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If you want one number that captures how much atherosclerosis has actually accumulated in your heart arteries, this is it. PAV (percent atheroma volume) measures the proportion of your coronary artery wall that has been replaced by plaque, across the entire coronary tree. It is not a guess based on cholesterol numbers or a risk calculator. It is a direct image of disease.
Unlike a calcium score, which only sees the hardened, calcified pieces of plaque, total PAV captures both soft and calcified plaque. That distinction matters because soft, non-calcified plaque is often the kind most likely to rupture and cause a heart attack. Knowing your PAV is knowing what your arteries actually look like inside.
Total PAV comes from one of two imaging methods. The most common in preventive care is coronary CT angiography (CCTA), a non-invasive scan that uses contrast dye to map your coronary arteries. The other, intravascular ultrasound (IVUS), is invasive and used mainly during cardiac catheterization. Both yield a number expressed as a percentage of vessel volume occupied by plaque.
Why a percentage instead of a raw plaque volume in cubic millimeters? Because arteries differ in size. A small woman with the same absolute plaque burden as a tall man has more concerning disease, since the plaque takes up a larger share of her smaller arteries. PAV adjusts for vessel size, making it more comparable across people. Research on 1,479 patients found PAV less influenced by body surface area and sex than absolute plaque volume, which is why many imaging groups now prefer it as the primary metric for whole-heart plaque burden.
Stenosis (the narrowing of an artery by plaque) has been the traditional focus of cardiology for decades. But most heart attacks happen at sites that were not severely narrowed before they ruptured. Total plaque burden, regardless of whether any single spot is narrowed, turns out to be a stronger predictor of future events.
In a long-term study of 1,311 symptomatic patients, every 1% increase in PAV was independently associated with roughly 3 to 4% higher risk of death, heart attack, or unstable angina over seven years. The relationship held even when myocardial perfusion (blood flow to the heart muscle) looked normal, meaning PAV captured risk that other tests missed.
The most important finding from the research base: plaque burden is reversible, and reversal lowers your risk. A meta-analysis of randomized trials found that every 1% absolute decrease in atherosclerotic plaque volume was associated with roughly 25% lower odds of major adverse cardiovascular events. An earlier analysis put the figure at about 20% per 1% reduction. The direction is clear and the magnitude is large.
Going the other way is just as predictive. In a study of 1,166 patients tracked over years with serial CCTA, whole-heart plaque progression of about 1% per year or more was independently linked to higher rates of heart attack, stroke, and cardiac death. This 1%-per-year threshold is now used as a working definition of rapid progression.
What this means for you: a single PAV reading tells you where you stand, but the trajectory matters more. A 7% PAV that is stable across two years is a very different clinical picture than a 7% PAV that climbed from 4% in the same period.
In a study of 1,005 patients, higher overall cardiovascular risk factor burden (smoking, diabetes, hypertension, dyslipidemia) was tied to faster annual progression of total, calcified, and non-calcified plaque. The more risk factors you carry, the faster the plaque grows. The same pattern holds for genetic risk. In 288 patients followed long-term, higher polygenic risk scores (a measure of inherited cardiovascular risk based on many DNA variants) predicted both higher baseline PAV and greater progression over years.
Plaque burden is not just a problem for the large arteries it lives in. In 142 patients without prior coronary disease, the highest tertile of PAV was associated with lower microvascular resistance reserve, a measure of how well the smallest blood vessels in your heart respond to demand. This suggests that significant plaque buildup affects circulation throughout the heart, not just in the visibly diseased segments.
In diabetics, PAV carries particular weight. Among 1,311 patients studied with both CCTA and PET imaging, PAV remained an independent predictor of long-term events in people with diabetes even when their stress perfusion testing came back normal. A clean stress test does not exclude meaningful plaque burden.
There is no single universal cutpoint for PAV, and exact values vary by imaging method, software, and reader. The most widely cited research staging system, based on 303 patients with invasive angiography and fractional flow reserve data, divides PAV into four stages. Use these as orientation, not as fixed targets.
| Stage | PAV Range | What It Suggests |
|---|---|---|
| Stage 0 | 0% | No detectable coronary plaque |
| Stage 1 | Greater than 0% to 5% | Mild plaque burden, early disease |
| Stage 2 | Greater than 5% to 15% | Moderate plaque burden |
| Stage 3 | Greater than 15% | Extensive plaque burden, high event risk |
Source: Min et al. 2022, Journal of Cardiovascular Computed Tomography. These ranges come from CCTA-based research and should be compared within the same imaging lab and software over time for the most meaningful trend.
A separate study of 2,271 patients using AI-based quantification proposed a much lower safety cutpoint of 2.6% PAV, below which long-term acute coronary syndrome risk was very low. The takeaway: any detectable plaque represents disease, and the goal of prevention is to find and act on it early.
A single PAV reading is a snapshot. The real value comes from serial imaging. Research using annual change in PAV defines progression of 1% or more per year as rapid and clinically significant. Tracking lets you see whether your interventions are working, whether your trajectory is flat, slowing, or reversing.
A sensible cadence for someone actively managing cardiovascular risk: a baseline CCTA in your 40s if you have any risk factors (or earlier with strong family history), a follow-up scan in 2 to 3 years if you are making lifestyle or medication changes, then every 3 to 5 years thereafter. The interval is longer than for blood tests because plaque changes slowly and the imaging involves contrast and radiation exposure.
Finding measurable plaque should not just sit in a report folder. It should trigger a decision pathway. The first move is to characterize your overall lipid and inflammatory picture. Order ApoB (the count of all cholesterol-carrying particles that can lodge in artery walls), Lp(a) (an inherited cholesterol particle that drives plaque independently of standard lipids), and hs-CRP (a marker of vascular inflammation). Combined with PAV, these tell you what is fueling the plaque so you can target it.
For a PAV in Stage 2 or higher, working with a preventive cardiologist or lipidologist is reasonable. Standard primary care often does not push lipid targets aggressively enough for people with documented plaque. Evidence-based goals for someone with established atherosclerosis include ApoB well below 60 mg/dL and LDL cholesterol well below 70 mg/dL, often requiring combination therapy.
If your PAV is rising despite treatment, the workup should include checks for under-treated drivers: poorly controlled blood pressure, elevated Lp(a), elevated hs-CRP, or unrecognized insulin resistance. A statin alone may not be enough. Adding ezetimibe, a PCSK9 inhibitor, or addressing inflammation directly may be warranted.
PAV is a robust imaging metric, but a few factors can distort a single reading:
Evidence-backed interventions that affect your Total PAV level
Total PAV is best interpreted alongside these tests.