Coronary Artery Calcium (CAC) Screening
A coronary artery calcium (CAC) score measures calcified plaque in your coronary arteries using a specialized CT scan—making it one of the few tools that gives direct, imaging-based evidence of whether atherosclerosis is already present in your body.
That's exactly what makes it so valuable. And exactly what makes interpretation so critical.
A CAC score is powerful evidence, but it has specific blind spots. A score of 0 can be falsely reassuring without the right context. A score of 20 in one patient may carry very different implications than the same score in another because of their differences in age, gender, ethnicity, other biomarkers, and other clinical conditions. Understanding what your result means, and what it doesn't, requires looking at the full picture.
This guide covers:
• What a CAC scan measures and its inherent limitations
• Who should get screened, per guidelines and beyond
• Why a CAC score of 0 is not necessarily an all-clear
• How CAC connects with Lp(a), LDL-P, ApoB, GlycA, and hsCRP
What Is a CAC Scan?
CAC screening uses a CT scanner to detect and quantify calcium deposits in the walls of the coronary arteries. Calcium is a marker of hardened, advanced atherosclerotic plaque which is soft plaque (not visibile in CAC screening) that has been present long enough to mineralize.
The test is fast (10-15 minutes), non-invasive, requires no contrast dye, and delivers a low radiation dose roughly equivalent to a mammogram. Most imaging centers offer it for $100-200 out of pocket, without a physician's order in most states.
The output is an Agatston score which is a standardized numerical measure of calcified plaque burden. A score of 0 means no calcified plaque was detected. Higher scores reflect progressively more extensive calcification.
Who Should Get a CAC Scan?
The clinical standard
The 2019 ACC/AHA prevention guidelines recommend CAC as a decision-making tool for intermediate-risk patients who are those with a 10-year ASCVD risk between 7.5% and 20% where the decision to start statin therapy is genuinely uncertain. A high CAC supports initiating therapy; a score of zero often supports deferring it.
CAC is also considered for borderline-risk patients (5-7.5% 10-year risk) when additional risk-enhancing factors are present: family history of premature heart disease, elevated Lp(a), metabolic syndrome, or chronic inflammatory conditions.
Beyond the guidelines: who else benefits
Traditional risk calculators have real limitations. They were built on population-level data and don't fully account for factors that significantly affect individual risk:
Strong family history of premature cardiovascular disease. A first-degree relative with an MI before age 55 (men) or 65 (women) raises concern for inherited risk that standard calculators underweight. CAC can clarify whether that genetic predisposition has translated into actual disease.
Elevated Lp(a). Present in roughly 1 in 5 people, elevated Lp(a) is an inherited cardiovascular risk factor with limited treatment options. Because Lp(a) drives non-calcified plaque specifically, knowing the Lp(a) level upfront changes how you interpret the CAC result.
Insulin resistance and metabolic dysfunction. Prediabetes, elevated fasting insulin, and metabolic syndrome accelerate atherogenesis in ways that 10-year calculators often underestimate. CAC can serve as a reality check.
People reconsidering lipid-lowering therapy. Whether considering stopping a current prescription or hesitant to start one, concrete imaging evidence often helps resolve the uncertainty.*
* We do not recommend stopping any lipid-lowering therapy without extensive consultation with your healthcare provider.
Who probably doesn't need one (yet)
Very low-risk adults (10-year ASCVD < 5%) without significant family history are unlikely to benefit. Adults under 35-40 rarely have detectable calcification. Patients already on high-intensity statin therapy where the result wouldn't change management don't add much by scanning.
What a CAC Score Measures and Its Limits
CAC scores are interpreted against two benchmarks. What matters is both (1) the absolute number and (2) where your score falls relative to others your age, sex, and ethnicity, because a score of 80 means something very different for a 45-year-old woman than a 68-year-old man.
| CAC Score | Clinical Significance |
|---|---|
| 0 | No detectable calcified plaque — generally reassuring, with an important caveat* |
|
>0 to 75th percentile
for your age, sex & ethnicity
|
Subclinical atherosclerosis confirmed; vascular disease is established |
|
>75th percentile
or ≥300 AU
|
Extensive burden — at this threshold, guidelines treat this as the clinical equivalent of a prior cardiovascular event1 |
1 Grundy SM et al. 2018 AHA/ACC Guideline on the Management of Blood Cholesterol. J Am Coll Cardiol. 2019;73(24):e285–e350.
Want to know where your score lands for your age, sex, and ethnicity? The MESA Coronary Artery Calcium Percentile Calculator lets you look it up directly.
