Blood Coagulation & Fibrinolysis最新文献

Background: Placenta-related obstetric complications (PROCs) such as miscarriage, fetal growth restriction, preeclampsia, and preterm birth are the major causes of maternal and fetal morbidity and mortality. The objective of this study was to search the relevance of plasminogen activator inhibitor-1 (PAI-1) polymorphisms and co-morbidities and the risk factors for PROCs such as miscarriage, fetal growth restriction, preeclampsia, and preterm birth.

Method: This retrospective study analyzed the PAI-1 genotype in a cohort of 268 multiparous women with poor obstetric history. Poor obstetric history was defined as the presence of at least one of the PROCs and/or poor gestational outcomes at the previous pregnancy/pregnancies.

Results: 5G allele frequency was higher than the 4G allele frequency in the cohort (0.767 vs. 0.233). The frequencies of having at least one risk factor are relatively similar among the different PAI-1 genotypes ( P  > 0.05). However, the presence of MTHFR polymorphisms (homozygous and compound heterozygous forms of C677T and A1298G) and hereditary thrombophilia (Factor V Leiden and prothrombin G20210A gene mutations, and FXIII deficiency) were found to be associated with PAI 4G/4G ( P  = 0.048) and 5G/5G ( P  = 0.022) genotypes, respectively. Significant differences were not observed in other risk factors and co-morbidities such as autoimmune disorders, chronic inflammatory diseases, history of venous thromboembolism, carbohydrate metabolism disorders, hyperlipidemia, cardiovascular and cerebrovascular diseases depending on PAI-1 genotypes ( P  > 0.05).

Conclusion: MTHFR polymorphisms were found to be associated with PAI 4G/4G genotype, while 5G/5G genotype was observed more frequently in hereditary thrombophilia cases.

Objectives: Angiographic high thrombus burden (HTB) is associated with increased adverse cardiovascular events in patients with ST-elevation myocardial infarction (STEMI). HbA1c and C-peptide are two interrelated bioactive markers that affect many cardiovascular pathways. HbA1c exhibits prothrombogenic properties, while C-peptide, in contrast, exhibits antithrombogenic effects. In this study, we aimed to demonstrate the value of combining these two biomarkers in a single fraction in predicting HTB and short-term mortality in patients with STEMI.

Methods: 1202 patients who underwent primary percutaneous coronary intervention (pPCI) for STEMI were retrospectively included in this study. The study population was divided into thrombus burden (TB) groups and compared in terms of basic clinical demographics, laboratory parameters and HbA1c/C-peptide ratios (HCR). In addition, short-term mortality of the study population was compared according to HCR and TB categories.

Results: HCR values were significantly higher in the HTB group than in the LTB group (3.5 ± 1.2 vs. 2.0 ± 1.1; P  < 0.001; respectively). In the multivariable regression analysis, HCR was determined as an independent predictor of HTB both as a continuous variable [odds ratio (OR): 2.377; confidence interval (CI): 2.090-2.704; P  < 0.001] and as a categorical variable (OR: 5.492; CI: 4.115-7.331; P  < 0.001). In the receiver operating characteristic (ROC) analysis, HCR predicted HTB with 73% sensitivity and 72% specificity, and furthermore, HCR's predictive value for HTB was superior to HbA1c and C-peptide. The Kaplan-Meier cumulative survival curve showed that short-term mortality increased at HTB. In addition, HCR strongly predicted short-term mortality in Cox regression analysis.

Conclusions: In conclusion, HCR is closely associated with HTB and short-term mortality in STEMI patients.

Autoimmune factor XIII/13 deficiency (aFXIII deficiency) is a rare hemorrhagic disorder, for which typical guideline-directed treatment is aggressive immunosuppressive therapy. Approximately 20% of patients are over 80 years old; however, and optimum management of such patients has not reached consensus. Our elderly patient had massive intramuscular hematoma, and aFXIII deficiency was diagnosed. The patient opted against aggressive immunosuppressive therapy, so he was managed with conservative treatment only. Thorough survey of other correctable causes of bleeding and anemia is also required in similar cases. Our patient's serotonin-norepinephrine reuptake inhibitor use and multivitamin deficiency (vitamin C, B 12 and folic acid) were revealed to be aggravating factors. Fall prevention and muscular stress prevention are also important in elderly patients. Our patient had two relapses of bleeding within 6 months, which were improved spontaneously by bed rest without factor XIII replacement therapy or blood transfusion. Conservative management may be preferred for frail and elderly patients with aFXIII deficiency when they opt against standard therapy.

The goal of this study was to describe hematologic and coagulation laboratory parameters and identify if these laboratory studies could predict blood loss in a cohort of pediatric patients undergoing complex cranial vault reconstruction (CCVR) for repair of craniosynostosis. We reviewed records from 95 pediatric CCVR patients between 2015 and 2019. Primary outcome measures were hematologic and coagulation laboratory parameters. Secondary outcome measures were intraoperative and postoperative calculated blood loss (CBL). Preoperative laboratory values were within normal limits and did not predict outcomes. Intraoperative platelet count and fibrinogen predicted CBL but without clinically relevant thrombocytopenia or hypofibrinogenemia. Intraoperative prothrombin time (PT) and partial thromboplastin time (PTT) predicted perioperative CBL, possibly reflecting surgically induced coagulopathy. Postoperative laboratory values did not predict postoperative blood loss. We found that standard hematologic and coagulation laboratory parameters predicted intraoperative and postoperative blood loss but provided limited mechanistic information to improve our understanding of coagulopathy in craniofacial surgery.

