Key result
Transient external pressurization of an in vitro arterial stenosis model led to reductions in downstream pressure and flow rate, and caused collapse of the stenosis model.
Why the study?
Does external pressure simulating Valsalva's maneuver or cough alter pulsatile flow and deformation in an arterial stenosis model?
Does external pressure simulating Valsalva's maneuver or cough alter pulsatile flow and deformation in an arterial stenosis model?
Transient increases in external pressure, such as those caused by Valsalva's maneuver or cough, can cause collapse of arterial stenoses and potentially trigger atherosclerotic plaque rupture.
Answers are grounded in this paper and cite their sources.
External pressure may collapse arterial stenoses; leaves open whether Valsalva or cough triggers plaque rupture in vivo.
High-grade stenoses can limit blood flow and produce conditions in which an artery may collapse. The resultant compression may be important in the development of atherosclerotic plaque fracture and subsequent thrombosis or distal embolization. We have developed stenosis models made of polyvinyl alcohol hydrogel, which closely approximate an arterial disease situation, and performed pulsatile flow experiments. Valsalva's maneuver and cough cause a sharp increase in jugular venous pressure to greater than 50 mmHg. Such transient pressure increases within the carotid sheath may augment the external pressure around the carotid artery. We applied external pressure to a stenosis model in two different forms and discussed the influences of external pressure on pulsatile flow and deformation in the stenosis model.
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Ji et al. (2008) studied Arterial stenosis. External pressure vs. Baseline external pressure (10 mmHg) was evaluated on Downstream pressure, flow rate, and model deformation. Transient external pressurization of an in vitro arterial stenosis model led to reductions in downstream pressure and flow rate, and caused collapse of the stenosis model.
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