Mitral valve regurgitation happens when the mitral valve, which sits between the two left chambers of your heart, doesn’t close tightly enough. Blood leaks backward with each heartbeat instead of flowing forward to the rest of your body. The causes fall into two broad categories: problems with the valve itself, and problems with the heart muscle that distort how the valve works. It’s the most common type of valve disease in older adults, affecting roughly 9.3% of people over age 75.
Primary vs. Secondary Regurgitation
This distinction matters because the underlying problem, and therefore the treatment approach, is fundamentally different depending on which category you fall into.
In primary mitral regurgitation, there’s direct, physical damage to some part of the valve apparatus: the leaflets (the flaps that open and close), the thin cords that anchor them (called chordae tendineae), the small muscles those cords attach to, or the ring of tissue that frames the valve. Something about the valve itself is broken or deformed.
In secondary mitral regurgitation, the valve itself is structurally normal. Instead, the left ventricle (the heart’s main pumping chamber) has enlarged or weakened, pulling the valve’s anchoring points apart so the leaflets can no longer meet in the middle. The valve isn’t damaged; it’s being stretched open by changes in the surrounding heart.
Mitral Valve Prolapse
Mitral valve prolapse is the most common primary cause. One or both valve leaflets become abnormally elongated or floppy, bulging backward into the upper chamber when the heart contracts. Over time this can worsen from a trivial leak into severe regurgitation.
Two specific mechanical failures drive the progression. First, the ring of tissue supporting the valve can gradually stretch and widen, preventing the leaflets from meeting properly. Second, the thin cords anchoring the leaflets can rupture, letting a leaflet flap freely. In a study of 83 patients who needed surgery for severe prolapse-related regurgitation, 58% had both a widened ring and ruptured cords, 19% had a widened ring alone, and 19% had ruptured cords alone. Cord rupture can happen suddenly, turning a stable mild leak into an acute emergency overnight.
Connective Tissue Disorders
Genetic conditions that weaken connective tissue throughout the body can also weaken the mitral valve. Marfan syndrome is the best-known example. People with Marfan often develop what’s called a Barlow’s valve, where the leaflets are unusually large and loaded with excess spongy tissue, making them prone to prolapse and progressive leaking. Loeys-Dietz syndrome and Ehlers-Danlos syndrome carry similar risks. These conditions affect the proteins that give tissues their strength and elasticity, so the valve’s structural integrity deteriorates earlier in life than it otherwise would.
Infection and Inflammation
Infective endocarditis occurs when bacteria enter the bloodstream and attach to the heart’s inner lining or valve surfaces. Once bacteria colonize a valve leaflet, they form clumps called vegetations that are extremely difficult for the immune system to clear, partly because the valve tissue has limited blood supply. The infection can erode holes through leaflets or destroy them entirely, causing sudden, severe regurgitation that often requires emergency surgery.
Rheumatic heart disease, triggered by repeated strep throat infections, causes a different kind of damage. The immune system’s inflammatory response scars and thickens the valve leaflets over years, making them stiff and unable to close fully. This was once the leading cause of mitral regurgitation worldwide and remains common in parts of the world where strep infections go untreated.
Heart Attacks and Ischemic Damage
A heart attack can cause mitral regurgitation through several pathways, and the timeline matters. In the acute phase, the affected section of heart muscle stops contracting, which can immediately distort the valve’s geometry. The small muscles that help pull the valve shut lose their blood supply and stop functioning properly. This type of regurgitation is sometimes reversible if blood flow is restored quickly.
In the longer term, scar tissue from the heart attack causes the ventricle to remodel, meaning it changes shape. The wall thins and stretches in the damaged area, pulling the valve’s anchoring points outward. This combination of leaflet tethering, a weakened pumping force, and a widening valve ring creates a leak that tends to worsen over months to years. About 8% of patients with chronic severe mitral regurgitation reach the point of needing surgery each year.
Heart Enlargement Without Valve Damage
Any condition that causes the left ventricle to dilate can produce mitral regurgitation even when the valve is perfectly intact. Dilated cardiomyopathy, long-standing high blood pressure, and chronic atrial fibrillation can all stretch the heart enough to pull the valve open.
For years, doctors assumed that widening of the valve ring itself was the main culprit. More recent research has shown that tethering of the valve’s anchoring cords, caused by displacement of the muscles they attach to as the ventricle enlarges, is actually the primary driver. Ring dilation alone doesn’t usually cause significant leaking. It’s the combination of a stretched ring, displaced anchor points, and a weakened pumping force that tips the balance.
How Symptoms Develop Over Time
Mild mitral regurgitation often produces no symptoms at all, and many people live with it for years without knowing. The heart compensates by pumping harder and gradually enlarging to handle the extra volume. You may feel completely fine during this phase.
As the leak worsens or the heart’s ability to compensate fades, symptoms emerge: shortness of breath during activity (and eventually at rest), fatigue, a fluttering or racing heartbeat, and swelling in the ankles or feet. The transition from “compensated” to “symptomatic” can be gradual over a decade or more with a slowly progressing leak. In acute cases, such as a ruptured cord or endocarditis, severe symptoms can appear within hours.
How Severity Is Measured
Doctors use an echocardiogram (an ultrasound of the heart) to grade the leak on a scale from 1 to 4. The key measurement is how much blood leaks backward per heartbeat. Grade 1 (mild) means less than 30 milliliters leaks back. Grade 2 (moderate) is 30 to 44 milliliters. Grade 3 (moderate-to-severe) is 45 to 59 milliliters. Grade 4 (severe) is 60 milliliters or more, meaning at least half the blood the ventricle pumps goes the wrong direction.
For people with severe primary regurgitation who aren’t yet experiencing symptoms, guidelines recommend echocardiograms every 6 to 12 months to watch for signs the heart is struggling, such as a declining pumping strength or an enlarging ventricle. When the heart begins to weaken or symptoms develop, surgical repair or replacement of the valve is typically recommended. For patients too frail for open-heart surgery, a catheter-based procedure that clips the valve leaflets together can reduce the leak significantly.