Patient-specific coupled CFD–DEM modelling of LDL-surrogate deposition in a middle cerebral artery bifurcation

Stroke remains one of the most devastating causes of adult disability and death worldwide, often stemming from a slow, silent process where fatty deposits build up inside the brain's blood vessels. This buildup, known as atherosclerosis, is driven by low-density lipoprotein, or LDL, particles sticking to the inner walls of arteries. For decades, doctors and scientists have tried to predict exactly where these dangerous deposits will form by looking at how blood flows. They have developed tools to measure the friction blood exerts on the vessel wall, the speed at which it swirls, and how long it lingers in one spot. These measurements have become the standard way to identify which parts of an artery are at risk. However, these tools only look at the surface of the vessel, treating the flow as a smooth sheet of water rather than a collection of individual particles moving through a complex, three-dimensional space.

A new study from researchers at the University of Leeds challenges the idea that surface measurements alone are enough to predict where plaque will form. Instead of just watching the flow, the team built a sophisticated computer simulation that tracks thousands of individual LDL particles as they move through a patient's actual brain artery. They combined a model of fluid motion with a method that treats each particle as a distinct object that can bounce, slide, and stick to the wall. By applying this approach to a real patient's middle cerebral artery, they discovered that the shape of the artery itself plays a role just as important as the blood flow in deciding where particles land. Their findings suggest that two sections of an artery can have nearly identical flow conditions yet behave very differently when it comes to catching particles, a detail that traditional methods completely miss.

The researchers focused their work on a specific branch of the brain's arterial network, a Y-shaped junction where a main vessel splits into two smaller branches. In the real world, this area is a common site for blockages, but scientists have struggled to explain why some branches collect more deposits than others when the blood flow looks the same. To solve this, the team created a digital twin of a patient's artery using medical scan data. They then ran a complex simulation that first calculated how the blood moved through the vessel, accounting for the fact that blood is thick and behaves differently than water. Once the flow was established, they injected over ten thousand tiny, computer-generated particles representing LDL into the stream. These particles were not just passive markers; the simulation tracked their physical interactions, including how they collided with the wall and whether they stuck there due to microscopic forces of attraction.

The results revealed a surprising asymmetry. The researchers divided the artery into three sections: the main junction where the split occurs, a left branch, and a right branch. As expected, the main junction showed the highest concentration of particle collisions, which aligns with the fact that it had the largest area of slow, low-friction flow. However, a closer look at the two branches told a different story. The left and right branches had almost identical flow conditions; the blood moved at similar speeds, and the friction on the walls was nearly the same. Yet, the right branch caught significantly more particles than the left. In fact, the right branch accounted for nearly half of all the particle collisions in the entire simulation, despite having flow metrics that suggested it should be just as safe as the left.

This discrepancy highlights a critical limitation in current medical assessments. The standard tools used to evaluate stroke risk rely on surface measurements like average wall friction and flow oscillation. In this simulation, those tools would have predicted that both branches were equally likely to develop plaque. The new method, however, showed that the physical shape of the right branch was actively steering particles toward the wall in a way that the surface measurements could not detect. The researchers found that the geometry of the vessel created subtle, three-dimensional currents that pushed particles into the right branch, a mechanism that remains invisible when looking only at the wall's surface.

To ensure this result was not just a fluke of the specific particle size they used, the team repeated the simulation with particles twice as large. The outcome was the same: the right branch continued to dominate the particle collisions, while the left branch remained relatively clear. This consistency confirmed that the pattern was driven by the geometry of the artery itself, not by the specific size of the particles. The study also showed that the main junction remained the most active area for particle accumulation overall, but the unexpected dominance of the right branch proved that local shape can override standard flow indicators.

The implications of this discovery extend beyond computer models. The researchers suggest that when doctors assess a patient's risk for stroke, they should consider the specific geometry of their blood vessels as an independent factor, not just a backdrop for flow calculations. A patient might have reassuring flow numbers on a standard report, but if their artery has a sharp curve or an unusual split, their vessel could still be trapping particles at a high rate. By integrating the physical shape of the vessel into risk assessment, clinicians could potentially identify high-risk patients who would otherwise be overlooked. This approach does not replace existing methods but adds a crucial layer of detail, moving the field from a two-dimensional view of blood flow to a more complete understanding of how particles actually behave inside the human body. The study concludes that while surface metrics are useful, they are not the whole story, and the hidden influence of vessel shape must be accounted for to truly understand where and why blockages form.