Jovan P Antovic

Karolinska University Hospital, Tukholma, Stockholm, Sweden

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Publications (43)112.69 Total impact

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    ABSTRACT: Introduction The oral direct thrombin inhibitor dabigatran is increasingly used to prevent thromboembolic stroke in patients with atrial fibrillation (AF). Routine laboratory monitoring is currently not recommended, but measurements of dabigatran and/or its effect are desirable in certain situations. We studied dabigatran exposure and compared different tests for monitoring of dabigatran in a real-life cohort of AF patients. Material and methods Ninety AF patients (68 ± 9 years, 67% men, mean CHADS2 score 1.5) were treated with dabigatran 150 (n = 73) or 110 mg BID (n = 17). Trough plasma concentrations of total and free dabigatran by liquid chromatography-tandem mass-spectrometry (LC-MS/MS) were compared to indirect measurements by Hemoclot thrombin inhibitors (HTI) and Ecarin clotting assay (ECA), as well as PT-INR and aPTT. Results Total plasma dabigatran varied 20-fold (12–237 ng/mL with 150 mg BID) and correlated well with free dabigatran (r2 = 0.93). There were strong correlations between LC-MS/MS and HTI or ECA (p < 0.001) but these assays were less accurate with dabigatran below 50 ng/mL. The aPTT assay was not dependable and PT-INR not useful at all. There were weak correlations between creatinine clearance (Cockcroft-Gault) and LC-MS/MS, HTI and ECA (p < 0.001 for all). A high body weight with normal kidney function was associated with low dabigatran levels. Conclusions HTI and ECA reflect the intensity of dabigatran anticoagulation, but LC-MS/MS is required to quantify low levels or infer absence of dabigatran. Most real life patients with a normal creatinine clearance had low dabigatran levels suggesting a low risk of bleeding but possibly limited protection against stroke.
    Thrombosis Research 01/2014; · 2.43 Impact Factor
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    ABSTRACT: Patients with haemophilia A have seriously impaired thrombin generation due to an inherited deficiency of factor (F)VIII, making them form unstable fibrin clots that are unable to maintain haemostasis. Data on fibrin structure in haemophilia patients remain limited. Fibrin permeability, assessed by a flow measurement technique, was investigated in plasma from 20 patients with severe haemophilia A treated on demand, before and 30 minutes after FVIII injection. The results were correlated with concentrations of fibrinogen, FVIII and thrombin-activatable fibrinolysis inhibitor (TAFI), and global haemostatic markers: endogenous thrombin potential (ETP) and overall haemostatic potential (OHP). Fibrin structure was visualized using scanning electron microscopy (SEM). The permeability coefficient Ks decreased significantly after FVIII treatment. Ks correlated significantly with FVIII levels and dosage, and with ETP, OHP and levels of TAFI. SEM images revealed irregular, porous fibrin clots composed of thick and short fibers before FVIII treatment. The clots had recovered after FVIII replacement almost to levels in control samples, revealing compact fibrin with smaller intrinsic pores. To the best of our knowledge, this is the first description of fibrin porosity and structure before and after FVIII treatment of selected haemophilia patients. It seems that thrombin generation is the main determinant of fibrin structure in haemophilic plasma.
    Thrombosis and Haemostasis 11/2013; 111(4). · 5.76 Impact Factor
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    ABSTRACT: Objective. Increased thrombin generation, as measured by the Calibrated Automated Thrombogram (CAT), has recently been reported to predict ischemic stroke, especially stroke with a cardioembolic source. However, there are few studies on thrombin generation using CAT in patients with manifest ischemic stroke, particularly in patients with cardioembolic stroke not yet on anticoagulation. Materials and methods. Therefore, a prospective cohort study of 205 stroke patients > 45 years of age was performed. They were recruited during their hospital stay or shortly thereafter. Inclusion criteria were ischemic stroke or TIA within two weeks and no atrial fibrillation (AF) in the history or at inclusion. Patients received a thumb ECG device in order to detect silent AF. Blood samples were collected at inclusion and after 1 month. Thrombin generation in plasma after addition of tissue factor was assessed in patients and in healthy controls. Results. Mean age of patients was 72 ± 7 years and 43% were females. Peak thrombin concentrations were variable among stroke patients but overall significantly higher at both time points (p < 0.0001) compared to controls, and tended to be highest in patients in whom paroxysmal atrial fibrillation was subsequently documented. Conclusion. Thrombin generation in patients with acute cardioembolic and non-cardioembolic schemic stroke/TIA is variable but overall higher compared to healthy subjects. The long-term prognostic value of thrombin generation in patients with a recent ischemic stroke deserves further investigation.
