An easy-to-use tool to flag patients at risk of poor INR control:A streak of subtherapeutic INRs

Introduction: Vitamin K antagonist therapy is safest and most effective with a high time within the therapeutic range (TTR). The TTR is difficult to calculate in the consultation room, therefore physicians need an easier-to-use tool to predict poor VKA control. We explored the prognostic value of subtherapeutic INRs on future TTR in two settings: (1) Clinical review setting, where a physician (bi) annually reviews a patient and uses the INRs since the last visit to predict the TTR up to the next visit; (2) Day-to-day INR management setting, where every new INR measurement prompts a new prediction over the next 90 days. Materials and methods: Retrospective cohort of 17,711 patients from a dedicated thrombosis service, using acenocoumarol (target range 2.0-3.0), with a "streak" defined as four consecutive INRs (1) Odds ratios of any streak in the last 180 days or 1 year on a TTR <45% over the same period in the future; (2) Odds ratio of a current streak on a TTR <45% over the next 90 days. Results and conclusions: Clinical review setting: The occurrence of any streak in the last 180 days or 1 year increased the odds of a TTR <45%: ORs 2.84 (95% CI 2.41-3.34) and 3.25 (95% CI 2.72-3.87), respectively. Day-to-day INR management setting: A current streak increases the odds of poor TTR over the next 90 days 3.58 (95% CI 2.64-4.87) fold. We conclude that a streak of four consecutive subtherapeutic INRs can aid physicians in flagging at-risk patients

Minimally invasive coronary artery bypass grafting versus percutaneous transluminal coronary angioplasty with stenting in isolated high-grade stenosis of the proximal left anterior descending coronary artery: Six months' angiographic and clinical follow-up of a prospective randomized study

AbstractObjective: We sought to compare minimally invasive coronary artery bypass grafting (surgical intervention) with percutaneous transluminal coronary angioplasty with primary stenting (stenting) in patients having an isolated high-grade stenosis (American College of Cardiology/American Heart Association classification type B2 or C) of the proximal left anterior descending coronary artery. At 6 months, both procedures were compared on the basis of quantitative angiography and clinical outcome. Methods: Both treatments were compared in a single-center, prospective, randomized study. The primary end point of this study was quantitative angiographic outcome at 6 months. The secondary end point was 6-month clinical outcome. Statistical analysis was performed in accordance with the intention-to-treat principle. Results: From March 1997 to September 1999, patients with angina pectoris caused by an isolated high-grade stenosis of the proximal left anterior descending coronary artery were randomly assigned to surgical intervention (n = 51) or stenting (n = 51). At 6 months, quantitative coronary angiography showed an anastomotic stenosis rate of 4% after surgical intervention and a restenosis rate of 29% after stenting (P <.001). Periprocedural events did not significantly differ between surgical intervention and stenting. After surgical intervention, 2 patients died; no patients died after stenting. After 6 months, no significant difference was found for major adverse cardiac or cerebral events and need for repeat target vessel revascularization. After 6 months, return of angina pectoris, physical work capacity, and use of antianginal drugs did not significantly differ between treatments. Conclusions: After 6 months, surgical intervention had a significantly better angiographic outcome than stenting in patients with an isolated high-grade stenosis of the proximal left anterior descending coronary artery. Clinical outcome did not significantly differ between treatments.J Thorac Cardiovasc Surg 2002;124:130-

Effect of nadroparin on anti-Xa activity during nocturnal hemodialysis

Background: Nadroparin is used during hemodialysis to prevent clotting of the extra corporeal system. During nocturnal hemodialysis patients receive an increased dosage of nadroparin compared to conventional hemodialysis. We tested whether the prescribed dosage regimen of nadroparin, according to Dutch guidelines, causes accumulation of nadroparin. Methods: Anti-Xa levels were used as an indicator of nadroparin accumulation. Anti-Xa was measured photometrically in 13 patients undergoing nocturnal hemodialysis for 4 nights a week. Nadroparin was administered according to Dutch dosage guidelines. We assessed anti-Xa levels at 4 time points during 1 dialysis week: before the start of the first dialysis session of the week (baseline), prior to (T1) and after the last dialysis session of the week (T2) and before the first dialysis of the following week (T3). Results: Patients received 71–95 IU/kg at the start of dialysis and another 50% of the initial dosage after 4 h with a total cumulative dosage of 128 ± 24 IU/kg. Anti-Xa levels increased from 0.017 at baseline to 0.019 at T1 (p = 0.03). Anti-Xa levels were 0.419 ± 0.252 IU/ml at T2 (p < 0.001 vs baseline and T1), whereas anti-Xa levels were not changed at T3 compared to baseline. Conclusion: Dosing of nadroparin according to Dutch guidelines in patients on nocturnal hemodialysis does not lead to accumulation of nadroparin. We therefore consider the Dutch dosage guidelines for nadroparin an effective and safe strategy. General significance: This article is the first to present data on anti-Xa activity during nocturnal hemodialysis which is a widely used and potentially dangerous therapy

Different risk of deep vein thrombosis and pulmonary embolism in carriers with factor V Leiden compared with non-carriers, but not in other thrombophilic defects. Results from a large retrospective family cohort study

The term factor V Leiden (FVL) paradox is used to describe the different risk of deep vein thrombosis and pulmonary embolism that has been found in carriers of FVL. In a thrombophilic family-cohort, we estimated differences in absolute risks of deep vein thrombosis and pulmonary embolism for various thrombophilic defects. Of 2,054 relatives, 1,131 were female, 41 had pulmonary embolism and 126 deep vein thrombosis. Annual incidence for deep vein thrombosis in non-carriers of FVL was 0.19% (95%CI, 0.16–0.23), and 0.41% (95%CI, 0.28–0.58) in carriers; relative risk (RR) 2.1 (95%CI, 1.4–3.2). For pulmonary embolism these incidences were similar in carriers and non-carriers 0.07%, respectively; RR 1.0 (95% CI, 0.4–2.5). When co-inheritance of other thrombophilic defects was excluded the RR for deep vein thrombosis in FVL carriers was 7.0 (95%CI, 2.3–21.7) compared to non-carriers and 2.8 (95%CI, 0.5–14.4) for pulmonary embolism. For other thrombophilic defects no such effect was observed. Thus the FVL paradox was confirmed in our study. However, a similar paradox in carriers of other thrombophilic defects was not observed