The Coronary Artery Calcium (CAC) score is a non-invasive screening tool that uses a computed tomography (CT) scan to detect calcium deposits in the walls of the coronary arteries, a direct sign of atherosclerosis or plaque buildup. The test provides a single numerical value, which is a powerful indicator of the extent of established coronary artery disease. A high score indicates significant disease burden, yet it does not automatically mean a person has an immediate physical blockage impeding blood flow. Understanding this distinction between the amount of calcified plaque and the severity of arterial narrowing is central to interpreting the test results and determining appropriate next steps.
Understanding the Calcium Score Measurement
The CAC score is quantified using the Agatston method, which calculates a weighted value based on the area and density of calcium found in the coronary arteries. Calcified lesions are identified on the CT scan as areas with a density above 130 Hounsfield units. The final score is the sum of these weighted values across all four major coronary arteries, reflecting the total burden of hardened, atherosclerotic plaque.
A score of zero signifies no detectable calcified plaque, correlating with a very low likelihood of a near-term cardiac event. Scores ranging from 1 to 100 indicate minimal to mild calcification. A score between 101 and 400 represents moderate calcification, placing the individual in a higher risk category. Scores exceeding 400 or especially 1,000 show extensive calcified plaque and are associated with a significantly elevated risk of future cardiovascular events.
Calcification Versus Stenosis
The core difference lies in the composition and stability of the plaque. Calcification, which the CAC score measures, represents older, more stable plaque that has developed a hard, mineralized shell. This hardened material is fixed within the artery wall and does not usually cause acute flow-limiting stenosis, which is a severe physical narrowing of the artery lumen.
Stenosis, or flow-limiting blockage, is often caused by soft, non-calcified, or unstable plaque. This vulnerable plaque has a thin fibrous cap and a lipid-rich core, making it prone to rupture. If this soft plaque ruptures, it can trigger a blood clot that rapidly blocks the artery, leading to a heart attack. Therefore, a person can have a very high CAC score, indicating a large burden of stable, calcified disease, without experiencing current flow obstruction.
Interpreting Risk When There Is No Blockage
A high CAC score, even without a severe physical blockage, is a powerful predictor of future cardiovascular events, including heart attack and stroke. The score serves as an independent marker of the total atherosclerotic burden, which is highly correlated with future problems. Individuals with a CAC score over 400 have a significantly increased risk of mortality and major adverse cardiac events compared to those with a score of zero. This prognostic value necessitates a change in therapeutic approach, as the score identifies patients who will benefit most from aggressive preventive interventions aimed at stabilizing the underlying disease.
Next Steps After a High Score
Receiving a high CAC score requires a comprehensive, tailored risk-reduction plan developed in consultation with a healthcare provider. The primary goal of management is to halt the progression of atherosclerosis and stabilize the existing plaque, preventing future acute events. Intensive lifestyle modifications form the foundation of this strategy, including adopting a heart-healthy diet and regular physical activity. Furthermore, smoking cessation and rigorous management of blood pressure and blood sugar levels are critical to slowing disease progression.
Pharmacological intervention is typically initiated or intensified with a high score. Statin therapy is recommended to lower low-density lipoprotein (LDL) cholesterol, often targeting a goal below 70 mg/dL, or even lower for very high scores. The use of low-dose aspirin may also be considered in certain patients to reduce the risk of clot formation, provided there are no contraindications for bleeding. These aggressive measures are designed to stabilize the underlying pathology and significantly reduce the likelihood of a future heart attack or stroke.