Intracoronary brachytherapy for in-stent restenosis using long sources reduces restenosis
Edge restenosis (candy wrapper effect) and late thrombosis remain a problem in various randomized intracoronary brachytherapy (ICBT) trials for the treatment of in-stent restenosis (ISR). Target vessel revascularization (TVR) due to target lesion revascularization (TLR) and edge restenosis can be decreased with the use of longer ICBT sources and debulking devices and has not been systematically studied. We analyzed 226 patients with ISR (240 vessels of 264 lesions; average lesion length 17.5+/-8.9 mm) who had lesion debulking followed by 90 Strontium (Sr) beta-irradiation using the Novoste Betacath system (30 mm source in 144 vessels and 40 mm source in 96 vessels). Dual antiplatelet therapy was recommended for one year. At follow-up of 12+/-2 months, clinical TVR occurred in 9.7%, with TLR in 7.1% and non-TLR in 2.6% of cases. There was no delayed or late subacute thrombosis. Beta-irradiation using a longer 90Sr source after lesion modification with cutting balloon (CB) and or rotational atherectomy (RA), along with the use of long-term dual antiplatelet therapy is safe and associated with single-digit clinical restenosis.
The activated clotting time can be used to monitor the low molecular weight heparin dalteparin after intravenous administration
OBJECTIVES: This study was designed to compare the dose response of dalteparin versus unfractionated heparin (UFH) on the activated clotting time (ACT), and to determine whether the ACT can be used to monitor intravenous (IV) dalteparin during percutaneous coronary intervention (PCI). BACKGROUND: The use of low molecular weight heparin (LMWH) during PCI has been limited by the presumed inability to monitor its anticoagulant effect using bedside assays. METHODS: This study was performed in three phases. In vitro, ACTs were measured on volunteer (n = 10) blood samples spiked with increasing concentrations of dalteparin or UFH. To extend these observations in vivo, ACTs were then measured in patients (n = 15) who were sequentially treated with IV dalteparin and then UFH. Finally, a larger monitoring study was undertaken involving patients (n = 110) who received dalteparin 60 or 80 international U (IU)/kg alone or followed by abciximab. We measured ACT (Hemochron), activated partial thromboplastin time (aPTT), plasma anti-Xa and anti-IIa levels, tissue factor pathway inhibitor (TFPI) concentration, and plasma dalteparin concentration. RESULTS: Dalteparin induced a significant rise in the ACT with a smaller degree of variance as compared to UFH. Five min after administration of IV dalteparin 80 IU/kg the ACT increased from 125 s (122 s, 129 s) to 184 s (176 s, 191 s) (p < 0.001). The aPTT, anti-Xa and anti-IIa activities, and TFPI concentration also demonstrated significant increases following IV dalteparin. CONCLUSIONS: The ACT and aPTT are sensitive to IV dalteparin at clinically relevant doses. These data suggest that the ACT may be useful in monitoring the anticoagulant effect of intravenously administered dalteparin during PCI.