Mitral Regurgitation I: Introduction

When the mitral valve fails to close entirely during systole, blood leaks backward from the left ventricle into the left atrium instead of being pumped forward. This abnormal backward circulation reduces the efficiency of cardiac output and forces the heart to work harder to maintain adequate blood flow throughout the body.

Primary mitral regurgitation originates from direct valve abnormalities such as mitral valve prolapse, rheumatic fever, and degenerative changes affecting the leaflets and chordae tendineae. Secondary mitral regurgitation results from indirect factors like ischemic heart disease, myocardial infarction, and infective endocarditis that damage supporting structures or alter ventricular geometry.

The regurgitated blood creates volume overload in the left atrium and ventricle, causing them to enlarge and stretch. Initially, this adaptive response of hypertrophy and dilation helps maintain cardiac output, but chronic volume overload eventually leads to progressive ventricular dilation and systolic dysfunction.

The mitral valve's supporting structures include the leaflets, chordae tendineae, annulus, and papillary muscles. Dysfunction or damage to any of these components prevents complete valve closure during systole, leading to incomplete valve closure and blood regurgitation into the left atrium.

Increased pressure in the left atrium due to regurgitated blood leads to pulmonary congestion and pulmonary hypertension. This back pressure strains the right ventricle, potentially causing right-sided heart failure and reducing overall cardiac output, which manifests as fatigue and exertional dyspnea.

Chronic volume overload and increased atrial pressures result in progressive ventricular dilation and dysfunction, culminating in systolic heart failure. The heart's pumping efficiency decreases over time, reducing cardiac output and causing symptoms such as reduced exercise tolerance and breathing difficulties.

Rheumatic fever causes scarring and deformation of the mitral valve leaflets, while degenerative changes cause the leaflets and chordae tendineae to thicken and become fibrotic. Both conditions impair the valve's ability to close completely, resulting in blood leakage during systole.