OBJECTIVE: We hypothesized that atheroemboli released during renal angioplasty could be responsible for the modest functional result of renal angioplasty even after anatomic reduction of renal artery stenosis. To test this hypothesis, we enumerated and sized fragments released during ex vivo angioplasty and stenting of human renal artery atherosclerotic specimens removed during aortorenal endarterectomy. METHODS: Thirty-three intact aortorenal atheroma specimens (16 pairs with adjacent aortic atheroma and one specimen with a single renal artery orifice) were removed from 17 patients with renal artery occlusive disease who underwent renal artery endarterectomy. specimens. Endarterectomy specimens were removed with a ring of aortic plaque and "fitted" with a polytetrafluoroethylene "adventitia". Ex vivo angioplasty was technically successful in 31 of the 33 specimens and was performed by using a 0.018-inch guidewire and 3.0-mm and 5.0-mm angioplasty balloons inflated for 30 seconds at 15 atmospheres pressure. Stenting was performed with either a 5-mm or 6-mm self-expanding Wallstent. Each artery was flushed with 20 mL of saline after guidewire placement, each angioplasty, and stent placement. The effluent was collected for analysis for counting with either a microscope (size >100 microm) or a Coulter counter (size <100 microm). The number and size of embolic fragments in the effluent collected after each manipulation was recorded. RESULTS: Each manipulation of the specimens, including simply advancing the guidewire through the atherosclerotic lesion, released thousands of fragments. The numbers of fragments in each size category increased with decreasing particle size. Positioning and deploying the Wallstent released an additional bolus of fragments similar to that released after balloon angioplasty. CONCLUSIONS: Ex vivo renal angioplasty releases thousands of atherosclerotic fragments of sufficient size to create vascular occlusions and initiate significant renal parenchymal damage. The results of renal angioplasty procedures could be improved by placing distal protection devices to prevent atheroembolization. CLINICAL RELEVANCE: Athero-emboli produce a local arteritis in the kidney and could cause substantial damage to the renal parenchyma. This report explores the quantity of athero-emboli released during ex vivo angioplasty and stenting of renal atheroma specimens. The number of emboli found in this ex vivo study suggest that the use of protection devices may be advisable to protect the end organ, as done with angioplasty of the carotid artery. Of necessity, this was an ex vivo study and direct application to the clinical setting will need further study. Fortunately, multi-center trials examining the value of protection devices are currently in progress.
OBJECTIVE: We hypothesized that atheroemboli released during renal angioplasty could be responsible for the modest functional result of renal angioplasty even after anatomic reduction of renal artery stenosis. To test this hypothesis, we enumerated and sized fragments released during ex vivo angioplasty and stenting of humanrenal artery atherosclerotic specimens removed during aortorenal endarterectomy. METHODS: Thirty-three intact aortorenal atheroma specimens (16 pairs with adjacent aortic atheroma and one specimen with a single renal artery orifice) were removed from 17 patients with renal artery occlusive disease who underwent renal artery endarterectomy. specimens. Endarterectomy specimens were removed with a ring of aortic plaque and "fitted" with a polytetrafluoroethylene "adventitia". Ex vivo angioplasty was technically successful in 31 of the 33 specimens and was performed by using a 0.018-inch guidewire and 3.0-mm and 5.0-mm angioplasty balloons inflated for 30 seconds at 15 atmospheres pressure. Stenting was performed with either a 5-mm or 6-mm self-expanding Wallstent. Each artery was flushed with 20 mL of saline after guidewire placement, each angioplasty, and stent placement. The effluent was collected for analysis for counting with either a microscope (size >100 microm) or a Coulter counter (size <100 microm). The number and size of embolic fragments in the effluent collected after each manipulation was recorded. RESULTS: Each manipulation of the specimens, including simply advancing the guidewire through the atherosclerotic lesion, released thousands of fragments. The numbers of fragments in each size category increased with decreasing particle size. Positioning and deploying the Wallstent released an additional bolus of fragments similar to that released after balloon angioplasty. CONCLUSIONS: Ex vivo renal angioplasty releases thousands of atherosclerotic fragments of sufficient size to create vascular occlusions and initiate significant renal parenchymal damage. The results of renal angioplasty procedures could be improved by placing distal protection devices to prevent atheroembolization. CLINICAL RELEVANCE: Athero-emboli produce a local arteritis in the kidney and could cause substantial damage to the renal parenchyma. This report explores the quantity of athero-emboli released during ex vivo angioplasty and stenting of renal atheroma specimens. The number of emboli found in this ex vivo study suggest that the use of protection devices may be advisable to protect the end organ, as done with angioplasty of the carotid artery. Of necessity, this was an ex vivo study and direct application to the clinical setting will need further study. Fortunately, multi-center trials examining the value of protection devices are currently in progress.
Authors: Mallik R Thatipelli; Sanjay Misra; Srinivas R Sanikommu; Robert M Schainfeld; Sandeep K Sharma; Peter A Soukas Journal: J Vasc Interv Radiol Date: 2009-03-27 Impact factor: 3.464