Coronary Artery Calcium (CAC) Score

The coronary artery calcium (CAC) score uses a non-contrast CT scan to directly quantify calcified plaque in the coronary arteries, producing an Agatston score that reflects the total burden of established, visible atherosclerosis. Unlike risk calculators that estimate probability from indirect factors like age, blood pressure, and cholesterol, CAC directly images disease already present in the arteries. The claim: a CAC score of zero indicates very low near-term cardiovascular risk, while an elevated score meaningfully reclassifies risk upward, even in people otherwise judged low or intermediate risk by standard calculators.

A large Multi-Ethnic Study of Atherosclerosis (MESA) analysis of 6,712 participants followed a median 16.7 years found the atherosclerotic cardiovascular disease event rate was 14.3 per 1,000 person-years with detectable CAC versus 4.1 per 1,000 person-years without any CAC, and CAC score was most strongly associated with increased risk precisely in low- and borderline-risk individuals (hazard ratio 1.35, 95% CI 1.22-1.50 in low-risk; 1.30, 95% CI 1.16-1.46 in borderline-risk) [1]. Adding the Agatston score to the standard pooled cohort equations improved the discrimination C-index from 0.593 to 0.640 in low-risk individuals and from 0.558 to 0.663 in borderline-risk individuals, and correctly reclassified 10.1% of low/borderline-risk individuals relative to standard risk equations using a 7.5% statin-eligibility threshold [1]. This is one of the largest and most direct demonstrations that CAC adds meaningful value specifically for people risk calculators might otherwise underestimate.

How to measure it: a low-dose, non-contrast CT scan of the heart, typically completed in under 15 minutes with no IV contrast needed, scored using the Agatston method based on calcium density and area [5]. A score of 0 indicates no detectable calcified plaque; scores are commonly categorized as 1-99 (mild), 100-399 (moderate), and 400+ (severe), with higher scores indicating a heavier established plaque burden [3].

How to intervene on it: CAC score itself does not reverse with treatment. Statins and other therapies stabilize plaque and can even modestly increase visible calcium density as soft, unstable plaque calcifies and becomes more stable, so a rising CAC score under treatment is not necessarily a treatment failure and can reflect plaque stabilization rather than progression of risk [4]. The clinical value of CAC lies mainly in one-time risk reclassification to guide whether to start statin therapy, not in tracking score changes over time as a treatment-response metric [2].

Critics note CAC involves radiation exposure, though a low dose comparable to several months of natural background radiation, and is not recommended for very low-risk younger adults where pretest probability of any calcium is already low, or for very high-risk patients where the test result is unlikely to change the treatment decision regardless [3]. It is best targeted at intermediate-risk adults where the test result can genuinely change the clinical decision, a framing Bryan Johnson's Blueprint protocol has cited in reporting its own zero CAC score as an n=1 data point [6].

The plain takeaway: CAC scoring directly visualizes existing coronary plaque and is one of the best-validated tools for reclassifying cardiovascular risk in people who appear low or borderline risk by standard calculators, but it is a one-time risk-stratification tool rather than a treatment-tracking metric, and a rising score under statin therapy does not necessarily mean worsening disease.