CAS-CARE: Cilostazol may inhibit in-stent restenosis after CAS
Cilostazol was associated with a trend toward reduction of in-stent restenosis in patients with carotid artery stenting at 2 years, according to findings presented at the International Stroke Conference.
However, compared with other antiplatelet agents, cilostazol did not affect CV events, mortality or bleeding, researchers from the CAS-CARE study reported.
The researchers randomly assigned 699 patients who underwent CAS (mean age, 70 years; 88% men) to receive cilostazol or other antiplatelet agents. There were no restrictions on use of other antiplatelet agents in either group.
“We previously reported the results of ReSISteR-CAS, a retrospective observational study of in-stent restenosis after CAS,” Nobuyuki Sakai, MD, director of neurosurgery at the Kobe City Medical Center General Hospital and director of neuroendovascular therapy at the Institute of Biomedical Research and Innovation in Kobe City, Japan, said during a presentation. “We found that periprocedural cilostazol treatment may suppress the occurrence of in-stent restenosis or target vessel revascularization after CAS. To the best of our knowledge, no randomized trial was ever conducted, thus we conducted the CAS-CARE trial.”
The primary endpoint of in-stent restenosis of at least 50% occurred in 10.8% of the cilostazol group and 19.6% of the control group (HR = 0.64; 95% CI, 0.41-1.02), Hiroshi Yamagami, MD, PhD, director of the department of stroke neurology at the National Hospital Organization Osaka National Hospital in Osaka, Japan said during the presentation.
In a landmark analysis, incidence of the primary endpoint was similar at 30 days (cilostazol, 0.6%; control, 0.3%; HR = 1.98; 95% CI, 0.17-20.8) but favored the cilostazol group between 31 days and 2 years (10.3% vs. 19.3%; HR = 0.62; 95% CI, 0.39-0.98), he said.
In an exploratory multivariate analysis, assignment to the cilostazol group was independently associated with in-stent restenosis (adjusted HR = 0.52; 95% CI, 0.32-0.84), and other predictors were stenosis of at least 70% at randomization (aHR = 2.07; 95% CI, 1.02-4.19) and stenosis of at least 13.5% after the procedure (aHR = 2.72; 95% CI, 1.63-4.53).
There were no differences in the secondary endpoints of stroke/CVD/death (HR = 0.95; 95% CI, 0.51-1.8), hemorrhagic events (HR = 1.66; 95% CI, 0.48-5.66), in-stent restenosis/out-of-stent restenosis/retreatment (HR = 0.81; 95% CI, 0.51-1.27), severe in-stent restenosis (HR = 0.5; 95% CI, 0.21-1.18), CV events (HR = 1.17; 95% CI, 0.12-1.89), stroke (HR = 1.21; 95% CI, 0.55-2.67), all-cause mortality (HR = 2.85; 95% CI, 0.3-27.4) and CV events/death/hemorrhagic events/in-stent restenosis/out-of-stent restenosis/retreatment (HR = 0.8; 95% CI, 0.56-1.15), according to the researchers.
“The addition of cilostazol to other antiplatelet agents in patients underwent carotid artery stenting tended to inhibit in-stent restenosis within 2 years after the procedure,” Yamagami said during the presentation. “Additional effects of cilostazol to prevent cardiovascular events or any death, and bleeding events, were not confirmed.” – by Erik Swain
Reference:
Yamagami H, et al. LB21. Presented at: International Stroke Conference; Feb. 19-21, 2020; Los Angeles.
Disclosures: The study was investigator-initiated and was funded in part by Otsuka Pharmaceutical Co. Ltd. Yamagami reports no relevant financial disclosures. Sakai reports he received honoraria from Biomedical Solutions and a research grant from Terumo.