SYNERGISTIC ACTION OF SEVERE WALL INJURY AND SHEAR FORCES ON THROMBUSFORMATION IN ARTERIAL-STENOSIS - DEFINITION OF A THROMBOTIC SHEAR RATE THRESHOLD

Objectives. This study attempted to determine the influence of progres sive degrees of stenosis on platelet deposition onto a severely damage d vessel wall. Background. The severity of wall injury and increased s hear forces have been proposed as the determinants of thrombus formati on and growth in arterial stenosis. Methods. Carotid angioplasty was p erformed in 15 mongrel dogs to produce severe wall damage. Group I (n = 9) had arteries with damage only. In group II (n = 14), progressive degrees of stenosis mere produced at the center of the dilated area. A cute thrombus formation was evaluated by angiography at the time of an gioplasty and platelet deposition/cm(2) quantified by indium-111 label ing 1 h after the procedure. Results. Severe wall damage (group I) pro duced a significant increase in platelet deposition compared with cont rol arterial segments (8.19 +/- 3.82 vs. 3.62 +/- 2.52 platelets x 10( 6)/cm(2) [mean +/- SD], p < 0.05), and the presence of a stenosis (gro up II) further increased platelet deposition (36.98 +/- 3.82 platelets x 10(6)/cm(2), p < 0.05). Angiographic filling defects or total occlu sion was found in seven of the arteries in group II but in none in gro up I (p < 0.05). A shear rate of similar to 5,000 s(-1), corresponding to a critical stenosis of 70% and a 1.5- to 1.6-mm diameter, was foun d to identify the arteries in which thrombosis was likely to occur (p < 0.05). Four of 5 arteries <1.5 to 1.6 mm in diameter had angiographi c filling defects or occlusion compared with 1 of 13 with less severe stenosis (p < 0.01). Conclusions. In low shear rate conditions, deep a rterial injury will lead to mural thrombosis without further thrombus growth. When deep arterial injury occurs under critical local shear co nditions, platelet deposition will be enhanced, and thrombosis may pro gress to total occlusion.