The most common cause of mitral regurgitation depends on where in the world you live. In developed countries, degenerative valve disease (where the valve tissue gradually weakens and stretches over time) is the leading cause. In developing countries, rheumatic heart disease, triggered by untreated strep throat, takes the top spot. A third major cause, relevant everywhere, is heart damage from a heart attack or heart failure that distorts the valve’s geometry without directly damaging the valve itself.
Degenerative Valve Disease
In the United States, Europe, and other high-income countries, the most frequent cause of mitral regurgitation is age-related degeneration of the valve leaflets. The mitral valve has two thin flaps (leaflets) that open and close with each heartbeat to keep blood flowing in one direction. Over time, the structural proteins that give these leaflets their strength and flexibility, primarily collagen and elastic fibers, begin to break down. The leaflets become thicker, stretchier, and less able to seal shut properly. This process is called myxomatous degeneration.
At a tissue level, what happens is an imbalance between how the body builds and breaks down the valve’s connective tissue scaffolding. Enzymes that normally remodel tissue become overactive, fragmenting the collagen and elastic fibers that hold the leaflet together. The spongy middle layer of the valve swells with water-attracting molecules, creating a boggy, weakened structure. The cords that anchor the leaflets to the heart muscle (chordae tendineae) also stretch, thin out, or even snap. When a cord ruptures, a section of the leaflet can flip backward into the upper chamber of the heart during each beat, allowing a significant volume of blood to leak in the wrong direction.
Genetics play a role. Some people inherit defects in the genes responsible for producing collagen and elastic fibers, which predisposes them to earlier or more severe valve breakdown. But for many people, this is simply a wear-and-tear process that becomes more likely with age. The global prevalence of moderate-to-severe mitral regurgitation reflects this: roughly 0.6% of people at age 50, climbing to about 2.9% at 70, 4.5% at 80, and 6.5% by age 90. Men and women are affected at nearly identical rates across all age groups.
Rheumatic Heart Disease
Globally, rheumatic heart disease is the single largest contributor to mitral valve problems, affecting an estimated 55 million people worldwide and causing approximately 360,000 deaths each year. The vast majority of cases occur in low- and middle-income countries where access to antibiotics for strep throat is limited.
The chain of events starts with a common strep throat infection. In some people, the immune system’s response to the bacteria accidentally attacks the body’s own tissues, including the heart valves. This autoimmune reaction, called rheumatic fever, inflames the valve leaflets. One episode may cause only minor damage, but repeated bouts of rheumatic fever scar and stiffen the valve over months and years. The leaflets can thicken, fuse together at the edges, or shrink, preventing the valve from closing completely.
Rheumatic heart disease is the most commonly acquired heart disease in people under 25. It is also the leading cause of heart complications in pregnant women in regions where the disease is endemic. Because it strikes young people and often goes undetected until the valve damage is advanced, it carries an outsized burden in populations with limited healthcare infrastructure.
Heart Damage That Distorts the Valve
The third major category is called functional (or secondary) mitral regurgitation. In this scenario, the valve leaflets themselves are structurally normal. The problem is that the heart around them has changed shape, pulling the valve apart so it can no longer close properly.
This most often happens after a heart attack. When a section of the heart muscle dies and scars, the left ventricle (the heart’s main pumping chamber) remodels. It may dilate, change shape, or develop weak spots. The two small muscles inside the ventricle that anchor the mitral valve’s cords, called papillary muscles, get pulled out of position. This tugs the valve leaflets downward and apart during each beat, creating a gap where blood leaks backward. Heart attacks affecting the bottom wall of the heart are particularly likely to cause this because the displacement of the papillary muscles is greatest in that direction.
Heart failure from causes other than a heart attack (such as viral infections, alcohol use, or long-standing high blood pressure) can produce the same result. As the ventricle enlarges globally, the ring-shaped base of the mitral valve stretches with it. The valve also loses its natural saddle shape, which increases stress on the leaflets. This creates a vicious cycle: the leaking valve forces the ventricle to pump extra volume, which makes the ventricle dilate further, which pulls the valve further apart, which worsens the leak.
How Symptoms Develop
Mild mitral regurgitation often causes no symptoms at all. Many people live for years without knowing they have it. As the leak worsens and the heart works harder to compensate, the first symptom is usually shortness of breath, initially during physical activity, then during rest, lying down, or trying to sleep. You may feel like you can’t fill your lungs or that breathing requires unusual effort.
Other symptoms that can develop include fatigue that feels disproportionate to your activity level, heart palpitations (a fluttering or skipping sensation), swelling in the legs or feet, chest discomfort, coughing, and near-fainting episodes. These symptoms can develop gradually over months or years with chronic mitral regurgitation. In some cases, particularly when a valve cord ruptures or a heart attack suddenly damages the valve apparatus, symptoms can appear within hours and escalate rapidly.
How Severity Is Assessed
Mitral regurgitation is typically detected and graded using an echocardiogram, an ultrasound of the heart. The test lets doctors visualize the valve in real time, see how much blood is leaking backward, and measure how the heart is responding to the extra workload.
Several measurements help determine whether the leak is mild, moderate, or severe. Doctors look at the width of the jet of blood flowing backward through the valve, the size of the opening through which blood escapes, the total volume of blood leaking per heartbeat, and whether blood flow in the pulmonary veins (which drain into the upper heart chamber) reverses direction during the heart’s pumping phase. A flail leaflet, where part of the valve flips backward freely, is considered a hallmark of severe disease. An enlarged left ventricle that is still pumping normally also suggests the heart has been compensating for a significant leak over time.
Why Timing Matters
Left untreated, severe mitral regurgitation carries a poor prognosis. Studies consistently show high rates of heart failure hospitalization and death when significant leaks are managed conservatively. Yet intervention rates remain surprisingly low. A large French national study found that only about 8% of patients with severe mitral regurgitation underwent repair or replacement within the first year of diagnosis, with those managed without intervention experiencing very high rates of adverse events.
The challenge is that the heart compensates well for a long time. By the time symptoms become obvious, the heart muscle may already be weakened in ways that are difficult to reverse. This is why regular monitoring matters once mitral regurgitation is identified, even when it’s mild. Tracking changes in heart size and pumping function over time helps determine the right window for intervention, ideally before irreversible damage sets in.