Mitral regurgitation overview

Mitral Regurgitation Microchapters
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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
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S; Mohammed A. Sbeih, M.D. [3].

Overview

Mitral regurgitation (MR), mitral insufficiency or mitral incompetence is a disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood. It is the abnormal leaking of blood from the left ventricle, through the mitral valve, and into the left atrium, when the left ventricle contracts, i.e. there is regurgitation of blood back into the left atrium . MR is the most common form of valvular heart disease . Diseases that weaken or damage the valve or the heart tissue around the valve cause mitral regurgitation. After age 55, some degree of mitral regurgitation is found in almost 20% of men and women who have an echocardiogram.

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

Anatomy

The mitral valve is typically 4–6 cm² in area. It has two cusps, or leaflets (the anteromedial leaflet and the posterolateral leaflet).

Pathophysiology

Mitral regurgitation is due to either perforation or prolapse of the leaflets, dilation of the mitral annulus or rupture of the papillary muscles or chordae tendineae. There are several phases of mitral regurgitation (acute, chronic compensated, and chronic decompensated). 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 pulomanry capillary wedge pressure which causes dyspnea, PND, orthopnea and rales. During the chronic compensated phase of mitral regurgitation, the left ventricle maintains forward cardiac output by filling with a larger volume of blood than usual to accomodate the fact that a portion of the blood will go backwards into the left atrium. In the decompensated phase, the left ventricle begins to dilate and fail. The markers of decompensation are as follows:

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

Epidemiology and Demographics

The incidence of mitral regurgitation is approximately 2% in a modern Western population. In the past, rheumatic heart disease was the leading cause of mitral regurgitation in Western countries, but now mitral valve prolapse is the leading cause and accounts for 45% of cases in Western countries. In Asia, North Africa, and the Middle East, and among some immagrant populations in the US, rheumatic heart disease remains the leading cause of mitral regurgitation.

Overall, mitral regurgitation affects both males and females equally . However, there are some minor imbalances when age is considered. In patients younger than 20 years, there is a male preponderance, and the severity of involvement is greater in males over the age of 50.

Complications

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

• Atrial Fibrillation
• Cardiogenic Shock
• Endocarditis
• Pulmonary Edema
• Pulmonary Hypertension
• Right Heart Failure
• Thromboembolism-Stroke

Prognosis

• Acute mitral regurgitation with cardiogenic shock is associated with an operative mortality of 80%.
• Patients with asymptomatic chronic severe mitral regurgitation have a high likelihood of developing symptoms or LV dysfunction over the course of 6 to 10 years . However, the incidence of sudden death in asymptomatic patients with normal LV function varies widely among these studies.

• The prognosis is poor in patients with severe symptomatic mitral regurgitation with an eight year survival rate of only 33% in the absence of surgical intervention. Heart failure being the common cause with sudden death attributing to ventricular arrhythmia .

• In patients with severe mitral regurgitation due to a flail posterior mitral leaflet, 90% of patients are either dead or require mitral valve surgery by 10 years with the mortality rate in patients with severe mitral regurgitation being 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 also predict 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. While in patients with NYHA functional class I/II symptoms before surgery survival rates at 5 and 10 years are 90 ± 2% and 76 ± 5%, respectively .

Causes

Mitral regurgitation is due to either perforation or prolapse of the leaflets, dilation of the mitral annulus or rupture of the papillary muscles or chordae tendineae. There are several phases of mitral regurgitation (acute, chronic compensated, and chronic decompensated).

Acute Mitral Regurgitation

• Heart attack or acute MI: Dysfunction or injury to the mitral valve following a heart attack. Papillary muscle rupture or dysfunction that is associated with ST elevation myocardial infarction.
• Endocarditis: The infaction may cause perforation of the leaflet, erosion of the surrounding structures, or a vagetation may not permit the leaflets to coapt.
• Trauma

Chronic Mitral Regurgitation

• Mitral valve prolapse: This disorder now accounts for 45% of cases of mitral regurgitation in the Western world.
• Ischemic heart disease / Coronary artery disease: This can be due to either papillary muscle dysfunction or left ventricular dilation and functional mitral regurgitation. Ischemia is responsible for 3% to 25% of MR cases.
• Rheumatic heart disease: In the past, this was the most common cause of MR in the Western world. In developing countries, rheumatic heart disease remains the most common cause.

Differentiating Mitral Regurgitation From Other Diseases

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

Diagnosis

History and Symptoms

Acute and decompensated mitral insufficiency is associated with symptoms of congestive heart failure including dyspnea, PND, orthopnea, and exercise intolerance. In chronic compensated mitral regurgitation there may be few symptoms.

