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Heparin Administration (heparin + administration)
Selected AbstractsAcute cardiorespiratory collapse from heparin: a consequence of heparin-induced thrombocytopeniaEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 5 2004Martha P. Mims Abstract: Background:, Heparin has rarely been reported to cause acute cardiorespiratory reactions or collapse. Some reports relate this to underlying heparin-induced thrombocytopenia. Objective:, To confirm and increase awareness of acute life-threatening cardiopulmonary events when patients with heparin-induced thrombocytopenia are re-exposed to heparin. Design:, Retrospective observational case series. Patients/setting:, Four cardiovascular surgery patients were identified in two adjacent large urban hospitals over a 2-yr-period who experienced eight episodes of cardiorespiratory collapse immediately following heparin administration. All had underlying heparin-induced thrombocytopenia. Results:, Intravenous boluses of unfractionated heparin were given to four patients with known or previously unrecognized heparin-induced thrombocytopenia. Two patients experienced severe respiratory distress within 15 min for which they required endotracheal intubation. Two other patients experienced cardiac arrest or a lethal arrhythmia within minutes of receiving intravenous heparin. Serologic tests for heparin-induced antibodies were positive in all patients. In three cases, the platelet count was normal or near normal but fell dramatically (71%) immediately following the heparin bolus. Three cases had prior diagnoses of heparin-induced thrombocytopenia, but health care workers administered heparin either unaware of the diagnosis or ignorant of its significance. No patients died, but all required some form of cardiopulmonary resuscitation and subsequent intensive care. Conclusions:, Heparin administration to patients with heparin-induced antibodies can result in life-threatening pulmonary or cardiac events. Appreciation of this phenomenon can unmask cases of heparin-induced thrombocytopenia and strengthens the mandate to avoid any heparin exposure in affected patients. Recognition is crucial to avoiding disastrous outcomes. [source] Prolonged activated partial thromboplastin time in thromboprophylaxis with unfractionated heparin in patients undergoing cesarean sectionJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 1 2010Shigeki Matsubara Abstract Aim:, Hemorrhage is an important complication of heparin-thromboprophylaxis after surgery. We attempted to clarify the incidence rate of prolonged activated partial thromboplastin time (APTT), representative of hemorrhagic tendency, in Japanese women who received thromboprophylaxis with unfractionated subcutaneous heparin administration after cesarean section (CS). We also determined factors which affected postoperative APTT. Methods:, We studied 280 women who were administered thromboprophylaxis with unfractionated subcutaneous heparin 5000 IU two times per day after CS. Postoperative APTT under heparin was measured and the incidence of its prolongation was determined. Preoperative APTT, blood loss during surgery, postoperative hematocrit, postoperative serum total protein level, and postpartum body weight were measured, and their correlation with postoperative APTT was determined. Results:, Preoperative and postoperative APTT values were 28.3 (26.7,30.3) and 33.8 (31.0,37.5) seconds for median (interquartile range), respectively. Overall, 7.1% of patients showed ,45 s postoperative APTT. Two patients (0.7%) showed ,60 s APTT, one of whom suffered subcutaneous hemorrhage around the abdominal incision with complete healing. There were no other hemorrhagic complications. Preoperative APTT positively, and postpartum body weight inversely, correlated with postoperative APTT. The amount of blood loss, postoperative hematocrit, and postoperative serum total protein level did not correlate with postoperative APTT. No discernible deep vein thrombosis or pulmonary embolism occurred. Conclusion:, Although 7.1% of women under heparin-thromboprophylaxis showed a prolonged APTT that was 150% of the preoperative APTT, serious side effects were not observed. Subcutaneous administration of unfractionated heparin, if checking APTT prolongation 1 day after surgery, may be safe method of thromboprophylaxis after CS. [source] Safety of plasmin in the setting of concomitant aspirin and heparin administration in an animal model of bleedingJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 12 2003S. Sadeghi Summary., Plasmin is a direct thrombolytic which has been shown to have a strikingly favorable benefit to risk profile in comparison with plasminogen activators, notably tissue plasminogen activator (t-PA). As heparin is known to increase the risk of hemorrhage when co-administered with a plasminogen activator, we asked whether adjunct antithrombotic agents such as aspirin and heparin would affect the safety of plasmin. Three groups of rabbits were administered plasmin at a dose (4 mg kg,1) designed to induce significant decreases in antiplasmin, fibrinogen and factor (F)VIII, to about 25, 40 and 40%, respectively, of baseline values, but not cause prolongation of the ear puncture bleeding time. In a blinded and randomized trial, the results show that an intravenous aspirin bolus plus heparin administered as a bolus followed by a maintenance continuous infusion did not significantly prolong the bleeding time during plasmin infusion. These data indicate that in the rabbit, concomitant use of aspirin plus heparin does not affect the safety of a therapeutic dose of plasmin. [source] When Should Heparin Preferably Be Administered During Radiofrequency Catheter Ablation?PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2001OLE-GUNNAR ANFINSEN ANFINSEN, O.