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Most people who have a heart attack never saw it coming. They had no symptoms, no warning, and often no prior diagnosis of heart disease. The coronary artery calcium score exists precisely to change that equation. It is one of the most powerful tools in preventive cardiology for finding silent disease before it becomes a catastrophic event, and it does so with a single, low-radiation CT scan that takes minutes to perform.
What makes it remarkable is not just that it detects plaque, but that it quantifies it. The resulting number, called the Agatston score, maps directly onto real-world event rates in ways that traditional risk calculators simply cannot match. Understanding your score is, in many respects, understanding your cardiovascular future.
Coronary artery calcium (CAC) scoring measures the total amount of calcified atherosclerotic plaque across all of the coronary arteries, the vessels that supply the heart with blood. Atherosclerosis, the process by which fatty and inflammatory material builds up inside artery walls, eventually leads to calcification of those deposits. Calcium in the arteries is therefore a reliable marker of cumulative plaque burden, essentially a record of how much arterial damage has accumulated over a lifetime.
The scan is performed using a non-contrast, ECG-gated CT, meaning no dye injection is needed and the imaging is timed to the heartbeat to reduce motion blur. The resulting Agatston score is calculated by multiplying the area of each calcified deposit by a density weighting factor, then summing the results across every coronary artery. The score ranges from 0, meaning no detectable calcified plaque, to well over 1,000 in cases of extensive disease. A score of zero is not merely reassuring; it is, as the research literature has come to call it, a demonstration of the "power of zero."
The predictive power of CAC scoring is robust and consistent across populations. In the Multi-Ethnic Study of Atherosclerosis (MESA), which followed 6,814 asymptomatic adults over approximately 11 years, ASCVD event rates rose in a stepwise fashion with increasing CAC scores. Critically, each doubling of the CAC score was associated with approximately a 14% increase in risk, a relationship that held independent of traditional cardiovascular risk factors and across sex and racial groups.
The score categories translate into clinically meaningful risk bands. A score of zero is associated with very low 5 to 10 year event rates, typically below 1 to 5%. In patients presenting with stable chest pain, a CAC of zero corresponded to a MACE (major adverse cardiovascular events) rate of approximately 0.5% over 3.5 years, along with very low rates of obstructive coronary artery disease. Scores between 1 and 100 indicate mild atherosclerosis with risk elevated above zero but generally below thresholds that would independently drive treatment decisions. Scores from 101 to 300 are associated with 10-year ASCVD risk typically exceeding 7.5%, which is the conventional threshold supporting statin therapy. At CAC scores of 300 to 400 and above, 10-year ASCVD event rates in population cohorts range from approximately 13% to 26%, and in the stable chest pain cohort, a CAC above 400 corresponded to a MACE rate of approximately 6.8%, with high rates of obstructive disease and revascularization.
| Agatston Score | Plaque Burden | Approximate 10-Year ASCVD Risk | Clinical Implication |
|---|---|---|---|
| 0 | None detectable | Very low, typically <1–5% | "Power of zero"; supports deferral of statin in borderline-risk patients |
| 1–100 | Mild | Elevated above zero, generally below treatment threshold | Risk-factor modification; statin decision depends on other factors |
| 101–300 | Moderate | Often >7.5% | Strong support for statin therapy |
| ≥300–400+ | High | 13–26% in population cohorts | Intensive prevention; equivalent to established coronary artery disease |
CAC scoring also adds predictive information beyond what traditional risk calculators can provide. A systematic review and meta-analysis published in JAMA Internal Medicine confirmed that CAC scores provide incremental value in cardiovascular risk assessment above and beyond standard risk factors. This matters most in patients at intermediate risk, where the decision to start preventive medications is genuinely uncertain, and a CAC score can meaningfully tip the clinical decision one way or the other.
Even in patients who have already had a heart attack, CAC score retains prognostic value. Among acute myocardial infarction patients, those in the top quartile of CAC burden (scores above approximately 5,300) experienced substantially more MACE even after statistical adjustment for other risk factors.
One important caveat: CAC does not measure non-calcified or soft plaque, and it does not directly assess whether an artery is blocked. Up to 14% of patients with flow-limiting stenoses may have a CAC score of zero, which means the test should not be used in isolation to rule out obstructive coronary artery disease in symptomatic patients.
On the methodological frontier, researchers have found that separately modeling calcium volume and density, rather than relying solely on the composite Agatston score, can modestly improve risk prediction. Artificial intelligence applied to CAC scans has also shown promise in further enhancing cardiovascular event prediction, potentially extracting additional prognostic signal from the same imaging data.