    Scandinavian journal of clinical and laboratory investigation 09/2013; · 1.38 Impact Factor
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    ABSTRACT: The soluble fibrin monomer (sFM) assay, like the D-dimer (DDi) assay, has the potential to be used both as an aid in the diagnosis of disseminated intravascular coagulation (DIC) and as a thrombotic marker. It differs from DDi in that it is a much earlier produced fragment produced only by thrombin action on fibrinogen, whereas DDi is a much later produced fragment formed by plasmin cleavage of cross-linked fibrin. In our study, we compared two commercially available automated sFM assays in the routine hospital setting using samples obtained from the general hospital ward and the emergency room. The results obtained with the two automated assays (Stago LIA sFM assays and the LPIA-Iatro SF assay) were compared with each other and with the results obtained using the routine semiquantitative hemagglutination assay. The study showed that both automated assays were comparable with each other. No patient sample previously classified as positive would be missed, but with the higher sensitivity in the automated tests, more samples are positive. In conclusion, we suggest that both automated tests are suitable for routine laboratory use. Both assays had the advantage over the hemagglutination assay in that previously frozen samples could be used, and the assays are easier and quicker to perform. The LIA sFM Stago has slightly better sensitivity but has a tendency to lower specificity than the Iatro SF test.
    International journal of laboratory hematology 06/2013; · 1.30 Impact Factor
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    ABSTRACT: BACKGROUND: Dabigatran is an oral direct thrombin inhibitor for which routine laboratory monitoring is currently not recommended. However, there are situations in which measurements of the drug and its effect are desirable. We therefore compared and validated different coagulation methods for assessments of dabigatran in clinical samples in relation to measurements of plasma dabigatran, without the purpose of establishing effective and safe concentrations of dabigatran in plasma. METHODS: Samples were obtained from 70 atrial fibrillation patients treated with dabigatran etexilate. Plasma concentrations were measured using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and were compared with coagulation methods Hemoclot thrombin inhibitors (HTI) and Ecarin clotting assay (ECA), as well as with prothrombin time-international normalized ratio (PT-INR) and activated partial thromboplastin time (aPTT). RESULTS: A wide range of dabigatran concentrations was determined by LC-MS/MS (<0.5-586 ng/mL). Correlations between LC-MS/MS results and estimated concentrations were excellent for both HTI and ECA overall (r(2) = 0.97 and 0.96 respectively, p < 0.0001), but the precision and variability of these assays were not fully satisfactory in the low range of dabigatran plasma concentrations, in which ECA performed better than HTI. aPTT performed poorly, and was normal (<40 s) even with dabigatran levels of 60 ng/mL. PT-INR was normal even at supratherapeutic dabigatran concentrations. CONCLUSION: LC-MS/MS is the gold standard for measurements of dabigatran in plasma. Alternatively, either HTI or ECA assays may be used, but neither of these assays is dependable when monitoring low levels or to infer total absence of dabigatran. The aPTT assay is relatively insensitive to dabigatran, and normal aPTT results may be observed even with therapeutic dabigatran concentrations.
    European Journal of Clinical Pharmacology 06/2013; · 2.70 Impact Factor
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    ABSTRACT: Multiple electrode aggregometry (MEA) is used to measure platelet function. Pneumatic tube transport systems (PTS) for delivery of patient samples to a central laboratory are often used to reduce turnaround time for vital analyses. We evaluated the effects of PTS transport on platelet function as measured by MEA. Duplicate samples were collected from 58 individuals. One sample was sent using PTS and the other was carried by personnel to the lab. Platelet function was measured by means of a Multiplate® analyzer using the ADP test, ASPI test, COL test, RISTO test and TRAP test. Samples transported using PTS showed a reduction of AUC-values of up to a 100% of the average as compared to samples carried by personnel and a majority showed reductions of AUC-values greater than 20% of the average. Bias±95% limits of agreement for the ADP test were 26±56% of the average. Bias±95% limits of agreement for the ASPI test were 16±58% of the average. Bias±95% limits of agreement for the COL test were 20±54% of the average. Bias±95% limits of agreement for the RISTO were 14±79% of the average. Bias±95% limits of agreement for the TRAP test were 19±45% of the average. We conclude that PTS transport affect platelet activity as measured by MEA. We advise against clinical decisions regarding platelet function on the basis of samples sent by PTS in our hospital settings.
