In a rabbit model of atherosclerosis, marked platelet accumulation occurs early after transluminal angioplasty and correlates with the extent of vascular dissection.
Since platelet accumulation may be an important determinant of restenosis after angioplasty, the time course of 51Cr-labeled platelet accumulation after experimental angioplasty was evaluated in a deendothelialized, hypercholesterolemic rabbit preparation of atherosclerosis. Marked platelet accumulation (39.5 +/- 8.7 X 10(6) platelets/1 cm vessel length) was observed at 30 min and remained active until 4 hr after angioplasty. Total accumulation over 24 hr was 56.4 +/- 4.7 X 10(6) platelets/1 cm length. Histologic dissection was directly related to the degree of platelet accumulation, with 64 +/- 15 X 10(6) platelets/1 cm in the group with marked dissection and 8.7 +/- 3.7 X 10(6) platelets/1 cm in the group with minimal dissection (p less than .05). Increasing angiographic dissection also resulted in a trend toward increased platelet accumulation, and angiographic change in luminal diameter showed a significant correlation with platelet accumulation. It is concluded that marked platelet accumulation occurs early after transluminal angioplasty and is related to the extent of dissection. Restenosis may result from a complex interaction of platelet accumulation, vascular damage, and blood flow.
Wilentz et al. (Sun,) studied this question.