Low responsiveness to thienopyridine in hemodialysis patients
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ORIGINAL ARTICLE
Low responsiveness to thienopyridine in hemodialysis patients Shuichi Oshima Æ Katsuo Noda Æ Hironobu Fukushima Æ Shinichi Nakamura Æ Makoto Shono Æ Fumihito Kugimiya Æ Kenichiro Higa
Received: 19 February 2009 / Accepted: 27 July 2009 / Published online: 1 October 2009 Ó Japanese Association of Cardiovascular Intervention and Therapeutics 2009
Abstract We sought to evaluate whether thienopyridine low responsiveness, a predictor of stent thrombosis, is found in hemodialysis patients. We measured platelet aggregation at the site of implantation of drug-eluting stents in 333 patients with angina pectoris undergoing dual anti-platelet therapy. Thirty-one patients were on hemodialysis (HD group), and 302 were not (N-HD group). We used a novel whole-blood aggregometer. The aggregometer used the screen filtration method, with adenosine diphosphate as an agonist. The concentration of agonist required to induce 50% of the maximum pressure rate was calculated and indicated as the platelet aggregatory threshold index (PATI). Low responsiveness for thienopyridine was defined if the PATI levels were \4 lmol/l. PATI levels (lmol/l) were significantly lower in the HD group than in the N-HD group (6.8 ± 4.8 vs. 9.1 ± 5.4, P = 0.023), and the rate of low responsiveness for thienopyridine was significantly higher in the HD group than in the N-HD group (45.7 vs. 26.8%, P = 0.019). Non-fatal myocardial infarction and stent thrombosis occurred in three of the HD group and in nine of the N-HD group (P = 0.122). Late stent thrombosis occurred at a significantly higher rate in the HD group than in the N-HD group (P = 0.002). The rate of target lesion revascularization was significantly higher in the HD group than in the N-HD group (38 vs. 11.8%, P = 0.0001). In conclusion, low responsiveness to thienopyridine, as an indicator of platelet reactivity, is found more frequently in hemodialysis patients.
Keywords Hemodialysis Drug-eluting stent Thienopyridine low responsiveness Introduction Dual anti-platelet treatment with clopidogrel or ticlopidine and aspirin is the standard treatment for the prevention of stent thrombosis in patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stent (DES) [1, 2]. Early discontinuation of this treatment is a strong predictor of DES thrombosis [3, 4]. However, high residual platelet reactivity during anti-platelet treatment is related to the risk of DES thrombosis [5–7]. Dialysis patients show a complex morphology of coronary artery lesions such as marked calcification [8] and are at higher risk for DES restenosis [9, 10]. Renal failure, in recent reports, has been identified as a predictor of DES thrombosis [4, 11]; however, the mechanism still remains unclear. In recent years, the screen filtration pressure (SFP) method for measuring whole-blood aggregability has become available and is being used in the clinical and research fields [12–14]. It is reported that whole-blood aggregability can be measured quickly and reliably using this method [15]. The object
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