    Thrombosis Research 05/2013; · 2.43 Impact Factor
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    ABSTRACT: Obesity is a known risk factor for venous and arterial thrombosis but the mechanisms are still unclear. In women, obesity is correlated with low-grade inflammation and recent data show that BMI is positively associated with thrombin generation. We explored the correlations between obesity, inflammation and thrombin generation in women with increased thrombotic risk by looking at a cohort of women with prior venous thrombosis. One hundred and fifty-six women age 18-65 years were enrolled at diagnosis of first venous thromboembolism (VTE). Plasma samples were obtained at least 3 weeks after cessation of anticoagulant treatment. Thrombin generation was determined with the calibrated automated thrombography (CAT) assay and the Innovance ETP assay. Thrombin generation started later but was more pronounced with higher endogenous thrombin generation potential (ETP) determined with CAT in patients with obesity. The Innovance ETP assay showed results consistent with CAT. Furthermore, patients with obesity had significantly higher levels of fibrinogen, C-reactive protein and plasminogen activator inhibitor-I (PAI-I) than patients without obesity. Increased levels of fibrinogen were the main determinant of the prolonged lag-time in patients with obesity whereas higher levels of prothrombin could account for the difference in the ETP between the groups. We found an association between BMI and ETP values using two different methods to measure thrombin generation. Obesity correlated with increased thrombin generation in women with VTE and the main determinants of this hypercoagulable state were increased levels of fibrinogen and prothrombin. This shows a possible link between obesity, low-grade inflammation and increased thrombin generation in women at increased risk for future thrombosis.
    Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis 03/2013; · 1.25 Impact Factor
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    ABSTRACT: BACKGROUND: Microparticles (MPs) are small membrane vesicles (0.1-1 μm) released from various cells after activation and/or apoptosis. There are limited data about their role in hemophilia A. PATIENTS AND METHODS: Blood samples were taken before and 30 minutes after FVIII injection in 18 patients with severe hemophilia A treated on demand. Flow-cytometric determination of total MPs (TMPs) using lactadherin, platelet MPs (PMPs) (CD42a), endothelial MPs (EMPs) (CD144) and leukocyte MPs (LMPs) (CD45) was performed. The results were compared with data on endogenous thrombin potential (ETP), overall hemostatic potential (OHP), fibrin gel permeability and thrombin-activatable fibrinolysis inhibitor (TAFI). RESULTS AND CONCLUSIONS: TMPs and PMPs decreased after treatment (to 1015±221 [SEM] and 602±134 × 10(6) /L in comparison with values before treatment (2373±618 and 1316±331; p<0.01). EMPs also decreased after treatment (78±12 vs. 107±13; p<0.05) while LMPs were not influenced. Both TMP and PMP counts inversely correlated, moderately but statistically significantly, with data on OHP, ETP, fibrin network permeability and TAFI/TAFIi (p<0.05 for all). EMP counts correlated only with ETP (p<0.05), while LMP counts did not show any correlation. TMP and PMP counts also inversely correlated with FVIII levels (p<0.05). TMP, PMP and EMP counts decreased after on-demand treatment with FVIII concentrate in hemophilia A patients. The decrease in circulating MPs, which inversely correlated with hemostatic activation, may imply that MPs are incorporated in the hemostatic plug formed after FVIII substitution at the site of injury. © 2012 International Society on Thrombosis and Haemostasis.
