Pressure and flow

November 28, 2011

The first large-scale simulation of blood flow in coronary arteries enlists a realistic description of the vessels’ geometries. Researchers reported on the simulation today at the SC10 supercomputing conference in New Orleans.

Heart disease is called the silent killer. Heart attacks occur in people who had no idea that deadly plaques lurked inside the tree of arteries that feed that life-sustaining muscle.

Because the medical tools that can measure and predict these problems involve expensive, painful and invasive tests, doctors want less invasive ways to tease out factors that put a patient at risk. Computational science provides one way to better understand blood flow in this complex biological system.

In research presented today at the SC10 supercomputing conference in New Orleans, a Harvard University-led team describes the first large-scale simulation of blood flow in coronary arteries. The simulation uses a realistic description of the arteries’ geometries, and it accounts for fluid flow and the shape and movement of 300 million red blood cells through this system. This multiscale simulation was carried out on the nearly 295,000 processors of the IBM Blue Gene/P system. The research is a finalist for the Gordon Bell Prize, awarded each year at the conference.

The geometry of human coronary arteries from a CTA scan, shown at 12.5 micron resolution. The inset shows blood-flow geometry detail. The red in the detail highlights red blood cells, not endothelial shear stress (ESS), which is represented as a color map on the arterial walls. (Image courtesy of the author.)

One goal of these simulations is to calculate the force – the endothelial shear stress – along the walls of the coronary arteries as blood flows through. Research suggests that such forces play a critical role in forming arterial plaques that lead to ruptured vessels and heart attacks.

“The only way to really determine the shear stress for a patient’s heart is to run a simulation like this,” says first author Amanda Peters, a recipient of the Department of Energy Computational Science Graduate Fellowship and a Harvard applied physics Ph.D. student.

The work, which requires expertise in physics, parallel computing methods and visualization, has grown into an interdisciplinary and international partnership to look at blood flow through the coronary arteries, says Efthimios Kaxiras, Peters’ advisor and John H. Van Vleck professor of pure and applied physics in Harvard’s  Department of Physics and School of Engineering and Applied Sciences.

Kaxiras developed the original project with Sauro Succi, the research director at the Istituto per le Applicazioni del Calcolo  (IAC) of the National Research Council of Italy. In the current study, Peters collaborated with Simone Melchionna, now a senior research scientist at the National Institute of Condensed Matter, Italy, and collaborateur scientifique at the Institute of Materials at École Polytechnique Fédérale de Lausanne (EPFL); and Massimo Bernaschi, IAC chief technology officer. Other co-authors include Mauro Bisson, IAC; Jonas Latt, EPFL; and Joy Sircar, Harvard.

Lecturer of Medicine Charles Feldman and cardiologist Peter Stone, both with Brigham and Women’s Hospital, have been looking at the relationship between plaques and blood flow forces and the progression of heart disease. Their radiologist colleague Frank Rybicki provided detailed medical imaging of the tree of coronary arteries for the study.

Calculating the geometry of coronary artery fluid flow is far more complex than it would be if the arteries were straight tubes, Peters says. The computational mesh of data points designed to emulate the system has to be small enough to account for the subtle kinks and branches of the 12 arteries that feed the heart. The resulting simulation was at a resolution of 12.5 microns, just larger than the average red blood cell, which led to a billion fluid nodes. The simulation looked at these effects for about 1 second, the length of an average heartbeat.


Because of the problem’s scale, the researchers chose a Lattice Boltzmann approach that approximates segments of fluid as particles and follows the momentum of their interactions with neighbors along a lattice structure within the geometry of the arteries. The approach was ideal because of the geometry’s complexity and the work across parallel processors.

Blood itself is not a simple fluid and contains a variety of suspended components such as red cells, white cells, lipids and platelets. In this simulation, the researchers focused on the movement of red blood cells, mimicking their bialy-like shapes as 300 million ellipsoids. Molecular dynamics methods helped calculate their movements and interaction in this vascular system.

With those nearly 300,000 processors involved, one important challenge was partitioning the data so it would use the whole Blue Gene system effectively. With the problems of both fluid flow and red blood cell movement layered on top of each other, Peters says, the team had to ensure that information about the momentum of red blood cells was coupled to momentum of fluid flow. “So you have two simulations going at two different length scales simultaneously, and [we’re] trying to keep those coupled and moving together.”

To link those effectively, the researchers chose the same partitioning method for the blood cells and fluid flow. Memory also presented a challenge, and the researchers tried several different file-processing schemes before finding one that worked.

Blood behaves as a non-Newtonian fluid, which accounts for its ability to flow through tiny capillaries without clogging them. Red blood cells are the component responsible for this type of fluid behavior, Kaxiras says. “You cannot capture that without accounting for red blood cells in the flow.”

Because red blood cells are just one of many components that comprise the complex mixture of blood, this simulation is just a first step in understanding the many factors that could contribute to endothelial shear stress and heart disease, Kaxiras says.

In further simulations, Peters and her colleagues will look at other factors that can contribute to a heart attack: white blood cells, motion within blood vessels and the complexities that arise when arterial geometry changes as blood pulses through.

Once researchers can identify the most important components, Peters adds, it might be possible to scale this type of simulation down to a tool that a physician could use to diagnose individual patients.


About the Author

Sarah Webb has been freelancing from the New York City area since 2004. She has covered chemistry and materials science for Science News and worked in-house at both Discover and Popular Science. She holds a Ph.D. in chemistry, an undergraduate degree in German and completed a Fulbright fellowship doing organic chemistry research in Germany. She is a member of the National Association of Science Writers, the American Society of Journalists and Authors, the Society of Environmental Journalists, the American Association for the Advancement of Science and is a past co-president of the Science Writers in New York (SWINY).

This article originally appeared on