ABSTRACT
Correction to: Clin Neuroradiol 2019 https://doi.org/10.1007/s00062-019-00776-2 The original version of this article unfortunately contained a mistake. The Acknowledgements were missing. The correct information is given .
ABSTRACT
BACKGROUND: Cerebral vasospasm (CVS) following subarachnoid hemorrhage occurs in up to 70% of patients. Recently, stents have been used to successfully treat CVS. This implies that the force required to expand spastic vessels and resolve vasospasm is lower than previously thought. OBJECTIVE: We develop a mechanistic model of the spastic arterial wall to provide insight into CVS and predict the forces required to treat it. MATERIAL AND METHODS: The arterial wall is modelled as a cylindrical membrane using a constrained mixture theory that accounts for the mechanical roles of elastin, collagen and vascular smooth muscle cells (VSMC). We model the pressure diameter curve prior to CVS and predict how it changes following CVS. We propose a stretch-based damage criterion for VSMC and evaluate if several commercially available stents are able to resolve vasospasm. RESULTS: The model predicts that dilatation of VSMCs beyond a threshold of mechanical failure is sufficient to resolve CVS without damage to the underlying extracellular matrix. Consistent with recent clinical observations, our model predicts that existing stents have the potential to provide sufficient outward force to successfully treat CVS and that success will be dependent on an appropriate match between stent and vessel. CONCLUSION: Mathematical models of CVS can provide insights into biological mechanisms and explore treatment approaches. Improved understanding of the underlying mechanistic processes governing CVS and its mechanical treatment may assist in the development of dedicated stents.
Subject(s)
Cerebral Arteries/physiopathology , Models, Cardiovascular , Stents , Vasospasm, Intracranial/therapy , Angioplasty/instrumentation , Angioplasty/methods , Biomechanical Phenomena/physiology , Blood Pressure/physiology , Extracellular Matrix/physiology , Humans , Muscle, Smooth, Vascular/physiopathology , Myocytes, Smooth Muscle/physiology , Subarachnoid Hemorrhage/complications , Vasospasm, Intracranial/etiology , Vasospasm, Intracranial/physiopathologyABSTRACT
Experimental and computational studies suggest a substantial variation in the mechanical responses and collagen fibre orientations of the two structurally important layers of the arterial wall. Some observe the adventitia to be an order of magnitude stiffer than the media whilst others claim the opposite. Furthermore, studies show that molecular metabolisms may differ substantially in each layer. Following a literature review that juxtaposes the differing layer-specific results we create a range of different hypothetical arteries: (1) with different elastic responses, (2) different fibre orientations, and (3) different metabolic activities during adaptation. We use a finite element model to investigate the effects of those on: (1) the stress response in homeostasis; (2) the time course of arterial adaptation; and (3) an acute increase in luminal pressure due to a stressful event and its influence on the likelihood of aneurysm rupture. Interestingly, for all hypothetical cases considered, we observe that the adventitia acts to protect the wall against rupture by keeping stresses in the media and adventitia below experimentally observed ultimate strength values. Significantly, this conclusion holds true in pathological conditions.