Carotid artery calcification (CAC) is the buildup of calcium deposits within the walls of the carotid arteries, the major blood vessels supplying oxygenated blood to the brain and head. This process indicates widespread atherosclerosis, the hardening and narrowing of arteries throughout the body. The presence of calcified plaques signals a heightened risk for serious cerebrovascular events, most notably stroke. Because CAC often produces no symptoms until advanced, its detection is important for assessing cardiovascular health and implementing preventive measures.
Understanding Carotid Calcification
The carotid artery system consists of two common carotid arteries, one on each side of the neck, which split into internal and external branches. The internal carotid artery is the primary source of blood flow to the brain. Calcification occurs as part of atherosclerosis, where fatty deposits and cellular debris accumulate in the inner lining of the artery wall (tunica intima).
This accumulation forms plaque. Over time, calcium salts are deposited within this plaque, transforming it from a soft lesion into a hardened, calcified one. This hardening reduces the artery’s flexibility and causes stenosis, which is the narrowing of the vessel, restricting blood flow to the brain. The presence of calcified plaque is a marker of long-standing, advanced arterial disease.
The composition of the plaque influences the risk of a stroke. Soft, lipid-rich plaques are often described as “vulnerable” because they can rupture easily, releasing debris that can travel to the brain and block smaller vessels. Large, dense calcifications may confer greater mechanical stability to the plaque, potentially making it less likely to break apart. However, calcification is also a marker for a large overall plaque burden, which contributes to the narrowing of the artery and poor blood flow.
Identifying the Causes
Carotid artery calcification develops due to a combination of unmodifiable and modifiable risk factors that promote atherosclerosis. Advancing age is the most consistent unmodifiable factor, as the probability of developing calcification increases significantly after age 40. Genetic predisposition and a family history of cardiovascular disease also increase susceptibility.
The progression of CAC is strongly influenced by several modifiable health conditions. High blood pressure (hypertension) damages the inner lining of the arteries, encouraging the inflammatory process that precedes plaque formation. High levels of low-density lipoprotein (LDL) cholesterol and triglycerides (dyslipidemia) provide the fatty material that accumulates within the artery walls.
Chronic inflammation, often driven by smoking and diabetes, accelerates the calcification process. Tobacco smoke toxins directly irritate the arterial lining, while diabetes impairs fat processing and increases overall inflammation. Obesity and a sedentary lifestyle compound these effects by contributing to hypertension, high cholesterol, and diabetes. Chronic kidney disease is also linked to a higher prevalence of vascular calcification, including in the carotid arteries.
Screening and Diagnosis
CAC is often considered a silent disease because most people do not experience symptoms until the artery is severely narrowed or a stroke occurs. When symptoms appear, they manifest as a transient ischemic attack (TIA) or a full stroke. These events present with sudden weakness, numbness on one side of the body, slurred speech, or temporary vision loss. Early detection relies heavily on medical imaging.
The gold standard for initial screening is the carotid duplex ultrasound, a non-invasive test using sound waves to image the arteries and measure blood flow velocity. This technique allows providers to visualize the plaque, assess the degree of stenosis, and determine the plaque’s composition for risk stratification. Advanced imaging modalities like Computed Tomography Angiography (CTA) and Magnetic Resonance Angiography (MRA) offer more detailed views of the plaque and the extent of calcification.
Carotid calcifications are often discovered incidentally during routine dental panoramic X-rays. The X-ray covers the jaw and neck, sometimes capturing the calcified deposits near the angle of the jaw as distinct, irregular masses. If found, this warrants immediate referral for a dedicated vascular ultrasound to confirm the presence and severity of the condition.
Management and Prevention Strategies
The primary goal of managing carotid artery calcification is to stabilize existing plaques and prevent new ones from forming, reducing the risk of stroke or heart attack. This approach focuses on controlling underlying risk factors through lifestyle changes and medical therapy. Lifestyle modifications are the core element of treatment and prevention for all patients with CAC.
Lifestyle Modifications
A heart-healthy diet, low in saturated and trans fats, cholesterol, and sodium, helps control blood pressure and lipid levels. Regular physical activity and maintaining a healthy body weight improve overall cardiovascular function. Smoking cessation is the most impactful intervention, as it immediately reduces arterial irritation and inflammation.
Pharmacological Management
Medications are initiated to reduce the risk of plaque progression and clot formation. Statins are frequently prescribed as intensive lipid-lowering therapy, aiming for low LDL cholesterol levels to stabilize existing plaques. Antiplatelet medications, such as daily low-dose aspirin, are used to reduce platelet stickiness, lowering the chance of a dangerous clot forming. Blood pressure medications are also administered to ensure blood pressure remains within a healthy range, minimizing damage to the artery walls.
Invasive Procedures
Invasive procedures may be considered for patients with severe carotid artery stenosis (typically 70% blockage or more) or those who have experienced a TIA or stroke. Carotid endarterectomy is a surgical procedure where the artery is opened to remove the plaque buildup directly. An alternative is carotid angioplasty and stenting, which involves using a balloon to widen the narrowed artery and placing a mesh tube (stent) to keep the vessel open. These revascularization options are reserved for high-risk cases where the severity of the blockage outweighs the procedural risks.