Is the endothelial cell responsible for the thrombus core and shell architecture?

Ischemia leading to heart attacks and strokes is the major cause of deaths in the world. This report explores the possibility that intracellular material from ruptured endothelial cells is partially responsible for the heterogeneous core-and-shell blood clot architecture, typically observed using intravital microscopy. As evidence, we present a fluid dynamic argument that platelet agonists emanating from the injury cannot activate platelets in the thrombus core, given that they would have to travel against flow of blood escaping into the extravascular.

In vivo measurement of blood clot mechanics from computational fluid dynamics based on intravital microscopy images.

Ischemia which leads to heart attacks and strokes is one of the major causes of death in the world. Whether an occlusion occurs or not depends on the ability of a growing thrombus to resist flow forces exerted on its structure. This manuscript provides the first known in vivo measurement of how much stress a clot can withstand, before yielding to the surrounding blood flow.