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How Does Age Affect Atherosclerosis? A Q&A Explainer

By: Peter Megdal PhD

How to Use This Article

Medical disclaimer: This article is for education only and is not medical advice. Always consult your clinician for personal guidance.

Easy Read

Does the risk of atherosclerosis increase as we age?

Yes. AtherosclerosisAtherosclerosis is the disease behind most heart attacks and many strokes. Cholesterol particles get stuck in the wall of an artery, the body sends immune cells to clean up, and over years that mess hardens into plaque. is considered a disease of aging. The likelihood and severity of plaquePlaque is the buildup of cholesterol, immune cells, scar tissue, and calcium inside an artery wall. buildup in the arteries increase with age, even when other risk factorsA risk factor is something that raises your chance of developing a disease — high cholesterol particles, high blood pressure, smoking, diabetes, family history. such as smokingSmoking damages the lining of your blood vessels, raises blood pressure, makes blood clot more easily, and speeds up plaque growth., high cholesterolCholesterol is a waxy substance your body needs. It goes into cell walls, hormones, vitamin D, and the bile that digests your food. You would die without it., or hypertensionHypertension is the medical term for high blood pressure. are controlled.

Research shows that by age 40, about half of adults have some form of atherosclerosis. By age 90, nearly everyone shows signs of it.
(Citation: Wang JC, Bennett MR. Circ Res. 2012;111(2):245–259.)

Atherosclerosis Progression

Adapted from Sports Plus Physio / Wikimedia Commons – educational reuse permitted.

Why does aging itself promote plaque buildup?

Aging affects the body’s cells, tissues, and immune system in several ways that make arteries more vulnerable to plaque formation.

  1. Vascular agingThe progressive structural and functional deterioration of arteries over time, characterized by loss of elasticity, increased stiffness, and accumulation of microscopic damage that makes arterial walls more susceptible to lipid deposition and chronic inflammation. – Over time, arteries lose elasticity and develop microscopic damage, making them more prone to lipid accumulation and inflammationInflammation is your immune system's response to injury or something it treats as an invader. It brings swelling, heat, and cleanup cells..
  2. Cellular senescenceCellular senescence is a state in which damaged cells permanently stop dividing but remain metabolically active, secreting inflammatory signals that can promote local tissue damage; in aging arteries, senescent cells cluster at plaque sites and contribute to chronic low-grade vascular inflammation. – Older cells stop dividing and repairing damage effectively. These senescent cellsCells that have permanently stopped dividing in response to stress or damage and instead secrete a cocktail of inflammatory cytokines, proteases, and growth factors; in the arterial wall, their accumulation with age drives chronic inflammation and accelerates plaque growth. release inflammatory chemicals that worsen plaque growth.
  3. Inflammation – Chronic, low-level inflammation (“inflammagingA chronic, low-grade, sterile inflammatory state that develops with advancing age as the immune system loses its ability to fully resolve acute inflammatory responses; in the arteries it promotes endothelial dysfunction, lipid retention, and plaque progression.”) contributes to arterial thickening and calcificationCalcification is when calcium gets deposited into a plaque, turning part of it hard and bony..

(Citations: Frismantiene A et al. Int J Mol Sci. 2023;24(24):17129; Zhang X et al. Ageing Res Rev. 2023;90:102041.)

Cellular Senescence Process

Adapted from Richardson et al., Cells (MDPI, open access).

How common is atherosclerosis in older adults?

Prevalence increases sharply with age:

  • 58% of adults aged 40–49
  • 87% of adults aged 60–69
  • Nearly 100% of adults over 90

These figures come from autopsy and imaging studies across decades of research.
(Citation: Roberts WC, Ferrans VJ. J Chronic Dis. 1961;14(6):614–631.)

Does plaque calcification increase with age?

Yes. Calcification, which makes plaques hard and brittle, accelerates with aging. The Agatston coronary artery calcium (CAC)Coronary artery calcium is a measure of calcified plaque deposits in the walls of the coronary arteries, quantified by CT scan and expressed as an Agatston score; higher scores indicate greater cumulative plaque burden and predict future cardiovascular events. score is one measure used to track this.

CT Example: CAC Scoring Visualization

Adapted from Thomas D et al., via ResearchGate (educational use).

Older adults often show significantly higher CAC scores, reflecting both the duration and intensity of plaque development.
(Citation: Bild DE et al. Circulation. 2005;111(10):1313–1320.)

Coronary CT Example of Calcified Plaques

Adapted from Cleveland Clinic Journal of Medicine (used for academic illustration).

What role does the immune system play as we age?

As we age, our immune system changes—a phenomenon called immunosenescenceThe age-related decline in immune system function, including reduced capacity to clear damaged cells and resolve inflammation, which allows atherosclerotic plaques to persist and enlarge rather than be kept in check.. It becomes less efficient at resolving inflammation, allowing plaque to persist and grow. Persistent, low-level inflammation (“inflammaging”) contributes to the worsening of atherosclerosis over time.
(Citation: Aiello A et al. Ageing Res Rev. 2024;99:102112.)

