Готові списки джерел за темами / Thrombotic risk

Добірка наукової літератури з теми "Thrombotic risk"

Автор: Grafiati
Опубліковано: 23 лютого 2024

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Статті в журналах з теми "Thrombotic risk"

1

Cheng, Hai, Dian Zhou, Jiang Cao, Wei Chen, Kunming Qi, Kailin Xu, and Jianlin Qiao. "A Study about the Relationship between Thrombotic Events and Peripheral Neutrophil-to-Lymphocyte Ratio in Patients with Newly Diagnosed Essential Thrombocythemia." Blood 132, Supplement 1 (November 29, 2018): 5465. http://dx.doi.org/10.1182/blood-2018-99-112785.

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Анотація:
Abstract To explore the role of neutrophil-to-lymphocyte ratio (NLR) in patients with newly diagnosed essential thrombocythemia (ET) and the relationship with thrombotic events.150 ET patients with ET from January 2013 to December 2017 were retrospectively enrolled in this study to investigate the risk factors of thrombosis and analyse the role of NLR in thrombotic events. The following parameters were evaluated: age, sex, blood routine examination, JAK2V617F mutation, cardiovascular risk factors, history of previous thrombosis, thrombosis during follow-up, examination and biopsy of bone marrow.Age(P=0.001) and JAK2 V617F mutation(P=0.003) were independent risk factors for thrombotic events at diagnosis after Logistic multivariate analysis. WBC count (P=0.047), NLR (P<0.001), age (P=0.037) and thrombosis at diagnosis (P=0.036) were independent risk factors for future thrombotic events and NLR was better for prediction of future thrombotic events than other risk factors in ROC curve. The thrombosis-free survival of thrombotic events in patients with higher NLR(median survival 22.3 months, 95% CI:17.8-26.8) was significantly shorter than that of patients with lower NLR(median survival 55.5 months, 95% CI:53.4-57.5) in Kaplan-Meier analysis (P<0.001). After 60 months of follow-up, patients with lower NLR had a thrombosis-free survival of 97.4%, while patients with higher NLR had a thrombosis-free survival of 46.7%. NLR at diagnosis was a better predictive parameter for future thrombotic events than other clinical parameters in ET patients, but was not associated with thrombosis at diagnosis. Disclosures No relevant conflicts of interest to declare.
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2

Mancuso, Salvatrice, Vincenzo Accurso, Marco Santoro, Simona Raso, Angelo Davide Contrino, Alessandro Perez, Florinda Di Piazza, Ada Maria Florena, Antonio Russo, and Sergio Siragusa. "The Essential Thrombocythemia, Thrombotic Risk Stratification, and Cardiovascular Risk Factors." Advances in Hematology 2020 (March 27, 2020): 1–5. http://dx.doi.org/10.1155/2020/9124821.

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Анотація:
Essential thrombocythemia is a rare hematological malignancy with good overall survival, but moderate to high risk of developing arterial or venous thrombosis lifelong. Different thrombotic risk scores for patients with essential thrombocythemia have been proposed, but only one of them (the IPSET-t scoring system) takes into account the classical cardiovascular risk factors as one of the scoring items. Currently, in clinical practice, the presence of cardiovascular risk factors in patients with diagnosis of ET rarely determines the decision to initiate cytoreductive therapies. In our study, we compared different risk models to estimate the thrombotic risk of 233 ET patients and the role of specific driver mutations and evaluated the impact that conventional cardiovascular risk factors (hypertension, cigarette smoking, diabetes, obesity, and dyslipidaemia) have on thrombotic risk in patients with ET. Perspective studies conducted on a polycentric large cohort of patients should be conducted to estimate the impact of cardiovascular risk factors in determining thrombosis in ET patients, evaluating the opportunity of initiating a cytoreductive therapy in patients with cardiovascular risk factors, even if classified into low to moderate risk groups according to other scoring systems.
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3

Yamamoto, J., T. Taka, K. Yamada, Y. Ijiri, M. Murakami, Y. Hirata, A. Naemura, et al. "Tomatoes have natural anti-thrombotic effects." British Journal of Nutrition 90, no. 6 (December 2003): 1031–38. http://dx.doi.org/10.1079/bjn2003988.

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The prevention of arterial thrombotic diseases has a high priority in developed countries. An inappropriate diet may be an important risk factor for thrombotic events. The daily intake of an anti-thrombotic diet may offer a convenient and effective way of prevention. The aim of the present study was to test tomato extracts for anti-thrombotic effects and to identify those varieties that have such an effect. A shear-induced platelet-function test (haemostatometry) was used to test anti-thrombotic potentialin vitro. Extracts from those tomato varieties that showed a significant anti-thrombotic activityin vitrowere further assessedin vivo, using a laser-induced thrombosis test in mice. One tomato variety (KG99-4) showed significant anti-thrombotic activity bothin vitroandin vivo. KG99-4 inhibited not only platelet-rich thrombus formation but also had a thrombolytic effect. It is concluded that haemostatometry can detect and classify the anti-thrombotic potential of fruits and vegetables and offers a simple way of screening for such effects.
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4

Navarro, Luana Magalhães, Damila Cristina Trufelli, Debora Rodrigues Bonito, Auro Del Giglio, and Patricia Weinschenker Bollmann. "Application of prognostic score IPSET-thrombosis in patients with essential thrombocythemia of a Brazilian public service." Revista da Associação Médica Brasileira 62, no. 7 (October 2016): 647–51. http://dx.doi.org/10.1590/1806-9282.62.07.647.