    Journal of Thrombosis and Haemostasis 12/2012; · 6.08 Impact Factor
  • Thrombosis Research 10/2012; 130:S116. · 2.43 Impact Factor
  • Thrombosis Research 10/2012; 130:S106. · 2.43 Impact Factor
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    ABSTRACT: Haemophilia A patients with similar levels of factor VIII (FVIII) may have different bleeding phenotypes and responses to treatment with FVIII concentrate. Therefore, a test which determines overall haemostasis may be appropriate for treatment monitoring in some patients. We studied two global haemostatic methods:endogenous thrombin potential (ETP) and overall haemostatic potential(OHP) before and after injection of FVIII concentrate in patients with haemophilia A treated prophylactically and on-demand. A significant correlation between FVIII and both ETP and OHP was observed, while ETP and OHP differed between patients with severe and mild clinical phenotypes. Both ETP and OHP differed significantly between severe, moderate and mild haemophilia A and controls. ETP and OHP increased after intravenous injection of FVIII concentrate in both groups of patients, but in spite of higher pre-treatment values of both ETP and OHP in patients treated prophylactically, and much higher post-treatment FVIII levels in comparison with the values in patients treated on-demand, no difference after treatment was observed for either ETP or OHP. ETP and OHP may be additional alternatives for monitoring (and even for individual tailoring) treatment in patients with haemophilia A.
    Thrombosis and Haemostasis 04/2012; 108(1):21-31. · 5.76 Impact Factor
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    ABSTRACT: D-dimer (DD) assays are effective for the exclusion of deep-vein thrombosis (DVT), but point-of-care (POC) DD assays have not been fully evaluated. We have compared five POC DD assays (Pathfast, Cardiac, Vidas, Stratus and NycoCard) with our routine DD method (Tinaquant), testing 60 samples from patients with suspected DVT. Using 0.5 μg/mL as a cut-off value, four samples tested negative with Tinaquant were positive with Pathfast. There were no Tinaquant-positive samples tested negative with Pathfast, while the overall agreement (k = 0.81) was very good. Four samples were discrepant between Tinaquant and Cardiac (cut-off, 0.4 μg/mL), while k = 0.72. One of two Tinaquant-negative samples was shown to be positive for either Vidas (cut-off, 0.5 μg/mL) or Stratus (cut-off, 0.4 μg/mL), respectively. The agreement with Tinaquant was excellent for both Vidas (k = 0.92) and Stratus (k = 0.94). Total CV was <10% for all four assays. Eight samples (of 27) were negative with NycoCard although they were positive with Tinaquant, while CV was 41%. Vidas cannot be considered a POC assay because the sample has to be centrifuged before testing. Our findings have also shown that the use of NycoCard is inappropriate. Stratus and Pathfast have a similar analytical profile in comparison with the Tinaquant method. Cardiac is potentially less sensitive but may still be acceptable for use. It seems that the employment of these three assays for rapid bed-side analysis offers a possibility to adequately rule out DVT in outpatients within minutes after admission.
    International journal of laboratory hematology 04/2012; 34(5):495-501. · 1.30 Impact Factor
  • Thrombosis Research 01/2012; 129(1):95-7. · 2.43 Impact Factor
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    Journal of Internal Medicine 08/2011; 270(5):496-9. · 5.79 Impact Factor
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    ABSTRACT: Thrombin activatable fibrinolysis inhibitor (TAFI) down-regulates fibrinolysis after activation by thrombin/thrombomodulin. We investigated the effect of treatment with FVIII concentrate on plasma levels of pro-TAFI and activated TAFI in haemophilia A patients. Samples were collected pre and posttreatment from patients treated prophylactically or on-demand. Pro-TAFI, TAFI/TAFIi and FVIII levels were measured in all samples. Treatment had no effect on pro-TAFI levels. Pro-TAFI was similar in both patient groups but higher than in controls. Patients from the prophylactic treatment group had measurable FVIII levels pretreatment while in the treatment-on-demand group FVIII levels were ≤0.01 IU/mL. In the prophylactic treatment group, the levels of TAFI/TAFIi were significantly lower pre- and posttreatment (4.31 ± 3.14 and 3.48 ± 2.65 ng/mL respectively) than in the on-demand group (13.02 ± 3.47 and 14.87 ± 3.47 ng/mL respectively). This difference may be due to release of tissue factor at the injury site in the on-demand group. This could induce thrombin and TAFI activation within the clot counterbalancing fibrinolysis in these patients. In the prophylactic group, no injury existed, thus there was insufficient thrombin generation within the clot to activate TAFI. These findings suggest that in patients to whom FVIII is administered on demand the fibrinolysis activity is more down regulated than in patients following a prophylactic treatment regime.
