“…Similarly, Kaluski et al 8 reported a 3.3% event rate for death, MI, and urgent revascularization with 2500 U of heparin before PCTA, but postprocedural creatine kinase was not routinely assayed, which likely underestimated the incidence of periprocedural MI. 8 Vainer and colleagues 15 performed a small trial of 404 patients randomized to either 5000 or 20 000 U of heparin before PCI. In the low-dose heparin group, only 22% of patients attained an ACT Ͼ275 s. This group had a composite event rate for death, MI, repeat revascularization, or acute occlusion of 13.2%; the rate for the high-dose group was 8% (PϭNS).…”
Section: Discussionmentioning
confidence: 99%
“…In the low-dose heparin group, only 22% of patients attained an ACT Ͼ275 s. This group had a composite event rate for death, MI, repeat revascularization, or acute occlusion of 13.2%; the rate for the high-dose group was 8% (PϭNS). This lack of statistical significance has been interpreted as support for low-dose heparin regimens, 8 although an inadequate sample size is a more likely explanation.…”
Section: Discussionmentioning
confidence: 99%
“…4 -6 Furthermore, in clinical practice, periprocedural heparin dosing varies markedly, with a recent emerging trend toward the use of lower heparin doses, despite the support of only a few small observational series. 7,8 Therefore, we performed an analysis combining individual patient data from 6 randomized, controlled trials to determine the optimum range of ACT for the suppression of periprocedural ischemic events after PCI.…”
Background-Unfractionated heparin has been the primary anticoagulant therapy for percutaneous coronary intervention for Ͼ20 years. Despite the availability of rapid "point of care" testing, little clinical data defining the optimal level of anticoagulation are available. Furthermore, recent reports have advocated the use of low-dose heparin regimens in the absence of large-scale, well-conducted studies to support this practice. Methods and Results-We pooled the data from 6 randomized, controlled trials of novel adjunctive antithrombotic regimens for percutaneous coronary interventions in which unfractionated heparin constituted the control arm. Patients were divided into 25-s intervals of activated clotting times (ACTs), from Ͻ275 s to Ͼ476 s. In a total of 5216 patients, the incidence of death, myocardial infarction, or any revascularization and major or minor bleeding at 7 days were calculated for each group and compared. An ACT in the range of 350 to 375 s provided the lowest composite ischemic event rate of 6.6%, or a 34% relative risk reduction in 7-day ischemic events compared with rates observed between 171 and 295 s by quartile analysis (Pϭ0.001). Conclusions-Contrary to recent reports, the optimal suppression of ischemic events with unfractionated heparin therapy in patients undergoing percutaneous coronary intervention demands treatment to ACT levels that are substantially higher than currently appreciated. These data define a goal for heparin dosing within coronary interventions and establish a benchmark of optimal unfractionated heparin therapy against which future trials of novel antithrombotic regimens in percutaneous interventions can be compared.