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What a CAC Score Measures and Its Limits
Before diving into score interpretation, it's essential to understand what CAC measures and doesn't measure.
CAC quantifies calcified plaque which is arterial plaque that has hardened and mineralized. This is a marker of established, advanced atherosclerosis. In that sense, it's backward-looking: it shows you a fire that's already been burning for years, not the fuel that's currently accumulating.
What CAC cannot detect is non-calcified (soft) plaque. Soft plaque is the earlier-stage, lipid-rich plaques that haven't yet hardened. Soft plaque is often more vulnerable to rupture and is closely associated with acute cardiovascular events, including sudden heart attacks in people with no prior symptoms.
Several common risk factors preferentially drive non-calcified plaque. This distinction is central to understanding why CAC must always be interpreted alongside other biomarkers covered in detail further below.
CAC = 0: What It Means, and What It Doesn't
A score of 0 is generally excellent news. In the landmark MESA cohort, adults with CAC = 0 had roughly a 3% 10-year cardiovascular event rate, compared to 14% for those with CAC > 100. In intermediate-risk patients, a zero score is often the strongest available evidence to support deferring statin therapy.
The concept of a "warranty period" captures this well: for most adults, CAC = 0 is reassuring for approximately 5-7 years. The scan doesn't need to be repeated until risk factors change meaningfully or that window passes.
But CAC = 0 is not a clean bill of health. Here's what a zero score cannot rule out:
Elevated Lp(a) and non-calcified plaque. Lp(a) drives lipid-rich, non-calcified plaque. This kind of plaque is missed by CAC screening. Someone with a CAC of 0 and an Lp(a) of 200 nmol/L may have significant atherosclerotic burden that simply hasn't calcified yet. In this setting, a zero score is not reassuring without knowing the Lp(a) level.
Active atherogenic particle burden (LDL-P / ApoB). CAC is a snapshot. If your LDL-P particle count or ApoB is elevated today, atherogenic particles are actively penetrating the arterial wall right now. A CAC = 0 today is not a guarantee of CAC = 0 in five years, especially with untreated high ApoB of 120+ mg/dL.
Inflammation (GlycA / hsCRP). Cardiovascular events aren't driven by plaque alone. They're triggered by inflammation destabilizing that plaque. The JUPITER trial showed that patients with CAC = 0 and elevated hsCRP (> 2 mg/L) still had meaningfully higher event rates than those with both CAC = 0 and normal hsCRP. Inflammation matters independently.
Insulin resistance (LP-IR / HOMA-IR). Metabolic dysfunction accelerates atherogenesis, often faster than risk calculators project. In someone with significant insulin resistance (elevated fasting insulin, impaired glucose tolerance, fatty liver) a CAC = 0 may have a shorter warranty period than population averages suggest.
The bottom line: A zero is a data point, not a verdict. Its meaning depends heavily on what else is going on in the rest of your cardiometabolic risk profile.
CAC + Biomarkers: The Complete Picture
CAC and labdrawn biomarkers are not redundant—they're complementary. CAC shows you the fire that's already burning. Biomarkers show you the fuel, the accelerants, and the inflammatory conditions that determine whether a new fire is starting and how fast it's spreading.
LDL-P and ApoB: The atherogenic fuel
ApoB or LDL-P particle count, measures the concentration of atherogenic particles in circulation. Every one of these particles can penetrate the arterial wall and contribute to plaque. In patients with high CAC, elevated ApoB signals that the established disease is being actively driven by ongoing particle burden. In patients with low or zero CAC, elevated ApoB means the underlying driver hasn't been addressed, even if the damage so far is limited.
Treatment decisions for lipid-lowering therapy like statins, ezetimibe, Nexlizet, or PCSK9 inhibitors, are best made by combining CAC and ApoB or LDL-P in the overall context of a Cardiometabolic Risk Assessment.
Lp(a): The hidden driver of soft plaque
Approximately 20% of the population carries an elevated Lp(a), almost entirely due to genetics. Unlike standard LDL, Lp(a) has pro-inflammatory and pro-thrombotic properties and preferentially drives non-calcified, lipid-rich plaque.
This creates a systematic interpretation problem: in high-Lp(a) individuals, CAC scans underestimate true atherosclerotic burden. Lp(a) should be measured at least once in every adult, independent of their CAC result. In those with elevated levels, the CAC number must be read in that context.
GlycA or hsCRP: The inflammatory dimension
GlycA and high-sensitivity C-reactive protein (hsCRP) measure systemic inflammation which is a key driver of plaque destabilization and acute events. The combination of high CAC + elevated inflammatory markers is associated with the highest near-term cardiovascular event risk of any combination. Even at CAC = 0, high inflammation carries measurable residual risk. Inflammation is a co-driver of events that imaging alone cannot capture.
