Glycoprotein IIb/IIIa antagonists during carotid artery stenting: results from the carotid artery stenting (CAS) registry of the Arbeitsgemeinschaft Leitende Kardiologische Krankenhausärzte (ALKK).
BACKGROUND
Glycoprotein II b/IIIa antagonists (GPII b/IIIa-A) lower the periprocedural rate of ischemic events during high risk percutaneous coronary interventions. Their clinical impact on carotid artery stenting (CAS) remains to be determined.


METHODS
We analyzed data from the Carotid Artery Stent (CAS) Registry.


RESULTS
From 01/ 2000 to 06/2005 1322 CAS interventions were registered. In 94 (7.1%) procedures a GPII b/IIIa-A was used: abciximab in 8 cases (8.6%), tirofiban in 53 cases (57%) and eptifibatide in 32 cases (34.4%). The use of a GPII b/IIIa-A during CAS decreased significantly over time: from 17.6% in 2000 to 3% in 2005, p for trend <0.0001. The mean use of a GPII b/IIIa-A at the hospitals was 5.2%. More than 50% of the hospitals never used a GPII b/IIIa-A. There were no significant differences in baseline characteristics and concomitant diseases in CAS patients treated with GPII b/IIIa-A compared to those without GPII b/IIIa-A. A bilateral intervention was performed more often in patients treated with GPII b/IIIa-A (2.1 vs 0.2%, p = 0.04), a thrombus was more often visible (27 vs 12.4%, p <0.001) and an ulcer more frequently diagnosed (50 vs 37.5%, p = 0.03). There was no significant difference in the combined death or stroke rate between the two groups (5.3 vs 3.0%, p = 0.22, OR = 1.81, 95% CI: 0.69-4.72), which was confirmed by logistic regression analysis after adjusting for possible confounders (OR = 1.67, 95% CI: 0.62-4.46, p = 0.31).


CONCLUSIONS
Our data neither demonstrate a significant benefit nor a significant risk with the use of GPIIb/IIIa-A during CAS. However, only an adequately sized randomized controlled clinical trial could establish the real value of GPII b/IIIa-A during CAS. Until then, considering the potential increase in cerebral hemorrhage, we should not use GPII b/ IIIa-A routinely during CAS.
Zahn
R
R
Kardiologie/Angiologie/Internistische Intensivmedizin, Klinikum Nürnberg, Breslauer Strasse 201, 90471 Nürnberg, Germany. erzahn@aol.com
Ischinger
T
T
Hochadel
M
M
Mark
B
B
Zeymer
U
U
Jung
J
J
Schramm
A
A
Hauptmann
K E
KE
Seggewiss
H
H
Janicke
I
I
Mudra
H
H
Senges
J
J
D000077284:Abciximab; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D016893:Carotid Stenosis / Q000628:therapy*; D000077542:Eptifibatide; D005260:Female; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D012042:Registries; D015607:Stents; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives / Q000627:therapeutic use
D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014443:Tyrosine; D000077466:Tirofiban; D000077542:Eptifibatide; D000077284:Abciximab