Predictors of embolization during protected renal artery angioplasty and stenting: Role of antiplatelet therapy.
OBJECTIVE
The objective of this study was to identify the predictors of distal embolization (DE) during protected renal artery angioplasty and stenting.


BACKGROUND
DE may contribute to worsening renal function after renal artery stenting. The factors associated with DE, rates of platelet-rich emboli, and treatments that may prevent DE during renal stenting have not been evaluated.


METHODS
The current study evaluated patients randomized to receive an embolic protection device (EPD) in the RESIST trial. Forty-two patients were identified for inclusion in this study. These patients were further randomized to abciximab (N = 22) or placebo (N = 20). Modification in Diet in Renal Disease glomerular filtration rate (GFR) was used as the primary measure of renal function. Creatinine was measured by a modified Jaffe reaction using the IDMS-traceable assay. The primary endpoint was capture of platelet rich emboli in the angioguard basket.


RESULTS
DE occurred in 15/42 (35%) of the patients and platelet rich DE in 10 (24%) of the patients who received an EPD. Of the angiographic characteristics only lesion length was significantly higher in patients with DE (16 +/- 7 mm vs. 10 +/- 5 mm, P = 0.04). Preprocedural abciximab reduced DE from 42 to 8% (P = 0.02). The rate of platelet rich emboli was 50% with neither abciximab nor a thienopyridine, 36% with thienopyridine only, 15% abciximab only, and 0% in patients who received both a thienopyridine and abciximab. Only Abciximab use was associated with improved renal function at 1-month, thienopyridine was not. Angiographic characteristics including percent stenosis, minimal luminal diameter (MLD), reference diameter, change in MLD, contrast volume, and procedure time were not predictors of DE during renal stenting.


CONCLUSIONS
Capture of DE and specifically platelet DE are common during protected renal stenting using a filter-type EPD. Abciximab use, and potentially combined thienopyridine and abciximab use, decreased the rate of platelet rich DE; however, only abciximab improved renal function at 1-month.
Kanjwal
Khalil
K
Department of Medicine, Division of Cardiology, The University of Toledo, 3000 Arlington Ave., Toledo, OH 43614, USA.
Cooper
Christopher J
CJ
Virmani
Renu
R
Haller
Steven
S
Shapiro
Joseph I
JI
Burket
Mark W
MW
Steffes
Michael
M
Brewster
Pamela
P
Zhang
Haifeng
H
Colyer
William R
WR
D000077284:Abciximab; D000368:Aged; D000369:Aged, 80 and over; D017130:Angioplasty / Q000009:adverse effects / Q000295:instrumentation*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D003404:Creatinine / Q000097:blood; D004359:Drug Therapy, Combination; D004617:Embolism / Q000209:etiology / Q000517:prevention & control*; D005260:Female; D005374:Filtration / Q000295:instrumentation*; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D011725:Pyridines / Q000627:therapeutic use*; D012078:Renal Artery Obstruction / Q000188:drug therapy / Q000628:therapy*; D018570:Risk Assessment; D012307:Risk Factors; D015607:Stents; D013997:Time Factors; D016896:Treatment Outcome; D014481:United States
D000911:Antibodies, Monoclonal; D015415:Biomarkers; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D011725:Pyridines; C446540:thienopyridine; D003404:Creatinine; D000077284:Abciximab