atherosclerosis.eu

MEDICINE × ENGINEERING

Atherosclerosis,
across scales.

A change in a molecule. A response in a cell.
A transformation of an artery.

Understanding plaque means connecting lipid biology, inflammation, blood flow and the living mechanics of the vessel wall.

Look inside the disease
THE ARTERY AS A LIVING SYSTEMFIG. 01
Blood flowLipid-rich regionVessel wall
Blood flow sets the mechanical environment at the endothelial surface.Conceptual illustration · not a patient scan or a simulation
A cardiovascular disease. A multidisciplinary challenge.From molecules to the whole patient
01 / THE DISEASE

It begins within
the artery wall.

Atherosclerosis is a chronic process in which lipids, inflammatory cells and altered tissue accumulate in arterial plaques. It can develop silently over many years.[1]

WHY IT MATTERS

A local plaque.
A systemic consequence.

Plaque can restrict blood supply. Rupture or erosion can trigger a clot and abruptly interrupt flow. The consequences depend on the artery affected.[1]

Plaque composition, inflammation and mechanical integrity matter alongside the degree of narrowing.[3]

CORONARY ARTERIES

The heart

Reduced oxygen supply, angina and myocardial infarction.

01
ARTERIES SUPPLYING THE BRAIN

The brain

Impaired circulation and the risk of ischaemic stroke.

02
PERIPHERAL ARTERIES

The limbs

Restricted circulation, exertional pain and tissue ischaemia.

03
02 / PATHOGENESIS

A process of
continuous feedback.

Lipid accumulation, immune activity and tissue remodelling reinforce or counteract one another. These mechanisms overlap; they are not a fixed timetable for every patient.[2]

TRANSPORT + VASCULAR BIOLOGY

From the circulation
into the wall.

Atherogenic lipoproteins enter and become retained in the arterial intima. Their modification and the endothelial response help recruit inflammatory cells to the developing lesion.

The modelling question: how do flow and permeability shape local lipid exposure?

03 / ACROSS SCALES

Different disciplines.
The same artery.

No single scale contains the whole disease. What happens in the blood changes the wall; the wall changes the flow. A useful description must connect both directions.[3][4]

BIOCHEMISTRY · LIPID SCIENCE · TRANSPORT

Lipoprotein retention, oxidation and signalling establish the local chemical environment. Transport and reaction models describe how exposure changes across the wall.

Molecular signalsCellular behaviour

Length scales are indicative. Molecular events, cellular responses, pulsatile flow and long-term remodelling also operate on different time scales.

04 / COMPUTATIONAL APPROACHES

Making the
connections explicit.

Computational models turn assumptions into equations and predictions that can be challenged with data. Their value lies in linking mechanisms, not just reproducing a curve.[4][5]

01 / DYNAMICS

Networks & differential equations

Represent lipid, inflammatory and tissue states as interacting variables. Compare mechanisms and functional responses while keeping the biological meaning of each connection visible.

change = inputs − losses
ODEs · regulatory graphs · interpretable model discovery
02 / TRANSPORT

Flow, filtration & reaction

Describe blood flow, endothelial exchange, diffusion and chemical reactions. Spatial models reveal gradients and local exposures that a well-mixed compartment cannot resolve.

accumulation + transport = reaction
CFD · advection–diffusion–reaction · endothelial permeability
03 / MECHANICS

Stress, growth & remodelling

Relate pressure, geometry and tissue composition to wall deformation and stress. Growth and remodelling models investigate how the living wall adapts as its constituents change.

composition ↔ mechanics ↔ remodelling
Finite elements · fluid–structure interaction · constrained mixtures
04 / INTEGRATION

Patient data & multiscale models

Combine imaging, systemic measurements and biological observations. Hybrid and agent-based models connect scales; uncertainty analysis tests how strongly the available data constrain an interpretation.

data + mechanisms + uncertainty
Medical imaging · agent-based modelling · calibration & validation

A good fit is a starting point. Agreement with observed trajectories does not uniquely identify a mechanism. Independent validation, uncertainty and alternative hypotheses remain essential.

A SHARED RESEARCH PERSPECTIVE

The artery does not
separate biology
from physics.

Neither should the way we study it.

Vascular biology ↔ Clinical medicine ↔ Applied mathematics ↔ Computational engineering
05 / SELECTED READING

Where to go deeper.

Clinical background, biological mechanisms and modelling perspectives.

  1. NHLBI / NIHWhat is atherosclerosis? Clinical overview
  2. SOEHNLEIN & LIBBY · 2021Targeting inflammation in atherosclerosis — from experimental insights to the clinic Biological mechanisms
  3. BROWN ET AL. · 2016Role of biomechanical forces in the natural history of coronary atherosclerosis Vascular biomechanics
  4. PARTON ET AL. · 2016Computational modelling of atherosclerosis Computational perspective
  5. CABALLERO ET AL. · 2026A personalized mechanobiology-driven multiscale model of atherosclerosis Hybrid modelling · preclinical study