    International journal of laboratory hematology 06/2011; 34(1):35-40. · 1.30 Impact Factor
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    ABSTRACT: We investigated the effects of statin treatment on platelet-derived microparticles (PMPs) and thrombin generation in atherothrombotic disease. Nineteen patients with peripheral arterial occlusive disease were randomised to eight weeks of treatment with atorvastatin or placebo in a cross-over fashion. Expression of GPIIIa (CD61), P-selectin (CD62P), tissue factor (TF, CD142) and phosphatidylserine (PS; annexin-V or lactadherin binding) was assessed on PMPs. Thrombin generation in vivo was assessed by measurement of prothrombin fragment 1+2 in plasma (F1+2) and ex vivo by using the calibrated automated thrombogram (CAT). During atorvastatin treatment, expression of TF, P-selectin and GPIIIa was significantly reduced vs. placebo (p<0.001 for all). No effect on annexin-V or lactadherin binding was seen. Thrombin generation was significantly reduced during atorvastatin as assessed by both the CAT assay (p<0.001) and by measurements of F1+2 (p<0.01). Subsequent in vitro experiments showed that when TF on microparticles (MPs) was blocked by antibodies, the initiation of thrombin generation was slightly but significantly delayed. Blocking PS on MPs using annexin-V or lactadherin resulted in almost complete inhibition of thrombin generation. In conclusion, atorvastatin reduces thrombin generation and expression of TF, GPIIIa and P-selectin on PMPs in patients with peripheral vascular disease. Microparticle-bound TF slightly enhances initiation of thrombin generation whereas negatively charged surfaces provided by MPs or lipoproteins could reinforce thrombin generation. Statins may inhibit initiation of thrombin generation partly through a microparticle dependent mechanism but the main effect is probably through reduction of lipoprotein levels.
    Thrombosis and Haemostasis 05/2011; 106(2):344-52. · 5.76 Impact Factor
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    ABSTRACT: Heparin-induced thrombocytopenia (HIT, type II) is an immune-mediated disorder due to antibodies formed against heparin-platelet factor 4 complexes, usually appearing at days 5 to 14 after initiation of heparin. It is important to recognize HIT because heparin prophylaxis or treatment paradoxically associates with new venous and/or arterial thrombosis. Early clinical suspicion and diagnosis together with proper pharmacotherapy and close laboratory monitoring are the cornerstones for successful management. This includes monitoring of Thrombocytopenia, its Timing to heparin administration, appearance of new Thrombosis or resistance to treatment, and differential diagnosis by exclusion of o Ther causes (the 4T's). Specific attention should be paid to the absence or presence of thrombosis and to tailoring thromboprophylaxis or anticoagulant therapy with a nonheparin alternative. Even in the absence of HIT-associated thrombosis, an active policy for prolonged thromboprophylaxis is demanded. Rapid and reliable assays should be developed for diagnosis and anticoagulation monitoring to secure safe management with nonheparins. Semiquantitative testing for on-call hours should be available and later confirmed as clinically needed. Alternative therapeutic options are available, but because their use is infrequent, experienced coagulation treatment centers should provide guidance in the treatment and in laboratory monitoring. Most of the evidence in HIT is grade IC, and thus the best evidence is provided by clinical experience. New anticoagulants and platelet inhibitors may offer future alternatives in the management of HIT, but the current treatment options provide the best experience and benefit. The joint clinical and laboratory guidelines provided in this article along with two practical case scenarios were prepared by a Nordic expert panel. They will be valuable for hematologists and colleagues who do not routinely encounter HIT.
    Seminars in Thrombosis and Hemostasis 04/2011; 37(3):328-36. · 4.22 Impact Factor
  • Thrombosis Research - THROMB RES. 01/2011; 127.
