Heart valve disease develops when one or more of the heart’s four valves stop opening or closing properly. The causes range from conditions you’re born with to damage that accumulates over decades from aging, infection, high blood pressure, or other heart problems. In many cases, more than one factor is at work.
Age-Related Calcium Buildup
The most common cause of heart valve disease in developed countries is the gradual deposit of calcium on valve leaflets, a process that mirrors what happens in arteries with atherosclerosis. It starts with damage to the thin lining of the valve, which triggers inflammation and oxidative stress. Over time, inflammatory cells transform into bone-like cells that actively deposit calcium, forming hard nodules on the valve surface. The leaflets stiffen, thicken, and eventually can’t open or close fully.
This process unfolds in two stages. First, the valve develops mild thickening and scarring, often without symptoms. In the second stage, calcium deposits become heavy enough to deform the leaflet and obstruct blood flow. The prevalence tells the story of how age-dependent this process is: 20 to 30 percent of people over 65 have some degree of calcific valve disease, and that jumps to 48 to 57 percent in people over 85.
Congenital Valve Defects
Some people are born with valves that have the wrong number of leaflets. The most common example is a bicuspid aortic valve, where the aortic valve has two leaflets instead of the usual three. About 1.5 percent of the population has this condition, making it the most frequent valve malformation. It’s roughly three to four times more common in males than females.
A bicuspid valve can function well for years, but its abnormal shape creates uneven mechanical stress. That accelerated wear and tear means calcium buildup and stiffening often begin decades earlier than they would in a normal three-leaflet valve. Some people with a bicuspid valve develop significant narrowing in their 40s or 50s rather than their 70s or 80s. Less commonly, a valve forms with just one leaflet (unicuspid), which tends to cause problems even earlier.
Infections That Damage Valves
Rheumatic Heart Disease
Globally, rheumatic heart disease remains a leading cause of valve damage, affecting an estimated 55 million people and killing roughly 360,000 each year, overwhelmingly in low- and middle-income countries. It starts with an ordinary strep throat infection. In some people, the immune system’s response to the bacteria mistakenly attacks heart valve tissue, causing inflammation and scarring. Repeated episodes of rheumatic fever compound the damage, fusing valve leaflets together and severely restricting their movement. Rheumatic valve disease most often affects the mitral and aortic valves, and it’s more common in women.
Infective Endocarditis
Bacteria, fungi, or other germs can enter the bloodstream and attach directly to heart valves, causing an infection called endocarditis. The germs tend to latch onto valves that are already abnormal or damaged. Risk factors include intravenous drug use with contaminated needles, poor dental health that allows mouth bacteria into the bloodstream, and long-term use of catheters or other devices that provide a direct route for germs to enter the body. The infection creates vegetations (clumps of bacteria and blood cells) on the valve surface, destroying tissue and sometimes perforating the leaflets.
Heart Failure and Heart Attacks
Valve disease doesn’t always start in the valve itself. When the heart muscle weakens or enlarges from a heart attack or chronic heart failure, the surrounding structures shift in ways that pull valve leaflets out of alignment. This is especially common with the mitral valve. As the left side of the heart stretches, it widens the ring of tissue that anchors the mitral valve and increases the pulling forces on the leaflets, preventing them from sealing shut. Blood then leaks backward with every heartbeat.
This type of valve dysfunction creates a vicious cycle. The leaking valve forces the already weakened heart to pump extra volume, because the blood that flows backward never reaches the rest of the body. That added workload accelerates the heart’s decline, which worsens the leak further.
High Blood Pressure
Chronically elevated blood pressure is a well-established long-term contributor to valve disease. A large UK cohort study of more than 5 million adults found that elevated blood pressure independently increases the risk of both aortic valve disease and mitral regurgitation. The mechanism is straightforward: higher pressure in the left side of the heart forces valves to work harder with every beat. Over years and decades, this extra mechanical load accelerates the same inflammatory and calcification processes that drive age-related valve deterioration.
Chest Radiation for Cancer
Radiation therapy aimed at the chest, commonly used for lymphoma, breast cancer, and other thoracic cancers, can damage heart valves years or even decades after treatment. The median gap between cancer treatment and the appearance of valve disease is 23 years, which means many patients don’t connect the two. The risk increases in a dose-dependent way, rising linearly above a certain threshold. Up to 26 percent of people who received chest radiation show valve damage at 10 years, and that figure climbs to 60 percent at 20 years.
Radiation primarily affects the left-sided valves (aortic and mitral), likely because the higher pressures on that side of the heart compound the damage to already fragile tissue. Leaking of the aortic valve is the most common finding, followed by aortic narrowing.
Connective Tissue Disorders
Genetic conditions that weaken connective tissue can make heart valves floppy and prone to leaking. Marfan syndrome is the best-known example. It’s caused by a mutation in fibrillin 1, a protein that gives elastic tissues their structure. Researchers initially thought the problem was purely structural, like building a bridge with substandard cables. But later discoveries showed that the mutation also disrupts a signaling pathway that controls how connective tissue develops and repairs itself. The result is valves that are too stretchy and don’t hold their shape under pressure, along with a widened aorta that can further distort the aortic valve.
Related conditions like Loeys-Dietz syndrome and Ehlers-Danlos syndrome cause similar valve problems through overlapping mechanisms involving the same signaling pathway.
Who Is More Affected
Most types of valve disease are more common in men than in women, with a few notable exceptions. Tricuspid regurgitation, mitral stenosis, and pulmonary stenosis are more prevalent in women. Women who develop aortic valve narrowing tend to have less calcium on their valves and more fibrous tissue compared to men with the same severity, suggesting the disease progresses through slightly different pathways depending on sex.
Race also plays a role. African Americans are less likely to have a bicuspid aortic valve and present less often with aortic stenosis overall. Rheumatic valve disease, while rare in wealthy nations, remains a major cause of valve problems in sub-Saharan Africa, South Asia, and the Pacific Islands, where access to treatment for strep throat is limited.
How Valve Disease Is Staged
Doctors classify valve disease into four stages based on how much the valve has changed, how well the heart is coping, and whether symptoms have appeared. Stage A means you have risk factors (like a bicuspid valve or high blood pressure) but no actual valve dysfunction yet. Stage B is progressive disease, where the valve is mildly or moderately abnormal but you feel fine. Stage C means the valve meets criteria for severe disease, though you may still have no symptoms. Your heart may be compensating well (C1) or starting to strain (C2). Stage D is when symptoms like shortness of breath, chest pain, or fatigue have developed because the valve can no longer keep up.
This staging system matters because treatment decisions, particularly the timing of valve repair or replacement, hinge on which stage you’re in. Many people live at Stage B for years with monitoring alone, while others progress to Stage D and need intervention relatively quickly.