Mitral Valve Regurgitation

Overview

Mitral Valve Regurgitation refers to inappropriate retrograde movement of blood from the left ventricle to the left atrium through the mitral valve during systole.

Etiologies

Proper closure of the mitral valve during systole requires the structural integrity of the valvular leaflets and annulus as well as proper functionality of the papillary muscles and chordae tendineae. A wide variety of etiologies can result in defects in any of these components and thus result in Mitral Regurgitation. We categorize these etiologies according to whether resultant regurgitation develops acutely or chronically.

Infective Endocarditis: Infection perforates valve leaflets or ruptures chordae tendineae
Myocardial Infarction: Dysfunction or rupture of papillary muscles

Mitral Valve Prolapse: Progressive structural weakening of the mitral valve leaflets
Rheumatic Fever: Fibrotic deformation of the leaflets and shortening of the chordae tendineae prevent valvular closure. Is less common that rheumatic mitral stenosis but both can co-exist
Ventricular Dilation: May be due to dilated cardiomyopathy or eccentric ventricular hypertrophy associated with end-stage left heart failure or myocarditis. Whatever the case, expansion of the mitral anulus prevents proper closure of the leaflets
Marfan Syndrome: Weakening of the valve leaflets and chordae tendineae.

Pathophysiology

Mitral Regurgitation results in some portion of the stroke volume ejected by the left ventricle entering the left atrium rather than the systemic circulation. This not only increases the left atrial pressure but also reduces the heart's total cardiac output. A number of factors determine what percentage of the stroke volume inappropriately enters the atrium; however, the most important factor appears to be the relative ease with which the ventricle can eject blood into the atrium.

During acute atrial regurgitation, atrial compliance is relatively low; consequently, atrial pressures rapidly rise even with small regurgitant volumes, thus directing the majority of the stroke volume appropriately into the systemic circulation. As a result, cardiac output is not severely compromised; however, the sharp rise in left atrial pressures are retrogradely transmitted to the pulmonary circulation rapidly resulting in profound pulmonary edema and thus dyspnea.

Long-term mitral regurgitation allows the left atrium to undergo remodeling and thus atrial dilation which substantially increases atrial compliance. When atrial compliance is high, the atrium can accommodate large blood volumes from the ventricle without a large increase in pressure, allowing much of the stroke volume to empty into the atrium. While this prevents sharp rises in left atrial pressure and protects the pulmonary circulation from edema, cardiac output is severely compromised as much of the stroke volume enters the atria rather than the systemic circulation. Consequently, the signs and symptomology of chronic mitral regurgitation center around poor cardiac output which manifests as fatigue and weakness.

Clinical Consequences

As described above the pathophysiological sequelae of acute and chronic mitral valve regurgitation are substantially different and are reflected in their distinct clinical presentation. Acute mitral regurgitation is dominated by increased left atrial pressures and thus pulmonary edema. In contrast, chronic mitral regurgitation is dominated by reduce cardiac output.

Patients with acute mitral regurgitation present with signs and symptomology of severe, rapidly progressive pulmonary edema such as profound dyspnea that constitutes a medical emergency.

Mild chronic mitral regurgitation is usually subclinical as the heart possesses significant functional reserve. Patients with chronic moderate regurgitation often display signs of deficient cardiac output which present as fatigue and an intolerance to physical exertion. If chronic regurgitation is severe then left atrial pressures do eventually rise to the point that signs and symptoms of pulmonary edema begin to manifest, first as dyspnea and then progressing to orthopnea. In such severe cases, chronic volume overloading of the left ventricle can lead to left heart failure which aggravates pulmonary hypertension and often yields concomitant right heart failure. Whatever the severity, dilation of the left atrium can cause atrial fibrillation.

Signs

A heart murmur spanning all of ventricular systole, termed a "Holosystolic Murmur", is typical of mitral valve regurgitation. In most patients with mitral regurgitation the murmur usually radiates toward the left axilla. However, in certain cases, such as dysfunction or rupture of the chordae tendineae, the regurgitant jet may be displaced from its prototypical angle and thus the murmur may radiate toward the left sternal edge, mimicking aortic stenosis. In addition, in cases of acute regurgitation, the murmur may decrescendo during systole, reflecting dissipation of the regurgitant jet as left atrial pressure rapidly rises.

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