Atherosclerosis is often discussed as though it were one thing: “plaque”. CT imaging shows a more complicated reality.
A plaque can contain calcium, fibrous tissue and lipid-rich material in different proportions. In twins, those components do not necessarily show the same genetic pattern — and that may change how we think about vascular ageing and prevention research.
Quick answer
Are calcified and noncalcified plaques equally genetic?
Not in the BUDAPEST-GLOBAL twin study. Calcified plaque volume showed a strong additive-genetic component in the model, while noncalcified plaque volume was explained predominantly by shared and unique environmental components. That finding needs replication and does not make one plaque type “genetic” and the other “caused by lifestyle”.
Key takeaways
- Plaque composition can be measured with coronary CT angiography.
- The 196-twin study estimated 78% additive genetic contribution to variation in calcified plaque volume.
- Noncalcified plaque volume was modelled with 63% shared-environment and 37% unique-environment components.
- The result is about variance between people in the study, not a causal percentage inside one artery.
- Different plaque phenotypes may reflect partly different biology and should not be merged into one genetic label.
Plaque is a structure, not a single substance
Atherosclerotic plaque develops within the artery wall and can include lipid-rich material, fibrous tissue and calcium. Coronary CT angiography can estimate the volume of calcified and noncalcified components.
Coronary artery calcium scoring is related to this process but is not a complete inventory of all plaque. A person can have noncalcified plaque even when calcium burden is low.
The BUDAPEST-GLOBAL natural experiment
Researchers studied 196 twins, including monozygotic and same-sex dizygotic pairs, with coronary CT angiography. None had known coronary artery disease at enrolment.
By comparing similarity across twin types, structural-equation models estimated additive genetic, shared environmental and unique environmental components for different plaque measurements.
A remarkable split between calcified and noncalcified plaque
For calcified plaque volume, the best-fitting model assigned 78% of variance to additive genetic effects and 22% to unique environment. For coronary calcium score, the corresponding genetic estimate was 58%.
Noncalcified plaque volume showed no additive-genetic component in the reported main model: 63% of variance was assigned to common environment and 37% to unique environment. The contrast is scientifically provocative because all three measurements sit inside the broad umbrella of coronary atherosclerosis.
What the study cannot tell us
The result does not mean a person can calculate how much of their plaque came from genes or lifestyle. It also does not prove that noncalcified plaque can simply be removed by changing behaviour.
Twin models rely on assumptions and estimates from a particular sample. Medication, age, risk-factor history and measurement choices matter. Replication in larger and more diverse cohorts is essential.
TwinPare perspective: precision begins by naming the phenotype correctly
One reason health information becomes misleading is that broad labels hide biological differences. “Atherosclerosis” contains multiple measurable traits, just as “bone health” contains more than bone density.
Twin research becomes more powerful when the phenotype gets more precise. Instead of asking whether atherosclerosis is inherited, researchers can ask which part of plaque biology shows genetic similarity — and which part diverges.
Source notes
The source has been verified and editorially reviewed for this article. The limitations below show which level of conclusion the sources support.
- [drobni-2022] Heritability of Coronary Artery Disease: Insights From a Classical Twin Study Zsofia D Drobni et al.. Circulation: Cardiovascular Imaging, 2022. Evidence type: Prospective coronary CT angiography twin study of 196 adult twins Limitation: Model estimates differed sharply by plaque phenotype: calcified measures had stronger genetic components, while noncalcified plaque volume was modelled predominantly by shared and unique environmental factors. These are population-level variance estimates. PubMed PMC DOI
Editorial source review
This section shows how the article's key factual claims are linked to the source.
Phrasings that require caution
- Do not infer individual causation from variance components.
- Do not call noncalcified plaque harmless or purely lifestyle-driven.
- Do not equate a calcium score with total coronary plaque burden.
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