“…Similarly, Kaluski et al 8 reported a 3.3% event rate for death, MI, and urgent revascularization with 2500 U of heparin before PCTA, but postprocedural creatine kinase was not routinely assayed, which likely underestimated the incidence of periprocedural MI. 8 Vainer and colleagues 15 performed a small trial of 404 patients randomized to either 5000 or 20 000 U of heparin before PCI. In the low-dose heparin group, only 22% of patients attained an ACT Ͼ275 s. This group had a composite event rate for death, MI, repeat revascularization, or acute occlusion of 13.2%; the rate for the high-dose group was 8% (PϭNS).…”
Section: Discussionmentioning
confidence: 99%
“…In the low-dose heparin group, only 22% of patients attained an ACT Ͼ275 s. This group had a composite event rate for death, MI, repeat revascularization, or acute occlusion of 13.2%; the rate for the high-dose group was 8% (PϭNS). This lack of statistical significance has been interpreted as support for low-dose heparin regimens, 8 although an inadequate sample size is a more likely explanation.…”
Section: Discussionmentioning
confidence: 99%
“…4 -6 Furthermore, in clinical practice, periprocedural heparin dosing varies markedly, with a recent emerging trend toward the use of lower heparin doses, despite the support of only a few small observational series. 7,8 Therefore, we performed an analysis combining individual patient data from 6 randomized, controlled trials to determine the optimum range of ACT for the suppression of periprocedural ischemic events after PCI.…”
Background-Unfractionated heparin has been the primary anticoagulant therapy for percutaneous coronary intervention for Ͼ20 years. Despite the availability of rapid "point of care" testing, little clinical data defining the optimal level of anticoagulation are available. Furthermore, recent reports have advocated the use of low-dose heparin regimens in the absence of large-scale, well-conducted studies to support this practice. Methods and Results-We pooled the data from 6 randomized, controlled trials of novel adjunctive antithrombotic regimens for percutaneous coronary interventions in which unfractionated heparin constituted the control arm. Patients were divided into 25-s intervals of activated clotting times (ACTs), from Ͻ275 s to Ͼ476 s. In a total of 5216 patients, the incidence of death, myocardial infarction, or any revascularization and major or minor bleeding at 7 days were calculated for each group and compared. An ACT in the range of 350 to 375 s provided the lowest composite ischemic event rate of 6.6%, or a 34% relative risk reduction in 7-day ischemic events compared with rates observed between 171 and 295 s by quartile analysis (Pϭ0.001). Conclusions-Contrary to recent reports, the optimal suppression of ischemic events with unfractionated heparin therapy in patients undergoing percutaneous coronary intervention demands treatment to ACT levels that are substantially higher than currently appreciated. These data define a goal for heparin dosing within coronary interventions and establish a benchmark of optimal unfractionated heparin therapy against which future trials of novel antithrombotic regimens in percutaneous interventions can be compared.
“…ACT levels vary substantially after a fixed dose bolus of heparin due to variation in body size [21], anginal syndrome [22], and conditions that predispose to heparin resistance [3]. Intravenous UFH has been used in PCI with and without GP IIb/IIIa inhibitors [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38].…”
Since the advent of percutaneous coronary intervention (PCI), intravenous unfractionated heparin has been the primary antithrombotic therapy to prevent periprocedural ischemic complications. As compared with unfractionated heparin, low molecular weight heparins (LMWHs) have a greater bioavailability and a more predictable therapeutic response. In several recent studies of patients undergoing PCI, LMWHs have been shown to be as safe and effective as unfractionated heparin; given their better pharmacokinetic profile and the lack of need for coagulation monitoring, they have the potential to replace unfractionated heparin during coronary interventions. This article reviews the current status of anticoagulation therapy with unfractionated heparin and LMWHs in the cardiac catheterization laboratory.
“…The rate of myocardial infarction post PCI was 3.1% to 3.3%. One very recent study [18] showed the safety and feasibility of using very-low-dose heparin (2,500 units) in PCI. The mean ACT achieved was only 185 sec.…”
We tested the approach of reversing anticoagulation following PCI and immediate sheath removal in 429 consecutive patients. On completion of the PCI, protamine was administered, and the vascular sheath was immediately removed. Stents were used in 364 patients (85%) and GP IIb/IIIa inhibitors were used in 52 patients (12%). Time to achieve hemostasis was 30 +/- 17 min. Minor groin bleeding occurred in six patients. One patient required repair of femoral pseudoaneurysm. Mean creatine kinase at 8 and 16 hr post-PCI were 129 +/- 35 and 145 +/- 32 units, respectively. Creatine kinase rose to > 3 times normal in 12 out of 350 patients (3.4%). Prior to 48 hr, eight patients (1.9%) required emergency PCI or coronary bypass surgery. Follow-up at 30 days observed no deaths and only three target vessel revascularizations (0.7%). In conclusion, immediate reversal of anticoagulation and sheath removal after PCI is safe and feasible.
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