A Coronary Artery Calcium (CAC) score is a measurement of the hardened, calcified plaque present in the walls of the heart’s arteries. The test uses a computed tomography (CT) scan to generate an Agatston score, which quantifies the total area and density of these calcium deposits. A higher score indicates a greater burden of coronary atherosclerosis, which is the underlying disease process that can lead to heart attacks. Patients often seek this test to understand their personal risk, and the immediate question that follows a positive result is whether this accumulation can be removed or reversed.
The Nature of Calcified Plaque and Reversal
The CAC score is highly effective because calcified plaque is a permanent marker of previously existing, soft, fatty plaque accumulation. Atherosclerosis begins with soft, vulnerable plaque composed of lipids and inflammatory cells, which can sometimes regress under intensive medical therapy. However, the CAC scan specifically detects the final stage of this process: the hardened calcium deposits. These calcified lesions function essentially as permanent scars within the artery walls, and current medical strategies cannot dissolve them.
The calcified plaque is biologically stable and inert, meaning it generally remains fixed in place. Therefore, the goal of treatment shifts away from reducing the existing score. Instead, the focus is on preventing the formation of new plaque and stabilizing any remaining soft, vulnerable plaque. The presence of a CAC score, particularly one over 400 Agatston units, is a strong predictor of future cardiac events.
Calcification itself is not the primary cause of a sudden cardiac event, but a sign of extensive disease. Soft plaques, which are often not detected by the CAC scan alone, are more dangerous because they have a thin fibrous cap that can rupture, triggering a blood clot. When therapeutic interventions cause these soft plaques to harden and calcify, the resulting plaque is more stable and less likely to rupture, which is a beneficial change even if the measured Agatston score increases slightly.
Non-Pharmacological Strategies to Limit Progression
While reversing established calcification is not feasible, non-pharmacological strategies can effectively halt disease progression and stabilize existing soft plaques. Dietary interventions are primary, with the Mediterranean diet being effective due to its anti-inflammatory properties and positive effects on endothelial function. This pattern emphasizes vegetables, whole grains, and healthy fats, while reducing saturated fats that contribute to harmful cholesterol levels.
Smoking cessation is the most impactful lifestyle change, as smoking severely damages the arterial lining and accelerates the atherosclerotic process. Maintaining a healthy weight and engaging in regular physical activity are also crucial for managing underlying risk factors like blood pressure and glucose levels. Studies show that keeping biomarkers like triglycerides, insulin, and body fat low is directly associated with a slower rate of calcification progression.
Specific micronutrients also play a role in calcium regulation. Vitamin K2, for instance, helps regulate calcium movement by activating Matrix Gla protein (MGP). This activated protein inhibits calcium from depositing in artery walls and directs it toward the bones. Research suggests that adequate Vitamin K2 intake may help slow the future progression of coronary artery calcification, particularly in high-risk individuals.
Clinical Interventions for Risk Reduction
For patients with a positive CAC score, clinical management focuses on reducing cardiovascular risk factors through prescribed medical therapy. Statins are the mainstay of this treatment, functioning beyond simple cholesterol reduction to actively stabilize existing atherosclerotic plaques. These medications convert vulnerable soft lesions into safer, hardened ones by reducing lipid content and increasing the fibrous, calcified component of the plaques.
Plaque stabilization by statins can sometimes lead to a paradoxical increase in the measured Agatston score over time. Clinicians interpret this increase as a sign that the treatment is working effectively to stabilize the disease, not that the patient’s condition is worsening. The primary goal of medical therapy is to lower low-density lipoprotein (LDL) cholesterol, with target levels often set below 70 mg/dL, or even below 50 mg/dL for those with extensive disease.
Managing hypertension and blood sugar is also a part of the risk reduction strategy. Blood pressure medications reduce mechanical stress on arterial walls, and strict control of blood glucose minimizes damage to the vascular endothelium in patients with diabetes. Regular clinical monitoring, including routine bloodwork and follow-up, ensures therapeutic goals are met to prevent dangerous outcomes of atherosclerosis, such as heart attack and stroke.