Abstract
When thrombus fractures and breaks off it can occlude vital vessels such as those of the heart, lung, or brain. These thromboembolic conditions are responsible for 1 in 4 deaths world-wide. This problem is also of significant current interest as 1 in 3 COVID-19 intensive care patients exhibit thromboembolic complications. Thrombus resistance to fracture is driven by its intrinsic fracture toughness as well as other, non-surface-creating dissipative mechanisms. In our current work, we identify and quantify these latter mechanisms toward future studies that aim to delineate fracture from other forms of dissipation. To this end, we use an in vitro thrombus mimic system to produce whole blood clots and explore their dissipative mechanics under simple uniaxial extension, cyclic loading, and stress-relaxation. We found that whole blood clots exhibit Mullins effect, hysteresis, permanent set, strain-rate dependence, and nonlinear stress-relaxation. Interestingly, we found that performing these tests under dry or submerged conditions did not change our results. However, performing these tests under room temperature or body temperature conditions yielded differences. Overall, we have demonstrated that whole blood clots show several dissipative phenomena - similarly to hydrogels - that will be critical to our understanding of thrombus fracture.
Competing Interest Statement
The authors have declared no competing interest.