-G., et al.: When Should Heparin Preferably be Administered During Radiofrequency Catheter Ablation? RF catheter ablation is complicated by thromboembolism in about 1% of patients. Limited knowledge exists concerning when and how to use anticoagulation or antithrombotic treatment. We studied the activation of coagulation (prothrombin fragment 1 + 2 [PF1 + 2] and D-dimer), platelets (,-thromboglobulin [,-TG]) and fibrinolysis (plasmin-antiplasmin complexes [PAP]) during RF ablation of accessory pathways in 30 patients. They were randomized to receive heparin (100 IU/kg, intravenously) (1) immediately after introduction of the femoral venous sheaths (group I) or (2) after the initial electrophysiological study, prior to the delivery of RF current (groups II and III). Group II additionally received saline irrigation of all femoral sheaths. After the initial bolus, 1,000 IU of heparin was supplied hourly in all groups. Within groups II and III, median plasma values of PF1 + 2 and ,-TG more than tripled (P , 0.007) during the diagnostic study and gradually declined during heparin administration despite RF current delivery. Median D-dimer tripled (P = 0.005) and PAP doubled (NS) before heparin administration; then both remained around the upper reference values. In the early heparin group, however, PF1 + 2, Ddimer, and PAP did not rise at all, and ,-TG showed only a slight increase towards the end of the procedure. The differences between group I versus groups II and III were statistically significant prior to the first RF current delivery (PF1 + 2, D-dimer, and ,-TG) and by the end of the procedure (PF1 + 2, D-dimer, and PAP). In conclusion, "late" heparin administration allows hemostatic activation during the initial catheterization and diagnostic study. By administering intravenous heparin immediately after introduction of the venous sheaths, hemostatic activation is significantly decreased. Saline irrigation of the venous sheaths added nothing to late heparin administration. [source] Quantification of heparin-induced TFPI release: a maximum release at low heparin doseBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 6 2002Michiel J. B. Kemme Aims Heparin releases tissue factor pathway inhibitor (TFPI) from the endothelium and this release may decrease after repeated high dose heparin administration. The primary aim was to investigate and quantify this phenomenon during a short low dose heparin infusion. Also, the effects of heparin on tissue plasminogen activator (t-PA) were studied. Methods Nine healthy, nonsmoking, male volunteers (range 19,23 years) received a continuous heparin infusion (2000 IU) over 40 min. The endothelial TFPI release rate was estimated from the total TFPI concentration profile using a pharmacokinetic model. Results , Mean ,±,s.d. ,total ,and ,free ,TFPI ,increased ,from ,62.9 ± 9.4/8.3 ± 2.1 ng ml,1 at baseline to 237.2 ± 40.9/111.0 ± 19.9 ng ml,1 after 40 min infusion. The relationship between heparin concentration (anti-IIa activity) and TFPI concentration followed a maximum effect model and a clockwise loop (proteresis) was observed. The TFPI release rate rapidly increased to maximum of 200 ± 45 µg min,1 after 17.5 min heparin infusion but did not increase further although heparin concentrations further doubled. In contrast to TFPI, t-PA antigen decreased from 5.6 ± 1.0 at baseline to 4.5 ± 1.0 ng ml,1 at the end of infusion (t = 40 min) (difference of 1.1 ng ml,1 (95% confidence interval; 0.9, 1.3). Conclusions Our application of concentration-effect models and pharmacokinetic principles to these haemostatic variables showed that endothelial TFPI release has a maximum that is already reached at low heparin dose, corresponding with an anti-IIa activity of 0.08 IU ml,1. The relationship between anti-IIa activity and TFPI release rate showed signs of acute tolerance (clockwise loop) indicating exhaustion of endothelial TFPI pools. These findings may be of importance for the heparin dose used in conditions such as unstable angina, in which the favourable effects of heparin have been ascribed to its ability to release TFPI. [source] Effect of low molecular weight heparin (dalteparin) and fondaparinux (Arixtra®) on human osteoblasts in vitro,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 2 2005A. E. Handschin Background: The prolonged administration of heparin for prevention and treatment of venous thromboembolism has been associated with a risk of heparin-induced osteoporosis. Fondaparinux is a new antithrombotic drug that specifically inhibits factor Xa. Because of the known interactions of other antithrombotic agents with bone remodelling, the effects of fondaparinux on human osteoblasts were analysed