The objective of this study was to examine the pharmacokinetics of intravenous dalteparin (Fragmin, Pharmacia-Upjohn, Peapack, NJ) and to assess the accuracy of standard coagulation-based monitoring techniques as an estimate of drug concentration with which to guide dosing. Knowledge of the kinetic behavior of low-molecular-weight heparins (LMWHs) and the possible utility of coagulation times for monitoring may aid in the development of safe and effective dosing algorithms for percutaneous coronary interventions. Twenty normal volunteers were treated at 2-week intervals with each of three intravenous dalteparin doses. Measurement of anti-IIa, anti-Xa, activated partial thromboplastin time (aPTT), activated clotting time (ACT), and low-range ACT was performed at baseline and at seven additional time points over 8 hours. The half-life of intravenous dalteparin is 77 minutes with slight dose-related variation. The aPTT, LR-ACT, and standard ACT are prolonged after dalteparin administration with the increase closely correlated to anti-Xa activity (aPTT, r = 0.85; LR-ACT, r = 0.79). Classification of anticoagulation intensity range using aPTT or LR-ACT in comparison to anti-Xa activity (0.5-0.99, 1.0-1.49, 1.5-2, >2) displays a level of agreement (kappa: aPTT = 0.69, LR-ACT = 0.59) that is comparable to values reported for coagulation time guidance of unfractionated heparin administration. Standard coagulation times are sensitive to the anticoagulant effect of dalteparin with a degree of correlation that suggests their utility for estimating drug concentration during high dose therapy. Trials establishing a relationship between monitoring and clinical efficacy, and the risk/reward of different treatment ranges alone or in combination with GPIIb/IIIa inhibitors and clopidogrel, are necessary.

Purpose: To report the benefits of rheolytic thrombectomy for treating aortic endograft thrombosis. Methods: Of 40 patients who received the Ancure bifurcated endograft to treat abdominal aortic aneurysm (AAA) during a 9-month period, 6 (15%) patients (6 men; mean age 62.6 years, range 53–77) developed thrombosis of the endograft at an average of 9 weeks (range 1–20 months). Five patients were taking aspirin, and 3 were on warfarin therapy for atrial fibrillation. Immediately after angiography, rheolytic thrombectomy was used to remove the thrombus, followed by adjunctive procedures to treat the underlying pathology. Results: Causes were kinking or extrinsic compression of the graft limb in 5 cases and thrombosis of the surgical closure site in a common femoral artery. Mechanical thrombectomy was successful in restoring circulation in all cases; thrombolysis was used in 1. All 6 patients had additional stents placed in the graft limbs, re-establishing patency. There was no mortality or recurrent thrombosis in a follow-up that has extended to 26 months, but 1 patient required additional stenting for subsequent focal kinking of a graft limb above the previously implanted stent. Conclusions: Rheolytic thrombectomy can safely and effectively treat endograft thrombosis after endovascular AAA repair. Additional thrombolytic agents, angioplasty, and stenting may be needed to correct the underlying causes of the thrombosis. Prophylactic stenting of iliac limbs at the time of implantation in patients with complex anatomy may prevent thrombosis of unsupported bifurcated endografts.