Objective: To compare the risk of readmissions for major bleeding within one year between apixaban and rivaroxaban as a component of triple antithrombotic therapy.

Methods: This study was a multicenter, retrospective cohort study conducted at two academic medical centers in the Western New York and New York City region between July 1, 2011 and September 25, 2019. Adult patients were included if they were diagnosed with atrial fibrillation or venous thromboembolism and discharged on new triple antithrombotic therapy. The primary outcome compared the rates of 1-year readmission for major bleeding between apixaban and rivaroxaban groups. Secondary outcomes included rate of ischemic outcomes. Time to event analysis was determined with a Kaplan-Meier plot and Cox proportional hazard ratios (HR).

Results: A total of 378 patients were included in the study, 212 in the apixaban group and 166 in the rivaroxaban group. Within 1 year, readmission for major bleeding events occurred in six (2.8%) patients in the apixaban group and four (2.4%) patients in the rivaroxaban group ( P  = 1.000). After adjustment, the major bleeding event rate was not statistically significantly different between apixaban and rivaroxaban [adjusted hazard ratio (aHR) 0.68, 95% confidence interval (CI) 0.12-3.77; P  = 0.6624]. Higher albumin levels were identified to be protective against major bleeding related readmission events (aHR 0.18, 95% CI 0.05-0.63; P  = 0.0072). The ischemic outcome occurred in seven (3.3%) patients in the apixaban group and three (1.8%) in the rivaroxaban group ( P  = 0.7368).

Conclusion: Use of apixaban or rivaroxaban in a triple antithrombotic regimen was not associated with bleeding or ischemic outcomes.

Limited data is available on factor XII deficiency in critically ill patients with prolonged activated partial thromboplastin time (aPTT). The association of factor XII deficiency with an increased risk of thromboembolism is unclear. This prospective observational study assessed the incidence of factor XII deficiency among critically ill patients with prolonged aPTT (>40 s), whether factor XII deficiency manifesting as prolonged aPTT was associated with an increased risk of thromboembolism, and clotting time on a viscoelastic (ROTEM) test was useful to predict factor XII deficiency. Of the 40 included patients, 48% [95% confidence interval (CI) 33-63) had a factor XII deficiency (mean ± standard deviation of factor XII level of all patients: 54% ± 29%). Factor XII levels were not significantly correlated with the measured aPTT ( r  = -0.163, P  = 0.315). Factor XII deficiency was significantly more common in patients who were less critically ill ( P  = 0.027), but it was not significantly related to Disseminated Intravascular Coagulation scores ( P  = 0.567). The incidence of symptomatic venous thromboembolism ( P  = 0.246), allogeneic blood transfusion ( P  = 0.816), and hospital mortality ( P  = 0.201) were not significantly different between those with and without factor XII deficiency. The clotting time on the viscoelastic test was not predictive of factor XII deficiency (area under the receiver-operating characteristic = 0.605, P  = 0.264). Factor XII deficiency was common in critically ill patients with a prolonged aPTT. There was no association between factor XII deficiency and risk of thromboembolism. The clotting time on ROTEM was not predictive of the presence of factor XII deficiency.

Acquired hemophilia A (AHA) is a rare, life-threatening hemorrhagic disease caused by autoantibodies against factor VIII (FVIII), and bypassing agents (BPA) are used to control bleeding. However, some cases need a change of BPA or BPAs given sequentially or in combination for refractory bleeding. A 71-year-old man was admitted with subcutaneous hemorrhage. Laboratory investigations showed prolongation of activated partial thromboplastin time (APTT) and low-coagulation FVIII activity and FVIII inhibitor; we, therefore, diagnosed AHA. He was treated with recombinant factor VIIa (rFVIIa) BPA and prednisolone. However, his symptoms did not improve sufficiently, thus we switched BPA to activated prothrombin complex concentrate. Unfortunately, this was not effective and he suffered hemorrhagic shock. Therefore, we selected rFVIIa, with plasma-derived FVIIa and factor X (pd-FVIIa/FX) as combination therapy, and hemostasis was achieved without thrombosis. This case suggests that the combination of rFVIIa and pd-FVIIa/FX short-term can be well tolerated for refractory hemorrhage in AHA.

Risk factors for venous thromboembolism (VTE) in elderly patients with acute myeloid leukemia (AML) are not known by race. The aim of this study was to determine the association of VTE with known risk factors and the impact of VTE on mortality in elderly white, black and Asian patients with AML. The merged SEER-Medicare database (2000-2015) was used for patients aged at least 65 years diagnosed with AML. Multivariable logistic regression was used to examine the association of VTE with known risk factors and Cox proportional hazards regression was used to evaluate the association of VTE with mortality in white, black and Asian patients. Among 21 403 AML patients aged at least 65years, VTE was diagnosed in 10.6% of 18 731 white patients, 13.4% of 1362 black and 5.6% of 1310 Asian patients. Overall, the adjusted risk of VTE in black patients was similar to white patients, but Asian patients had a lower risk of VTE. Risk factors for VTE in white patients were age less than 75 years, female sex, chemotherapy and comorbid medical conditions, including hypertension, anemia, chronic kidney and lung disease, hyperlipidemia, heart failure and obesity. In black patients, hyperlipidemia, and heart failure and in Asian patients, age less than 75 years, female sex, chemotherapy and hypertension and myocardial infarction were associated with VTE. Central venous catheter placement was a predictor of VTE in all three races. Our study identified risk factors for VTE by race in elderly white, black and Asian AML patients.