Abstract

to evaluate whether systemic administration of cilostazol reduces neointimal hyperplasia in iliac arteries of pigs submitted to balloon catheter angioplasty. twenty pigs underwent angioplasty with a 6x40 mm balloon catheter in the right common iliac artery, guided by Doppler ultrasound. The animals were randomized into two groups: group 1 (n=10), which received 50mg cilostazol twice a day, and group 2 (n=10), control. After 30 days, the animals were killed and the iliac arteries prepared for histological analysis. The histological sections were digitized and analyzed by digital morphometry. Statistical analysis was performed using the Student t and Mann-Whitney tests. when comparing the iliac arteries submitted to angioplasty with those not subjected to angioplasty, there was significant neointimal hyperplasia (0.228 versus 0.119 mm2; p=0.0001). In arteries undergoing angioplasty, there was no difference between group 1 (cilostazol) and group 2 (control) as for the lumen area (2.277 versus 2.575 mm2; p=0.08), the tunica intima (0.219 versus 0.237 mm2; p=0.64), the tunica media (2.262 vs. 2.393 mm2; p=0.53) and the neointimal occlusion percentage (8.857 vs. 9.257 %; p=0.82). the use of cilostazol 50mg administered in two daily doses did not reduce neointimal hyperplasia in iliac arteries of pigs submitted to balloon angioplasty catheter.

Highlights

  • Peripheral arterial disease has a prevalence of up to 20% in patients over 70 years old and is an important cause of morbidity[1]

  • The objective of this study is to evaluate whether the systemic administration of cilostazol reduces neointimal hyperplasia in iliac arteries of pigs submitted to balloon catheter angioplasty

  • In this study there was significant neointimal hyperplasia, even using the balloon catheter oversizing of up to 20% commonly used in clinical practice and one single inflation of the Restenosis after balloon catheter angioplasty is caused by the negative elastic remodeling and the proliferation and migration of vascular smooth muscle cells (VSMC)[17]

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Summary

Introduction

Peripheral arterial disease has a prevalence of up to 20% in patients over 70 years old and is an important cause of morbidity[1]. The sequence of events stimulates the rapid regeneration of endothelial cells, which inhibits neointimal formation by two mechanisms: blockage of the abnormal growth of vascular smooth muscle cells (VSMC) and endothelial function improvement[5,6,8,9,10,11,12]. These mechanisms may be responsible for reducing restenosis after coronary stent insertion observed in clinical trials and metanalyses[13,14]

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