Mitral regurgitation overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S. [3]; Lakshmi Gopalakrishnan, M.B.B.S. [4]; Mohammed A. Sbeih, M.D. [5]; Rim Halaby, M.D. [6] Khizer Yaseen, M.B.B.S.[7]
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 valvular heart disease in the United States. 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. Mitral Regurgitation is classified as primary when caused by intrinsic pathology of mitral valve leflets and secondary when caused by abnormalities involving the left atrium or left ventricle.
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 mitral regurgitation (MR) arises from intrinsic abnormalities of the mitral valve (leaflets, chordae, or papillary muscles) and initially causes volume overload, leading to increased preload, reduced afterload, and eccentric left ventricular hypertrophy and dilation. During the compensated phase, left ventricular ejection fraction (LVEF) may remain preserved (~60%) despite progressive remodeling. Over time, increased wall stress and early myocardial dysfunction mark a transitional phase, and if untreated, decompensation occurs with irreversible left ventricular systolic dysfunction and heart failure. Markers of decompensation include left ventricular end-diastolic dimension >70 mm, end-systolic dimension >45–47 mm, and LVEF <50–55%. Notably, irreversible myocardial injury can precede the onset of symptoms, emphasizing the importance of early recognition and monitoring.
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
Mitral regurgitation is the most common valvular diseases in the United States. 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. Severe primary mitral regurgitation is associated with adverse prognosis if left untreated, with over 90% of patients developing heart failure or death within 10 years; timely surgical repair restores near-normal life expectancy.
Chronic mitral regurgitation may lead to progressive cleft atrial enlargement, and may results in atrial fibrillation, pulmonary hypertension, right ventricular dysfunction and 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.
Assessment of mitral regurgitation severity requires a comprehensive echocardiographic evaluation rather than reliance on a single Doppler parameter. Left atrial and left ventricular enlargement and elevated pulmonary pressures support chronic severe mitral regurgitation when Doppler findings are equivocal. When echocardiographic findings are discordant, transesophageal echocardiography or cardiac magnetic resonance imaging should be performed.²⁵
Cardiac MRI
Cardiac magnetic resonance imaging (CMR) is the reference standard for assessing left atrium and left ventricule size and function and provides accurate quantification of mitral regurgitant volume, particularly in cases with eccentric or multiple jets. It is especially valuable when echocardiographic findings are inconclusive, as it allows comprehensive evaluation of both left atrial and ventricular structure and function, as well as precise assessment of the severity of mitral regurgitation.
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.
Biomarker and advnaced imaging
Emerging markers of myocardial dysfunction include brain natriuretic peptide levels, global longitudinal strain, left ventricular volumes, and myocardial fibrosis detected by cardiac magnetic resonance imaging.
Treatment
Treatment Overview
Vasodilator therapy with ACE inhibitors and hydralazine is the foundation of medical therapy.Surgery is indicated for symptomatic severe primary mitral regurgitation or when left ventricular ejection fraction is ≤60% or left ventricular end-systolic dimension ≥40 mm. Early surgical repair should be considered in asymptomatic patients with severe mitral regurgitation when a durable repair is highly likely and operative risk is low. 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.
Successful mitral valve repair is defined by perioperative mortality <1%, mild or less residual regurgitation, preserved ventricular function, and low transmitral gradient. Transcatheter mitral therapies are options for symptomatic patients who are not surgical candidates.
Follow Up
In patients with asymptomatic mitral regurgitation and preserved left ventricular function, regular follow-up is essential. Ongoing surveillance allows early detection of progressive ventricular enlargement or declining ejection fraction, which are key indicators of impending decompensation and the need for timely intervention to prevent adverse outcomes.
References