Impact of solitons on the progression of initial lesion in aortic dissection

Abstract

Aortic dissection (AD) is the most common catastrophic disease reported at cardiovascular emergency in hospitals. Herein, a tear in the tunica intima results into separation of layers of aortic wall leading to rupture and torrential bleed. Hypoxia and oxidative stress are associated with AD. The release of hypoxia inducible factor (HIF)-1[Formula: see text] from the initial flap lesion in the tunica intima is the basis for aneurysmal prone factors. We framed a boundary value problem (BVP) to evaluate homeostatic saturation for oxygen dynamics using steady-state analysis. We prove uniqueness and existence of the solution of the BVP for gas exchange at capillary–tissue interface as a normal physiological function. Failure of homeostatic mechanism establishes hypoxia, a new quasi-steady-state in AD. We model permeation of two-layer fluid comprised of blood and HIF-1[Formula: see text] through tunica media as a generalized [Formula: see text]-dimensional nonlinear evolution equation and solve it using Lie group of transformations method. We note that the two-layer fluid permeates the tunica media as solitary wave including solitons such as bright soliton, dark soliton, peregrine soliton, topological soliton, kink soliton, breather soliton and multi-soliton complex. Also, we introduce the main result and discuss the implications of soliton solution, using graphic interpretation, to describe the early stage of progression of AD.