Effect of stenosis on wall motion. A possible mechanism of stroke and transient ischemic attack.

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Abstract
The mechanism by which atherosclerotic plaque causes stroke and transient ischemic attack is not fully understood. One possibility is that the plaque stenosis may set up hemodynamic conditions causing local arterial wall collapse. Arterial wall collapse may, in turn, affect the integrity of the plaque. This study was designed to define the effects of stenosis on the production of arterial wall collapse using a latex tube model. Stenoses ranging up to 81% by diameter were tested in a Starling resistor chamber under pulsatile pressure conditions upstream of the tube. Increasing the degree of stenosis progressively decreased the external pressure necessary to produce collapse, from 37 mm Hg with the 0% stenosis to 24 mm Hg for the 81% stenosis. The stenoses greater than 70% produced a new phenomenon of "systolic wall collapse" just distal to the stenosis. The maximum diameter decrease was 2.83 mm from the baseline diameter of 6.41 mm. Cyclic wall motion just downstream of the stenosis increased with the increased degree of stenosis from 0.34 mm at 0% stenosis to -1.28 mm at 75% stenosis. The phenomena are discussed in terms of simplified Bernoulli pressure drops. We conclude that local arterial stenosis can produce conditions favorable for wall collapse and increased wall motion at physiologic pressure and flow. This collapse may be important in the development of atherosclerotic plaque fracture and subsequent thrombosis or distal embolization.