What are the cardiovascular consequences?

Age-related plaque progression increases the risk of:

  • Heart attackA heart attack happens when blood flow to part of the heart muscle is cut off and that muscle starts to die. (myocardial infarctionSee Heart Attack for the full entry.)
  • StrokeA stroke happens when blood flow to part of the brain stops, either from a blockage or from bleeding.
  • Peripheral artery diseasePeripheral artery disease is plaque narrowing the arteries in your legs.

These risks rise because plaques not only enlarge but can rupture, triggering clot formation.
(Citations: Wang JC, Bennett MR. Circ Res. 2012;111(2):245–259; Mortensen MB et al. Interv Cardiol Rev. 2024;19:e04.)

Plaque Rupture Illustration

Adapted from research illustration, educational reuse allowed (ResearchGate).

Can measuring plaque help personalize prevention?

Yes. Coronary artery calcium (CAC) scoringA non-contrast, ECG-gated CT scan that detects and quantifies calcified plaque in the coronary arteries; the resulting Agatston score reflects the extent of coronary calcification and serves as a direct, disease-based measure of atherosclerotic burden rather than a statistical estimate of risk. using CT imaging helps determine risk levels and guide preventive therapy. Higher CAC scores strongly predict cardiovascular events.
(Citation: Arnett DK et al. J Am Coll Cardiol. 2019;74(10):e177–e232.)

What can older adults do to counteract arterial aging?

Older Adults Exercising

Adapted from Wikimedia Commons (“Old people walking in winter, Croatia”).

Even modest lifestyle changes can slow plaque progression and lower the risk of heart disease at any age.

Are there emerging anti-aging treatments for atherosclerosis?

Scientists are exploring senotherapeuticsAn emerging class of experimental drugs designed to selectively eliminate (senolytics) or suppress the harmful secretions of senescent cells (senostatics), with the goal of reducing inflammation and slowing age-related diseases including atherosclerosis.—drugs that remove or modify senescent cells—to reduce inflammation and plaque formation. These are experimental but could, in the future, become part of cardiovascular diseaseCardiovascular disease is the umbrella term for problems with the heart and blood vessels, including heart attacks, strokes, and blocked leg arteries. prevention.
(Citation: Farr JN et al. Trends Cardiovasc Med. 2024;34(10):e123–e135.)

Takeaway

Aging itself drives the development of atherosclerosis by altering cellular and immune processes. While we can’t stop aging, understanding its effects helps us take proactive steps—through lifestyle, screening, and possibly future therapies—to maintain cardiovascular health.

Image Credits (Generic, Public Sources)

References

  1. Wang JC, Bennett M. Aging and atherosclerosis: mechanisms, functional consequences, and potential therapeutics for cellular senescence. Circ Res. 2012;111(2):245-259. doi:10.1161/CIRCRESAHA.111.261388
  2. Molnár AÁ, Pásztor DT, Tarcza Z, Merkely B. Cells in Atherosclerosis: Focus on Cellular Senescence from Basic Science to Clinical Practice. Int J Mol Sci. 2023;24(24):17129. Published 2023 Dec 5. doi:10.3390/ijms242417129
  3. Adav SS, Ng KW. Recent omics advances in hair aging biology and hair biomarkers analysis. Ageing Res Rev. 2023;91:102041. doi:10.1016/j.arr.2023.102041
  4. Leigh JP. Interpreting regression coefficients. J Chronic Dis. 1986;39(3):243-244. doi:10.1016/0021-9681(86)90029-9
  5. Bild DE, Detrano R, Peterson D, et al. Ethnic differences in coronary calcification: the Multi-Ethnic Study of Atherosclerosis (MESA). Circulation. 2005;111(10):1313-1320. doi:10.1161/01.CIR.0000157730.94423.4B
  6. Damarkusuma A, Mota P, Patel B, Oommen M. Consequences and Management of Excessive Ostial Stent Protrusion: A Case Report. Interv Cardiol. 2024;19:e04. Published 2024 Mar 11. doi:10.15420/icr.2023.34
  7. Hu C. Prevention of cardiovascular disease for healthy aging and longevity: A new scoring system and related “mechanisms-hallmarks-biomarkers”. Ageing Res Rev. 2025;107:102727. doi:10.1016/j.arr.2025.102727
  8. Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019;74(10):e177-e232. doi:10.1016/j.jacc.2019.03.010
  9. Wann LS. Editorial commentary: Therapeutic ultrasound in atherosclerotic cardiovascular disease. Trends Cardiovasc Med. 2023;33(7):441. doi:10.1016/j.tcm.2022.06.009

Deep Dive

Transparency Note: This blog post was created with assistance from AI tools. The final content has been carefully reviewed and edited by the author, who is responsible for its accuracy. The information provided is for educational purposes only and does not constitute medical advice.

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