Mitral valve regurgitation (MR) is a common heart valve disorder. It occurs when the heart’s mitral valve, which separates the upper left chamber (left atrium) from the lower left chamber (left ventricle), fails to close completely. This incomplete closure allows blood to flow backward into the left atrium during the heart’s contraction cycle. This backflow reduces the amount of blood pumped forward to the rest of the body. The heart must then work harder to compensate for this inefficiency, potentially leading to complications like heart failure or irregular heart rhythms.
How the Mitral Valve Fails
The mitral valve is a structure designed to ensure one-way blood flow. It consists of two flaps, called leaflets, which open to allow blood to pass from the left atrium into the left ventricle. When the ventricle contracts to pump blood out to the body, these leaflets must meet precisely, or coapt, to form a tight seal. This seal is supported by a network of thin, fibrous cords called chordae tendineae, which are anchored to small muscles in the ventricle wall known as papillary muscles.
The entire system relies on the synchronized function of its components. Regurgitation occurs when the leaflets fail to coapt fully during the heart’s contraction. This mechanical failure can happen if the leaflets are damaged, the supporting chords rupture, or the entire valve structure is pulled out of alignment. The underlying causes of MR are categorized based on whether the problem originates within the valve itself or in the surrounding heart muscle.
Causes Originating in the Valve Structure
Problems that arise directly from damage or abnormality to the valve’s leaflets, chords, or ring (annulus) are known as primary mitral regurgitation. The most frequent cause of this type is Mitral Valve Prolapse (MVP). MVP is a condition where one or both leaflets become “floppy” due to weakened tissue (myxomatous degeneration), causing them to bulge backward into the left atrium during contraction. This ballooning effect prevents the leaflets from forming a proper seal, resulting in a leak.
Rupture of one or more chordae tendineae can cause a portion of the valve to “flail” into the atrium, leading to sudden, severe regurgitation. This rupture can occur spontaneously in patients with MVP or as a result of trauma.
Infective Endocarditis is another direct cause, involving a bacterial or fungal infection that colonizes the valve tissue. These infectious growths, called vegetations, can physically damage and destroy the leaflets, or they can cause the supporting chords to tear. The rapid destruction of tissue often leads to an abrupt and severe onset of regurgitation.
Rheumatic heart disease, a complication of untreated streptococcal throat infection, causes scarring and thickening of the mitral leaflets over time. This scarring makes them rigid and deformed. This prevents the valve from opening and closing properly, often causing both regurgitation and narrowing (stenosis).
Causes Originating in the Heart Muscle
When the mitral valve apparatus is structurally normal, but the valve leaks because of changes in the heart muscle’s shape or function, the condition is referred to as secondary or functional mitral regurgitation. This type of failure results from forces external to the valve pulling the leaflets out of alignment. The underlying issue is often the enlargement and weakening of the left ventricle.
Dilated Cardiomyopathy, the general enlargement and weakening of the left ventricle, is a common culprit. As the muscular walls stretch outward, the ring around the mitral valve (the annulus) also widens and the papillary muscles are pulled apart. This distortion prevents the leaflets from meeting in the center, even though the leaflets themselves are healthy.
Ischemic MR occurs after a heart attack (myocardial infarction). Damage to the heart muscle can cause the left ventricle to remodel and stretch, or it can directly injure the papillary muscles. This damage results in the leaflets being pulled down and tethered into the ventricle cavity, preventing them from coapting correctly.
Chronic conditions like long-standing high blood pressure or other forms of heart failure can gradually cause the left ventricle to remodel and dilate. The resulting ventricular enlargement stretches the entire mitral apparatus, creating an imbalance that exacerbates the leak. This process creates a continuous cycle where the regurgitation contributes to further ventricular remodeling.
The Difference Between Acute and Chronic Causes
Mitral regurgitation is also classified by its timeline, which affects the patient’s symptoms and treatment needs. Acute MR is characterized by a sudden onset, often caused by a catastrophic mechanical failure in a previously healthy valve. Examples include an abrupt rupture of the chordae tendineae due to endocarditis or trauma, or a tear in a papillary muscle following a large heart attack.
Because the left atrium and ventricle have no time to adapt to the sudden volume overload, acute MR can quickly lead to severe symptoms such as pulmonary edema and cardiogenic shock, requiring immediate medical intervention.
Chronic MR develops slowly and progressively over months or years. Causes like degenerative MVP or slow ventricular dilation from chronic heart failure fall into this category.
In chronic cases, the heart chambers gradually enlarge and remodel to accommodate the increased blood volume leaking backward. This adaptation allows the patient to remain compensated and often without severe symptoms for an extended period. The distinction between acute and chronic onset is a fundamental difference in how the body handles the mechanical failure and how the condition is managed by physicians.