Physical Examination

Chronic compensated mitral regurgitation causes a blowing holosystolic murmur which radiates to the axilla. The severity of the murmur is not associated with the volume of regurgitation. A third heart sound (S3) may be present. In patients with mitral regurgitation due to mitral valve prolapse, a click may be present.

Chest X-Ray

The chest x-ray in individuals with chronic mitral regurgitation is characterized by enlargement of the left atrium and the left ventricle. In acute mitral regurgitation, pulmonary edema is present, but the heart is not enlarged.

Ventriculogram

Echocardiography is the primary imaging modality that is used to diagnose and serially evaluate mitral regurgitation, but the ventriculogram can also be used to quantitate the magnitude of mitral regurgitation.

Electrocardiogram

In severe cases of mitral regurgitation, left ventricular hypertrophy with strain; left atrial enlargement, and signs of pulmonary hypertension may be observed on the resting EKG. Chronic mitral regurgitation is associated with an increased risk for atrial fibrillation.

Echocardiography

Transthoracic echocardiography should be performed in a patient with suspected mitral regurgitation 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 transthoracic echocardiogram (TTE) will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole. Echocardiographic features that suggest severe mitral regurgitation include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.

Cardiac Catheterization

In patients with mitral regurgitation who have risk factors for Coronary artery disease, such as advanced age, hypercholesterolemia, and hypertension, or when there is a suspicion that mitral regurgitation is ischemic in origin, coronary angiography should be performed before surgery.

Assessment of Severity

The severity of MR can be assessed by both clinical and echocardiographic criteria. Careful history is important to establish an estimate of baseline exercise tolerance of the patient.

The 2006 ACC/AHA guidelines included recommendations for echocardiographic monitoring in asymptomatic patients with chronic MR . Echocardiography is performed to assess the left ventricular ejection fraction and end-systolic dimension.

Determination of the degree of mitral regurgitation

Degree of mitral regurgitation	Regurgitant fraction	Regurgitant Orifice area
Mild mitral regurgitation	< 20 percent
Moderate mitral regurgitation	20 - 40 percent
Moderate to severe mitral regurgitation	40 - 60 percent
Severe mitral regurgitation	> 60 percent	> 0.3 cm2

Treatment

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

Afterload Reduction

• Afterload reduction should be instituted with the use of vasodilators such as ACE inhibitors and hydralazine.

Diuretics

• Diuretics are useful in reducing left ventricular volumes to improve functional mitral regurgitation and to improve pulmonary edema.

Digitalis

• Digitalis may be used to strengthen contractility, and potentially reduce hospitalization in patients with congestive heart failure.

Diet

• A low-sodium diet may be helpful.

Activity

• Most patients with chronic compensated mitral regurgitation have no symptoms; but if a person develops symptoms, activity should be restricted.

Beta Blockers

Beta blockers are generally not recommended as they would slow the compensatory tachycardia and would allow greater time over which the regurgitation could occur and increase the regurgitant volume.

Calcium Channel Blockers

• In the presence of atrial fibrillation, a calcium channel blocker or digoxin can be administered to slow the heart rate down and improve left ventricular filling.

Cardioversion

Cardioversion should be considered in the patient with atrial fibrillation or flutter who is hemodynamically unstable.

Anticoagulation

• Anti-coagulation therapy should be considered in patients with atrial fibrillation and in patients with prosthetic mitral valve replacement surgery.

Antibiotic Prophylaxis

• Prophylactic antibiotics prior to a periodontal procedure which involves manipulation of gingival tissue, the periapical region of a tooth, or perforation of oral mucosa is recommended in patients with previous infective endocarditis, patients who have a prosthetic mitral valve implanted and in those with congentital heart disease.

Surgery

Vasodilator theray with ACE inhibitors and hydralazine is the mainstay of therapy in patient with chronic compensated mitral regurgitation. Acute mitral regurgitation requires urgent mitral valve repair or mitral valve replacement. MV surgery is beneficial for patients with chronic severe MR and NYHA functional class II, III, or IV symptoms in the absence of severe LV dysfunction (severe LV dysfunction is defined as ejection fraction less than 0.30) and/or end-systolic dimension greater than 55 mm. MV surgery is beneficial for asymptomatic patients with chronic severe MR and mild to moderate LV dysfunction, ejection fraction 0.30 to 0.60, and/or end-systolic dimension greater than or equal to 40 mm. MV repair is recommended over MV replacement in the majority of patients with severe chronic MR who require surgery, and patients should be referred to surgical centers experienced in MV repair.