocardial infarction, endocarditis, cardiac tumors, hypertension, and Marfan’s syndrome.

The mitral valve is composed of two valve leaflets, the mitral valve annulus, a ring around the valve leaflets, the papillary muscles which tether the valve leaflets to the left ventricle thereby preventing them from prolapsing into the left atrium, and the chordae tendineae, which connect the valve leaflets to the papillary muscles.

Any part of the mitral valve apparatus can cause mitral regurgitation.

The most common cause of mitral regurgitation is mitral valve prolapse (MVP), which is caused by myxomatous degeneration.

About 50% of primary cases of mitral regurgitation related to myxomatous degeneration of the valve, which is more common in women and increases with age.

Myxomatous degeneration causes stretching of the valve leaflets and the chordae tendineae and such elongation of these structures prevent the valve leaflets from fully coapting when the valve is closed, causing the valve leaflets to prolapse into the left atrium, thereby causing mitral regurgitation.

Ischemic heart disease can cause dysfunction of the papillary muscles, and dilatation of the left ventricle, with displacement of the papillary muscles and the dilatation of the mitral valve annulus.

Other causes of MR include Marfan’s syndrome and rheumatic failure.

Dilatation of the left ventricle can cause secondary MR by causing stretching of the mitral valve annulus and displacement of the papillary muscles.

Dilatation of the left ventricle can be due to any cause of dilated cardiomyopathy, including aortic insufficiency and nonischemic dilated cardiomyopathy.

Functional mitral regurgitation, because the papillary muscles, chordae, and valve leaflets are usually normal.

Acute onet of mitral regurgitation is most often caused by endocarditis.

Papillary muscle rupture or dysfunction are also common causes in acute cases.

The clinical course has three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase.

A diagnosis of severe MR is made if 50% of the total stroke volume is diverted to regurgitation flow.

Acute presentation with sudden volume overload of the left atrium and ventricle may be related due to the sudden rupture of a chorda tendinea or papillary muscle: this results in an increase in the stroke volume of the left ventricle-made up of forward stroke volume and regurgitant flow.

In asymptomatic patients with severe mitral regurgitation watchful waiting is a reasonable strategy if meticulous regular follow up for symptoms and change and left ventricular performance are performed.

Most patients with severe and chronic primary mitral regurgitation are asymptomatic and remain so for many years due to a compensated ventricular dilation.

Symptoms of dyspnea on exertion, and exercise intolerance slowly develop as compensatory mechanisms are overwhelmed by volume overload and reversible left ventricular dysfunction.

Application of therapy in patients with mitral regurgitation before the onset of left ventricular dysfunction can result in improved survival.

It is important to diagnose MR and left ventricular volume as early as possible.

The increased stroke volume of the left ventricle leads to its dysfunction, decreased ejection fraction, overload of the left atrium and pulmonary congestion.

The compensatory response to volume overload is an increase in left ventricular volume with a normalization of eall stress, resulting in chronic asymptomatic stage of MR.

Long-standing volume overload can result in progressive left ventricular enlargement and stretching of the myocytes beyond their normal contractile length, leading to a decreased contractile state from reduced myofiber content and interstitial fibrosis with increasing left atrial and left ventricular diastolic pressures, producing dyspnea.

Left ventricular dysfunction may occur before the onset of symptoms, and may not be identified by conventional measures of ejection fraction and portends poor prognosis.

When mitral regurgitation develops slowly over months to years, or the acute phase is managed with medical therapy, the process can evolve into chronic compensated phase of the disease.

In chronic compensated MR the left ventricle develops eccentric hypertrophy and with an increased diastolic volume, combine to increase the stroke volume so that the forward stroke volume approaches normal levels.

In chronic compensated MR the atrium enlarges, allowing filling pressure to decrease, pulmonary vein drainage to increase and pulmonary congestion to improve.

In chronic compensated MR patients may be asymptomatic and have normal exercise tolerance.

In chronic compensated MR the left ventricle will eventually develop left ventricular failure and the development of chronic decompensated phase of disease.

Decompensated phase is characterized by calcium overload within the cardiac myocytes and the myocardium has impaired ability to compensate for volume overload and left ventricle stroke volume decreases, eventually resulting in CHF.

With decompensated phase the left ventricle dilates and causes dilation of the mitral valve annulus with worsening mitral regurgitation.

The ejection fraction with chronic decompensated MR is less than in acute phase MR or chronic compensated MR.

Severity of mitral regurgitation associated with diastolic blood pressure, with higher pressures associated with more severe disease.

Symptoms associated with mitral regurgitation are dependent on which phase of the disease is present.

With acute MR signs and symptoms of decompensated congestive heart failure, as well as low cardiac output state.

With acute mitral regurgitation due to papillary muscle rupture or rupture of a chorda tendinae, cardiogenic shock may the presentation.

With chronic compensated mitral regurgitation patients may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure, but are are prone to develop CHF.

Clinical findings depend on severity and duration of MR and include: a lateral displaced apical beat with possible heave, a holosystolic murmur radiating to the back or clavicle, a loud and palpable P2 sound and commonly a third heart sound.

Typically the murmur is holosystolic.

The murmur is most often found in patients with fixed rheumatic mitral regurgitation and may not be heard in patients with the more prevalent mitral regurgitation due to mitral valve prolapse.

The loudness of the murmur does not correlate well with the severity of MR, but generally the intensity of the murmur correlates with the hemodynamic severity of mitral regurgitation.

