Threshold of microvascular occlusion: injury size defines the thrombosis scenario

TL;DR

This study uncovers how injury size influences thrombus formation, revealing a critical threshold that determines whether a blood vessel remains open or becomes occluded, based on a mathematical model of platelet dynamics and blood flow.

Contribution

It introduces a mathematical model explaining the threshold behavior of thrombosis based on injury size and hemodynamics, highlighting a saddle-node bifurcation mechanism.

Findings

Thrombosis exhibits a critical injury size determining occlusion or non-occlusion.

A mathematical model demonstrates a saddle-node bifurcation causes regime switching.

Experimental observations align with the model's predictions.

Abstract

Damage to the blood vessel triggers formation of a hemostatic plug, which is meant to prevent bleeding, yet the same phenomenon may result in a total blockade of a blood vessel by a thrombus, causing severe medical conditions. Here, we show that the physical interplay between platelet adhesion and hemodynamics in a microchannel manifests in a critical threshold behavior of a growing thrombus. Depending on the size of injury, two distinct dynamic pathways of thrombosis were found: the formation of a nonocclusive plug, if injury length does not exceed the critical value, and the total occlusion of the vessel by the thrombus otherwise. We develop a mathematical model that demonstrates that switching between these regimes occurs as a result of a saddle-node bifurcation. Our study reveals the mechanism of self-regulation of thrombosis in blood microvessels and explains experimentally observed distinctions between thrombi of different physical etiology. This also can be useful for the design of platelet-aggregation-inspired engineering solutions.