Introduction: Statins were previously shown to suppress cellular tissue factor (TF) in vitro. Here, we investigated the effect of atorvastatin on the TF-pathway and thrombin generation after coronary angioplasty and stenting in vivo.
Materials And Methods: A cohort of 30 patients with coronary artery disease (CAD) was randomised to treatment with either none (n=10), 10 mg (n=10) or 80 mg (n=10) atorvastatin per day for the postinterventional period of 6 months starting the day before percutaneous coronary intervention (PCI). Fasting blood samples were collected on admission and after 6 weeks and 6 months of statin therapy to determine sTF, free tissue factor pathway inhibitor (TFPI) and prothrombin fragment F1.2 by immunoassay.
Results: Soluble TF (sTF) significantly correlated with thrombin generation as measured by prothrombin fragment F1.2 at baseline. This correlation was lost 6 weeks and 6 months after initiation of statin therapy. In vivo, F1.2 was significantly lowered after 6 months of statin therapy by both, low dose (0 vs. 10 mg: 1.3+/-0.3 vs. 0.7+/-0.2 ng/ml; P<0.05) and high dose (0 vs. 80 mg: 1.2+/-0.3 vs. 0.6+/-0.2 ng/ml; P=0.01) atorvastatin compared to control. However, sTF and free TFPI did not change significantly with atorvastatin therapy when compared to baseline or control.
Conclusions: Our results demonstrate reduced in vivo generation of thrombin six months after percutaneous coronary intervention and statin therapy independent of sTF and free TFPI.
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http://dx.doi.org/10.1016/j.thromres.2004.09.017 | DOI Listing |
Neurol Neurochir Pol
December 2024
Department of Thromboembolic Diseases, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.
Clinical Rationale For Study: We have reported that intracerebral haemorrhage (ICH) of unknown cause at a young age is associated with lower prothrombin and factor VII and higher antithrombin activity, along with the formation of looser fibrin networks displaying enhanced lysability. Patients with mild-to-moderate bleeding of unknown cause have elevated levels of free plasma tissue factor pathway inhibitor alpha (fTFPIα), inhibiting the tissue factor-factor VII complex and prothrombinase.
Aim Of Study: We hypothesised that patients with an intracerebral haemorrhage (ICH) of unknown cause may also exhibit higher fTFPIα.
J Microbiol Immunol Infect
December 2024
Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan; Department of Pediatrics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, 704, Taiwan; Department of Pediatrics, National Cheng Kung University Hospital Dou-Liou Branch, College of Medicine, National Cheng Kung University, Yunlin 640, Taiwan. Electronic address:
Background: Previously we identified a complex of non-structural protein (NS) 1 - Thrombin (NST) in dengue infected patients. Here, we investigated how the concentration of NS1 and NST differ in various dengue severity levels as well as their demographic and clinical features. Several comorbid (hypertension, diabetes, and chronic renal failure) often found in dengue patients were also measured and analyzed.
View Article and Find Full Text PDFBMJ Open
December 2024
Department of Paediatrics, Nara Medical University, Kashihara, Japan.
Introduction: Emicizumab prophylaxis is approved for people of all ages with haemophilia A (HA) including infants and children. Although previous studies have demonstrated the efficacy and tolerability of emicizumab in infants with HA, real-world data on emicizumab use in infants are limited. The Haemophilia A in Infancy and NewbOrns: multi-instituional prospective observational study to assess the efficacy anD safety of Emicizumab (HINODE) study aims to evaluate the coagulation potential and safety of emicizumab prophylaxis in infants with congenital HA from birth to <12 months of age.
View Article and Find Full Text PDFAnn Hematol
December 2024
Department of Clinical Laboratory, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Shangcai Village, Ouhai District, Wenzhou, 325000, China.
This study aims to investigate the clinical characterization and molecular pathogenic basis of hereditary protein C (PC) deficiency in two independent Chinese families, and conduct in vitro expression studies on the newly discovered p.Trp444Arg mutation. The PC activity (PC: A) was tested using the chromogenic substrate, and PC antigen (PC: Ag) was detected via enzyme-linked immunosorbent assay (ELISA).
View Article and Find Full Text PDFJ Thromb Haemost
December 2024
Department of Gastrointestinal and Minimally Invasive Surgery, Shaoxing Second Hospital, Shaoxing, Zhejiang, China. Electronic address:
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