The predictive value of the heart murmur auscultation exam is poor in patients with secondary mitral regurgitation and 75% of such patients with moderate to severe mitral regurgitation by echocardiograph are without audible murmur.

Atrial fibrillation is commonly found in MR.

With mitral valve prolapse a mid-to-late systolic click and a late systolic murmur is often present.

Electrocardiogram may show evidence of left atrial enlargement and left ventricular hypertrophy or atrial fibrillation

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Symptoms are often lacking.

When present symptoms include: cough, fatigue, dizziness, heart palpitations, and dyspnea.

A cardiac thrill may be palpable over the heart.

Findings of congestive heart failure may be present.

Surgical repair or replacement of the valve is recommended if heart function is poor or symptoms are severe.

A large proportion of patients with severe MR in older population have comorbidities and remain untreated, because of the high risk of complication from surgery.

Currently it is recommended that early surgery be performed for severe primary mitral regurgitation, but the management of secondary mitral regurgitation, which is essentially a disease of the left ventricle, is more controversial.

With severe regurgitation, surgical correction is indicated, as the disease progresses rapidly and can lead to heart failure.

Current guidelines recommend surgical intervention for symptomatic patients as well as asymptomatic patients With Left ventricular dysfunction, described as left ventricular ejection fraction less than 60% or left ventricular dilation and asymptomatic patients with normal left ventricular ejection fraction, no lLV dilation and the likelihood of success repair more than 95% and expected mortality less than 1%.

Patients who have left ventricular dysfunction and secondary mitral regurgitation of any severity have a worse prognosis in patients who have left ventricle dysfunction without mitral regurgitation.

Average interval from diagnosis to onset of symptoms is 16 years.

The performance of transthoracic echo cardiography allows the identification of the cause, mechanism, severity and consequences of MR by evaluating characteristics in motion of the mitral valve leaflets, their size, and calcification of the anulus, left ventricular and left atrial volumes, global and regional left ventricular systolic function, pulmonary vein flow, pulmonary artery pressures, right ventricular function, in the presence of tricuspid regurgitation.
Transthoracic echocardiography often reveals a greater mitral regurgitation that can be detected on physical examination.
Transesophageal echocardiography and cardiac magnetic resonance imaging can provide more specific anatomical and hemodynamic detail of the anatomy and function of the mitral valve.

Cardiac catheterization with hemodynamic assessment, coronary angiography and left ventriculography can be beneficial in selecting patients with suspected coronary artery disease.

In patients with chronic heart failure and reduce the left ventricle ejection fraction, severe is secondary mitral valve occur you Tatian is associated with the poor prognosis.

For patients with severe ischemic mitral regurgitation associated with limiting symptoms despite medical and possible resynchronization is mitral repair or chordal sparing replacement.

Conclusive evidence of whether to repair or replace the mitral valve is presently lacking.

Among patients with severe secondary mitral regurgitation, the rate of death or unplanned hospitalizations for heart failure at one year did not differ significantly between patients who underwent percutaneous mitral valve repair in addition to receiving medical therapy in those who receive medical therapy alone (Obadia JF)

Repair is associated with lower perioperative mortality, whereas replacement provides better long-term correction with a lower risk of recurrence: recurrence of mitral regurgitation predisposes the heart failure.

Heavy calcification of mitral annulus as well is calcification, thickening, and retraction of the mitral valve leaflets may preclude a successful and durable repair of the mitral valve.

Deciding between reduced operative mortality and morbidity with repair versus better long-term correction of ischemic mitral regurgitation with valvular replacemen remains the source in the variability in surgical practice for this process.(Cardiothoracic Surgical Trials Network).

In the above study replacement provided a more durable correction of mitral regurgitation, without significant between group difference in clinical outcomes.

Quantitative assessment of mitral regurgitation with proximal isovelocity surface area is standard to establish mitral regurgitation severity and provides the measurements of effective orifice area, regurgitant volume and regurgitant fraction.

In the above study there was no significant differences in mortality at 30 days or 12 months.: The observed 30 day rates of death were 1.6% in the repair group 4% in the replacement group.

The above studies contradict much of published literature which suggests advantages of mitral valve repair over replacement, including low operative mortality, improved left ventricular function, higher rates of long-term survival.

Meta-analysis show long- term risk of death 35% higher in replacement group than in a repair group (Magne J et al).

Patients undergoing mitral valve replacement are older and have more comorbidities than those undergoing repair.

No medical therapy has altered the natural history of patients with severe primary mitral regurgitation.

Patients who are symptomatic with severe primary mitral regurgitation may benefit from diuretics, afterload reduction, but ultimately treatment is interventional.

In a multicenter, randomized controlled trial involving patients with severe secondary mitral regurgitation, the rate of primary outcome of death or unplanned hospitalization for heart failure at 12 months did not differ significantly between a percutanouus mitral clip repair and a control group (MITRA-FR investigators).

Transcatheter mitral valve repair for degenerative MR  uses an edge to edge microvalve leaflet repair technique.

Outcomes of transcatheter mitral valve repair for high risk surgical patients and isolated degenerative MR results in successful repair in almost 89% of patients.

In a randomized clinical trial, minithoracotomy repair for degenerative mitral regurgitation, through mini thoracotomy, failed to demonstrate superiority over a sternotomy repair approach.

In a report of 19,088, patients with moderate or severe degenerative, mitral regurgitation treated by transcatheter edge to edge repair, there was a low 30 day mortality of 2.7%.


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