Calcification of the heart is the buildup of calcium deposits in the heart’s arteries, valves, or surrounding tissue. These deposits are made of a mineral called hydroxyapatite, the same substance found in bones and teeth. Over time, this buildup stiffens the affected structures, restricting blood flow or impairing valve function. It’s extremely common as people age, and many people live with mild calcification for years without knowing it.
Where Calcification Occurs in the Heart
Calcium can accumulate in several different parts of the heart, and the location matters because each type produces different problems.
Coronary artery calcification is the most frequently discussed form. Calcium deposits build up inside the walls of the arteries that supply blood to the heart muscle, typically within fatty plaques (atherosclerosis). As the deposits grow, they stiffen the artery walls and can narrow the channel blood flows through. This is the type measured by a coronary calcium scan.
Heart valve calcification most often affects the aortic valve, which controls blood flow from the heart to the rest of the body. Early on, calcium causes mild thickening of the valve leaflets, a condition called aortic valve sclerosis. Over time, heavier deposits stiffen the leaflets so much they can’t open fully, a condition called aortic stenosis. The mitral valve, which sits between the heart’s upper and lower left chambers, can also calcify, though this is less common. Both coronary artery disease and valve calcification share overlapping risk factors like high cholesterol, high blood pressure, and male sex, and the early stages of both involve lipid accumulation and inflammation.
Pericardial calcification affects the sac surrounding the heart. It’s rarer and usually results from prior infection or inflammation. When severe, the rigid, calcified pericardium can squeeze the heart and prevent it from filling properly.
What Causes Calcium to Build Up
Heart calcification isn’t simply a matter of eating too much calcium. It’s driven by disruptions in how your body handles minerals, combined with damage to blood vessel and valve tissue.
The process begins when smooth muscle cells in the artery or valve walls are exposed to excess phosphate or calcium in the blood. High phosphate levels trigger these cells to either die or transform into bone-like cells that actively deposit minerals. In a sense, the soft tissue starts behaving like bone. The formation of calcium-phosphate crystals can also happen passively, without any cellular activity at all, simply because the mineral concentrations in the blood are too high.
Under normal conditions, your body produces natural inhibitors that prevent calcium from settling in soft tissue. When those protective mechanisms fail, or when phosphate levels climb, calcification accelerates.
The major risk factors include:
- Age: Calcification becomes increasingly common after 60 and is nearly universal in older adults to some degree.
- Chronic kidney disease (CKD): Failing kidneys can’t excrete phosphate properly, leading to high blood phosphate levels. CKD also disrupts vitamin D activation, parathyroid hormone regulation, and other mineral-balancing systems. Vascular calcification is one of the leading causes of cardiovascular death in CKD patients.
- High cholesterol and high blood pressure: Both contribute to arterial damage that sets the stage for calcium deposits.
- Vitamin D deficiency: Low vitamin D can worsen the lining of blood vessels, making them more vulnerable to calcification. This is especially relevant in people with kidney disease, where vitamin D deficiency is common due to reduced kidney function.
- Diabetes and smoking: Both accelerate vascular damage and inflammation.
Symptoms and When They Appear
Mild to moderate heart calcification often causes no symptoms at all. Many people discover it incidentally during imaging for another condition. This silent phase can last years or even decades.
Coronary artery calcification typically only produces symptoms when the narrowing becomes severe enough to limit blood flow. At that point, you might notice chest pain or pressure during physical activity, shortness of breath, or unusual fatigue.
Valve calcification, particularly aortic stenosis, follows a similar pattern. Early stages are silent. As the valve stiffens and the opening narrows, symptoms emerge gradually: shortness of breath during exertion, chest tightness, dizziness or fainting during activity, fatigue that worsens with exercise, and a rapid or fluttering heartbeat. In advanced stages, aortic stenosis can lead to heart failure, loss of consciousness, and in some cases, sudden death. The progression from “no symptoms” to “serious problem” can happen slowly, which is why regular monitoring matters once calcification is detected.
How It’s Detected and Measured
A CT scan of the heart is the primary tool for detecting and quantifying coronary artery calcification. The scan produces a number called a coronary artery calcium (CAC) score, measured in Agatston units. This score reflects how much calcium is present in your coronary arteries and helps predict your risk of future heart events.
The score breaks down into straightforward risk categories:
- 0: Very low risk of significant coronary artery disease.
- 1 to 10: Low probability.
- 11 to 100: Mild coronary narrowing likely present.
- 101 to 400: Non-obstructive disease is likely, and significant blockages are possible.
- Above 400: High likelihood of at least one major coronary artery obstruction.
These categories help guide decisions about whether to start or intensify cholesterol-lowering treatment. A score of zero is reassuring but doesn’t guarantee zero risk permanently.
For valve calcification, echocardiography (ultrasound of the heart) is the standard tool. It shows how well the valve opens and closes, how thickened the leaflets are, and whether blood flow is obstructed. CT scans can also detect valve calcium and provide additional detail about vessel walls, including thickening and the presence of blood clots.
Can Heart Calcification Be Reversed?
No current treatment can dissolve or remove existing calcium deposits from the coronary arteries or heart valves. Once the mineral has been laid down, it stays. The goal of treatment is to slow the progression of calcification and reduce your overall risk of a heart attack or other cardiovascular event.
Statins, the most widely prescribed cholesterol-lowering drugs, are a key part of that strategy. They substantially lower LDL cholesterol and reduce cardiovascular events. However, their effect on calcium scores is more complicated. A 2023 systematic review and meta-analysis of randomized trials found that statins did not significantly reduce coronary calcium scores over an average follow-up of about 1.25 years. Some research has even suggested statins might paradoxically accelerate calcification through a separate mechanism, though this hasn’t been shown to increase heart attack risk. The working theory is that statins may stabilize dangerous soft plaques by converting them into denser, more calcified plaques that are less likely to rupture, a trade-off that favors safety even if the calcium score rises.
Lifestyle changes remain foundational: regular physical activity, a heart-healthy diet, not smoking, and managing blood pressure and blood sugar. For people with chronic kidney disease, controlling phosphate levels through diet and medications is critical to slowing vascular calcification. Vitamin D supplementation has shown promise in protecting blood vessel linings and may help reduce calcification in CKD patients with vitamin D deficiency.
When Surgery Becomes Necessary
Severe valve calcification that significantly obstructs blood flow often requires a procedure to restore normal heart function. For aortic stenosis, this typically means replacing the valve entirely, either through open-heart surgery or a less invasive catheter-based procedure where a new valve is threaded through a blood vessel and expanded inside the old one.
Mitral valve replacement in the setting of heavy calcification is more complex. Surgeons must carefully remove enough calcium to fit a replacement valve of adequate size, while avoiding damage to the surrounding heart muscle. A patch of tissue is often used to reinforce the area where calcium was removed, providing a secure anchor for the new valve and reducing the risk of calcium fragments breaking loose. This is considered a highly specialized operation.
For pericardial calcification that restricts the heart’s ability to fill, a procedure called decortication can strip away the rigid, calcified outer layer. This is uncommon and reserved for cases where the calcified pericardium is causing significant symptoms.