in vitro. Methods: Primary human osteoblast cell cultures were incubated with either the low molecular weight heparin dalteparin at concentrations of 30, 300 and 900 µg/ml or with fondaparinux at concentrations of 25, 50, 100, 150, 200 and 250 µg/ml. Cellular proliferation rate and protein synthesis were measured. Expression of genes encoding osteocalcin, collagen type I and alkaline phosphatase was examined by reverse transcriptase,polymerase chain reaction. Results: Incubation with dalteparin led to a significant, dose-dependent inhibition of osteoblast proliferation, inhibition of protein synthesis, and inhibited expression of phenotype markers (osteocalcin and alkaline phosphatase genes) after 3 and 7 days. No inhibitory effects were observed in the fondaparinux-treated cells. Conclusion: Fondaparinux did not inhibit osteoblast proliferation in vitro and may reduce the risk of heparin-induced osteoporosis associated with long-term heparin administration. Copyright © 2004 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Prospective Study of the Clinical Features and Outcomes of Emergency Department Patients with Delayed Diagnosis of Pulmonary EmbolismACADEMIC EMERGENCY MEDICINE, Issue 7 2007Jeffrey A. Kline MD Objectives:The authors hypothesized that emergency department (ED) patients with a delayed diagnosis of pulmonary embolism (PE) will have a higher frequency of altered mental status, older age, comorbidity, and worsened outcomes compared with patients who have PE diagnosed by tests ordered in the ED. Methods:For 144 weeks, all patients with PE diagnosed by computed tomographic angiography were prospectively screened to identify ED diagnosis (testing ordered from the ED) versus delayed diagnosis (less than 48 hours postadmission). Serum troponin I level, right ventricular hypokinesis on echocardiography, and percentage pulmonary vascular occlusion were measured at diagnosis; patients were prospectively followed up for adverse events (death, intubation, or circulatory shock). Results:Among 161 patients with PE, 141 (88%) were ED diagnosed and 20 (12%) had a delayed diagnosis. Patients with a delayed diagnosis were older than ED-diagnosed patients (61 [±15] vs. 51 [±17] years; p < 0.001), had a longer median time to heparin administration (33 vs. 8 hours; p < 0.001), and had a higher frequency of altered mental status (30% vs. 8%; p = 0.01) but did not have a higher frequency of prior cardiopulmonary disease (25% vs. 23%). Patients with a delayed diagnosis had equal or worse measures of PE severity (right ventricular hypokinesis on echocardiography, 60% vs. 58%; abnormal troponin I level, 55% vs. 24%); on computed tomographic angiography, ten of 20 patients with a delayed diagnosis had PE in lobar or larger arteries and >50% vascular obstruction. Patients with a delayed diagnosis had a higher rate of in-hospital adverse events (9% vs. 30%; p = 0.01). Conclusions:In this single-center study, the diagnosis of PE was frequently delayed and outcomes of patients with delayed diagnosis were worse than those of patients with PE diagnosed in the ED. [source] EFFECT OF BAY 41-2272 IN THE PULMONARY HYPERTENSION INDUCED BY HEPARIN,PROTAMINE COMPLEX IN ANAESTHETIZED DOGSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2007Cristiane F Freitas SUMMARY 1BAY 41-2272 is a potent activator of the nitric oxide-independent site of soluble guanylate cyclase and has been recently introduced as a new therapeutic agent to treat chronic pulmonary hypertension (PH) in neonatal sheep. Because the in vivo heparin,protamine interaction may lead to severe PH, the aim of the present study was to evaluate the effects of BAY 41-2272 in the PH induced by heparin,protamine interaction in anaesthetized dogs. 2Sixteen male dogs (10 mongrel dogs and six Beagles) were anaesthetized and instrumented for acquisition of mean arterial blood pressure (MABP), mean pulmonary arterial pressure (MPAP), heart rate (HR), pulmonary capillary wedge pressure (PCWP), cardiac index (CI) and indices of systemic and pulmonary vascular resistance (ISVR and IPVR, respectively). Plasma cGMP levels and Spo2 were evaluated. 3Intravenous administration of heparin (500 IU/kg) followed 3 min later by protamine (10 mg/kg) caused marked PH, as evaluated by the increase in MPAP, PCWP and IPVR. This was accompanied by a significant fall in MABP and a transient increase in HR. Infusion of BAY 41-2272 (10 µg/kg per h, starting 10 min before heparin administration) augmented plasma cGMP levels and slightly and significantly increased HR and CI, without affecting the other cardiovascular parameters. The elevation in IPVR, MPAP and PCWP triggered by the heparin,protamine interaction was significantly reduced in animals exposed to BAY 41-2272. 4In vehicle-treated dogs, the Spo2 values decreased significantly at the peak of the PH and this was significantly attenuated by treatment with BAY 41-2272. In addition, BAY 41-2272 (10 µmol/L) had no effect on the activated partial thromboplastin time of citrated plasma after the addition of heparin,protamine. 5In conclusion, BAY 41-2272 was effective in reducing canine PH induced in vivo by the heparin,protamine interaction, thus indicating its potential in the treatment of this type of disorder. [source] | ||||||||||