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    ABSTRACT: Activation of haemostasis during physical stress or during myocardial ischemia could be an important mechanism to trigger coronary and stent thrombosis. We examined changes in haemostatic parameters and its association with myocardial ischemia during adenosine-exercise-SPECT (adeno-EX) stress test in coronary patients at least 4 months after coronary stenting. The aim of this study was to examine relationship between changes in haemostatic parameters and stress induced myocardial ischemia quantified by perfusion scintigraphy in stented coronary patients. Thirty-seven patients on dual antiplatelet therapy (26 on clopidogrel plus aspirin and 11 on aspirin only) 4-8 months after successful intracoronary stent implantation were enrolled in the study. We determined the levels of platelet aggregability (PA) on ADP (PA-ADP) and epinephrine (PA-EPI), beta-thromboglobulin, platelet factor-4, protein C (PC) and antithrombin (AT) before and 15 minutes after intravenous injection of 150 micro/kg adenosine for4 minutes concomitant with supine ergo-bicycle exercise test for 50 W. The size of stress perfusion defect was measured 15 minutes after stress and in rest 4 hours later by 99mTc-tetrofosmin single photon emission computed tomography (SPECT) within 17 myocardial segments. There were no differences between haemostatic parameters before and after stress. A significant myocardial ischemia after exercise was registered in 12 patients on combined antiaggregation therapy and in 5 patients on aspirin. In this preliminary report, because of a small number of patients in the aspirin group we did not analyse difference in the levels of haemostatic markers and their correlations with the size of perfusion defect. The only significant difference between measured haemostatic parameters in the patients with stress induced ischemia compared to the patients without it, was a lower level of AT activity after stress (81.0% vs. 87.5%; p = 0.027). Antithrombin activity before stress had significant negative correlation with the size of perfusion defect in rest (R2 = 0.219; p = 0.016) and PC activity before stress had significant linear correlation with stress perfusion defect (R2 = 0.248; p = 0.010). Baseline activities of natural anticoagulant proteins AT and PC are associated with the size of myocardial perfusion defect during adeno-EX-SPECT test. Patients with significant stress-induced ischemia had lower levels of AT activity after stress.
    Srpski arhiv za celokupno lekarstvo 01/2010; 138 Suppl 1:28-32. · 0.17 Impact Factor
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    ABSTRACT: Flow cytometry (FCM) is the most commonly used method for detection of platelet-derived microparticles (PDMPs), but it is poorly standardized and mainly used for "bedside" analyses in fresh samples. If PDMPs could be analyzed in previously frozen samples it would increase the usefulness of the method. However, cell membrane fragments from contaminating cells created during freezing/thawing may cause artifacts and disturb measurements. PDMPs were labeled with monoclonal antibodies directed against CD42a and CD62P, or CD42a and CD142. The PDMP gate was determined using forward scatter (FSC) and CD42a expression. The mean fluorescence intensities (MFIs) of CD62P or CD142 positive particles were translated into MESF -values (Molecules of Equivalent Soluble Fluorochrome) using a standard curve. FITC-labeled phalloidin (which binds to intracellular actin) was used to detect destroyed cells/cell fragments. Phalloidin-positive particles were significantly more common in supernatants of frozen/thawed platelet rich and platelet poor plasma samples compared with supernatants of platelet free plasma. High-speed centrifugation was then used to obtain PDMP samples with low contamination of cell fragments. Electron microscopy showed that these samples contained numerous round stained particles with cellular membranes of a size of 100-700 nm. Reproducibility experiments using plasma samples from healthy individuals showed that the coefficients of variation (CVs) of MESF values of CD62P and CD142 (both intra- and interassay) were <10%, and the variation between two cytometers in two different laboratories was <5%. We also found that PDMP expression of CD142 (i.e. tissue factor [TF]) and CD62P (i.e P-selectin) was around two times higher in samples from type 1-diabetes patients compared with those from healthy controls (p<0.001). The use of MESF values to quantify PDMP expression of P-selectin and TF yields reproducible data and enables comparison of data between laboratories. If high-speed centrifugation is performed, contamination of cell fragments is low in frozen/thawed samples.
    Thrombosis Research 11/2009; 125(3):e110-6. · 2.43 Impact Factor

Publication Stats

245 Citations
112.69 Total Impact Points


  • 2001–2014
    • Karolinska University Hospital
      • • Department of Clinical Chemistry
      • • Department of Pediatric Anesthesiology and Intensive Care
      • • Clinical Pharmacology Trial Unit
      • • Department of Hematology
      Tukholma, Stockholm, Sweden
  • 2001–2013
    • Karolinska Institutet
      • • Institutionen för kliniska vetenskaper, Danderyds sjukhus
      • • Institutionen för molekylär medicin och kirurgi
      Solna, Stockholm, Sweden
  • 2011
    • Institut za transfuziju krvi Srbije
      Beograd, Central Serbia, Serbia
  • 2007
    • Danderyds Sjukhus AB
      Tukholma, Stockholm, Sweden
  • 1993
    • University of Niš
      • Department of Biochemistry
      Niš, Serbia