Fasting insulin and metabolic markers
Insulin resistance is one of the most underappreciated drivers of cardiovascular risk. Elevated fasting insulin, impaired glucose tolerance, and HbA1c > 5.7% are early indicators that atherogenesis is being accelerated by metabolic dysfunction—often before it shows up in a CAC score. Addressing insulin resistance isn't just a diabetes prevention strategy; it's an independent component of cardiovascular risk reduction.
Frequently Asked Questions about Coronary Artery Calcium Scoring
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Yes. This is one of the most important things to understand about CAC screening. A score of 0 means no calcified plaque was detected, but it doesn't rule out non-calcified (soft) plaque, which is earlier-stage and often more prone to rupture. People with elevated Lp(a), high LDL particle counts (ApoB or LDL-P), or significant insulin resistance can have meaningful atherosclerotic burden that simply hasn't hardened yet. A zero is excellent news, but it needs to be read alongside the rest of your biomarker profile.
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There's no universal threshold that automatically triggers treatment. It depends on your age, ethnicity, gender, other risk factors, and what biomarkers show. That said, a CAC score above 100 is generally considered significant enough to support starting statin therapy in most adults, and a score above 300 (or above the 75th percentile for your age and sex) typically warrants aggressive risk reduction. A score of 0 in an intermediate-risk patient often supports deferring statins. The score is most useful as a tie-breaker alongside your full risk picture, not a standalone directive.
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Most guidelines suggest that a score of 0 provides reassurance for approximately 5–7 years. This is sometimes referred to as the "warranty period." After that window, or sooner if your risk factors change significantly, a repeat scan may be worthwhile. For those with elevated scores, repeat scanning is sometimes used to track plaque progression, though the value of serial testing is still an active area of research. Your physician can help determine the right interval based on your overall risk profile.
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Usually not, though this is changing. Most commercial insurance plans and Medicare don't routinely cover CAC screening outside of specific clinical criteria. The good news is the test is inexpensive and typically $100–200 out of pocket at most imaging centers. It typically doesn't require a physician's order in most states. You can often schedule it directly. You can find a list of noninvasive imaging centers here or use a resource like the MESA CAC center locator to find a location.
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They measure very different things. A stress test evaluates how well your heart functions under exertion. It is good at detecting significant blockages that are already affecting blood flow. A CAC scan evaluates structure. Different than a stress test, it shows whether plaque has formed in your coronary arteries, even before any blockage or symptoms exist. CAC is a screening tool for detecting early or subclinical atherosclerosis; a stress test is more appropriate when symptoms like chest pain or shortness of breath are already present. Most people who benefit from CAC screening would have a normal stress test.
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This is the most common situation. A CAC score without the context of your lipid particle counts, inflammatory markers, Lp(a), and metabolic health, and other risk factors, only tells part of the story. The number itself doesn't tell you whether your LDL is actively building more plaque, whether inflammation is destabilizing what's there, or whether genetic factors like elevated Lp(a) are driving risk that the scan can't see. The Precision Health Reports Cardiometabolic Risk Assessment was built to answer exactly this: what does your CAC score actually mean, given everything else going on?
Putting It All Together
A CAC scan is best understood as one imaging piece of a multi-dimensional risk assessment. It answers: "Has atherosclerosis already formed?" But it can't answer: "Is it actively forming right now?" This is better addressed by ApoB and LDL-P and best addressed by a comprehensive Cardiometabolic Risk Assessment. A CAC score alone can't answer: "Am I at risk despite clean imaging?".
The Precision Health Reports Cardiometabolic Risk Assessment was designed specifically to integrate your CAC score with the biomarkers that give it meaning. Your result is placed in the context of your lipid particle counts, inflammatory markers, metabolic indicators, and genetic risk factors — with guideline-driven, outcome-proven recommendations for what to do next.
References
1. Detrano R, et al. Coronary arterial calcium and the 10-year incidence of coronary heart disease (MESA). New England Journal of Medicine, 2008.
2. Ridker PM, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein (JUPITER). New England Journal of Medicine, 2008.
3. Grundy SM, et al. 2018 AHA/ACC Guideline on the Management of Blood Cholesterol. Journal of the American College of Cardiology, 2019.
4. Blaha MJ, et al. Importance of coronary artery calcium zero for decision making in MESA. Journal of the American College of Cardiology, 2016.
5. Budoff MJ, et al. Non-calcified plaque identification by coronary computed tomography angiography in intermediate-risk patients. Journal of the American College of Cardiology, 2007.