Fabián A. Azzari

Clopidogrel 600-Mg Double Loading Dose Achieves Stronger Platelet Inhibition Than Conventional Regimens : Results From the PREPAIR Randomized Study

OBJECTIVES The objective of this study was to compare the level of platelet inhibition achieved by 3 different clopidogrel loading regimens in patients undergoing elective angiography and percutaneous coronary intervention when appropriate. BACKGROUND Optimal platelet inhibition is a key therapeutic goal for patients undergoing percutaneous coronary intervention. Although 600 mg has been described as the maximum absorbed dose when given as a single bolus, the effects of 2 boluses given 24 h apart have not been described. METHODS Patients (n = 148) were randomly assigned to one of 3 regimens: Group A, clopidogrel 300 mg the day before (>or=15 h) + 75 mg the morning of the procedure; Group B, clopidogrel 600 mg the morning of the procedure (>or=2 h); and Group C, clopidogrel 600 mg the day before (>or=15 h) and 600 mg the morning of the procedure (>or=2 h). Blood samples were obtained at baseline and immediately before angiography. Peak and late platelet aggregation were measured in platelet rich plasma, with researchers blinded to treatment allocation. RESULTS There was a consistent difference favoring Group C in all aggregation parameters. Percent inhibition in Groups A, B, and C was 31.4%, 29.0%, and 49.5%, respectively, for peak aggregation (5 micromol/l adenosine diphosphate; p < 0.0001) and 54.1%, 57.7%, and 81.1%, respectively, for late aggregation (p < 0.0001). Similar striking reductions were observed when 20 micromol/l adenosine diphosphate was used. All comparisons between Group C and the other 2 groups were statistically significant, and those between Groups A and B were not. CONCLUSIONS Clopidogrel 600-mg double bolus achieves greater platelet inhibition than conventional single loading doses.

Midterm Results of a Sirolimus-Eluting Stent Implanted for Recurrent Carotid In-Stent Restenosis

One of the concerns about carotid artery stenting (CAS) is the development of restenosis. Although the incidence of restenosis is low (3% to 8% in large series) due to the large reference vessel diameter, the number of cases will continue to rise as more CAS procedures are performed each year. While drug-eluting stent implantation has replaced balloon angioplasty and brachytherapy for the treatment of in-stent restenosis in the coronary arteries, there is scarce information regarding their use for carotid in-stent restenosis. In 2007, Iancu and Lazar reported sustained patency of a drug-eluting stent 1 year after treatment for carotid in-stent restenosis. We have recently documented 30-month follow-up in a patient we treated for recurrent in-stent restenosis with a drugeluting stent. The 53-year-old diabetic woman with multiple comorbidities was seen for symptoms of bilateral carotid artery disease. Her left internal carotid artery (ICA) was chronically occluded, and the right ICA had an 80% stenosis (Figure, A); the intracranial circulation was free of hemodynamically significant lesions. An 8340-mm Wallstent under FilterWire EZ embolic protection (Boston Scientific, Natick, MA, USA) was implanted in the right ICA with excellent results (Figure, B). The patient was discharged on aspirin and clopidogrel, but 1 year later, she was seen for dizziness and left arm paresthesia. A high-grade in-stent restenosis was treated with balloon dilation without complications. Nine months later, the patient was admitted for unstable angina and left arm paresthesia. Ultrasound suggested a highgrade recurrent in-stent restenosis (Figure, C). Surgery was proposed but dismissed by the vascular surgeon due to the high cervical location of the stenosis and contralateral carotid occlusion, so we implanted a 3.5-333mm Cypher coronary stent (Cordis, Miami, FL, USA) under cerebral protection (Figure, D,E); the stent was further expanded with a 4.5-mm balloon. The patient was discharged on longterm aspirin and clopidogrel therapy. Thirty months later, she was admitted for left leg critical ischemia, but she was free of any neurological deficit or symptom. Carotid angiography showed no evidence of restenosis (Figure, F) in the right ICA stent.