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Анотація:
Summary Introduction: In patients with essential thrombocythemia (ET), the vascular complications contribute to morbidity and mortality. To better predict the occurrence of thrombotic events, an International Prognostic Score for Thrombosis in Essential Thrombocythemia (IPSET-thrombosis) has recently been proposed. We present the application of this score and compare its results with the usual classification system. Method: We retrospectively evaluated the characteristics and risk factors for thrombosis of 46 patients with a diagnosis of ET seen in the last 6 years at Faculdade de Medicina do ABC (FMABC). Results: Thrombosis in the arterial territory was more prevalent than in venous sites. We observed that cardiovascular risk factors (hypertension, hypercholesterolemia, diabetes mellitus, and smoking) were also risk factors for thrombosis (p<0.001). Age over 60 years and presence of JAK2 V617F mutation were not associated with the occurrence of thrombotic events. No patient classified by IPSET-thrombosis as low risk had a thrombotic event. Furthermore, using the IPSET-thrombosis scale, we identified two patients who had thrombotic events during follow-up and were otherwise classified in the low-risk group of the traditional classification. Leukocytosis at diagnosis was significantly associated with arterial thrombosis (p=0.02), while splenomegaly was associated with venous thrombotic events (p=0.01). Conclusion: Cardiovascular risk factors and leukocytosis were directly associated with arterial thrombosis. IPSET-thrombosis appears to be better than the traditional classification at identifying lower risk patients who do not need specific therapy.
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5

Chang, Simon, Christian Fynbo Christiansen, Anders Bojesen, Svend Juul, Anna-Marie B. Münster, and Claus H. Gravholt. "Klinefelter syndrome and testosterone treatment: a national cohort study on thrombosis risk." Endocrine Connections 9, no. 1 (January 2020): 34–43. http://dx.doi.org/10.1530/ec-19-0433.

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Анотація:
Objectives Klinefelter syndrome (KS), 47,XXY, can be viewed as a disease model for investigating the risk of thrombosis in male hypogonadism and the subsequent risk related to testosterone treatment. We describe rates of thrombotic risk factors, thrombosis and thrombosis mortality in KS and the association with testosterone treatment. Methods National registry-based matched cohort study with follow-up from 1995 to 2016 set in Denmark. For the study, 1155 men with KS were each matched by year and month of birth to 100 men from the background population. First thrombotic events and thrombosis mortality was evaluated by event rates and hazard ratios (HRs) and by applying testosterone treatment as a time-dependent covariate. Results The KS cohort had higher incidence of venous thromboembolism relative to the comparison cohort (HR, 3.95; 95% CI, 2.83–5.52). Total thrombotic deaths were increased in KS (HR, 1.76; 95% CI, 1.18–2.62), and all-cause mortality was increased in KS following arterial thrombosis (HR 1.73; 95% CI 1.22–2.47). Only 48.7% of men with KS redeemed prescriptions for testosterone. Untreated men with KS were on average born 12 years before those treated, and the majority of untreated men with KS with available biochemistry were hypogonadal. Testosterone treatment in KS was associated with a non-significant decrease in venous thromboembolism and thrombotic deaths. Conclusion Thrombosis and thrombotic deaths are increased in KS. Only half of the men with KS ever received testosterone treatment, despite overt hypogonadism in the non-treated. Testosterone treatment in Klinefelter syndrome was insignificantly associated with lower incidence rates of venous thrombosis and thrombotic deaths.
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6

Henni, Samir, Pierre Ramondou, Guillaume Duval, Jean Picquet, Georges Leftheriotis, and Pierre Abraham. "The risk of lower-limb superficial vein thrombosis relative to lower-limb venous thrombotic events is not increased in winter months." Phlebology: The Journal of Venous Disease 35, no. 7 (January 10, 2020): 533–37. http://dx.doi.org/10.1177/0268355519896729.

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Objectives Ambient temperature (that impacts differently venous flow in superficial and deep veins) could have a different effect on the risk of superficial and deep venous thrombosis. We searched for a trimestral variation of the risk of superficial venous thrombosis among all lower-limb thrombotic events (lower-limb thrombotic events = superficial venous thrombosis + deep venous thrombosis). Methods We retrospectively analyzed the results of venous ultrasound investigations performed among 11,739 patients (aged 67 ± 19 years old, 56.1% males) referred for suspected lower-limb thrombotic events over a 12-year period. Chi-square test was used to compare the superficial venous thrombosis/lower-limb thrombotic events ratio observed by trimesters to a homogeneous distribution. Results The proportion of lower-limb thrombotic events were 30.7%, 28.8%, 31.1%, and 31.4% (Chi2: 0.133; p = 0.987) of total investigations, while that of superficial venous thrombosis among all lower-limb venous thrombotic events were 27.2%, 30.0%, 31.4%, and 31.0%, for the first, second, third, and fourth trimesters respectively (Chi2: 0.357; p: 0.949). Conclusion No trimestral variation of the superficial venous thrombosis/lower-limb venous thrombotic events ratio was observed.
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7

Lim, Sunghee, Ji Yoon Lee, Seok Jin Kim, and Won Seog Kim. "The International Prognostic Index Is a Better Predictor of Thrombotic Complications Than the Khorana Score for Patients with Diffuse Large B-Cell Lymphoma Treated with R-CHOP: Results of a Single Center Prospective Cohort Study." Blood 120, no. 21 (November 16, 2012): 5095. http://dx.doi.org/10.1182/blood.v120.21.5095.5095.

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Abstract Abstract 5095 Background Thrombotic complication is a major life threatening condition in lymphoma patients because chemotherapy as well as lymphoma cell itself can result in thrombosis. Although high rates of thrombotic complication have been reported in patients with lymphoma, the majority of data were from retrospective studies with heterogeneous group of patients. Furthermore, the frequency of thrombotic complications varied depending o the nature of studies and subtypes of lymphoma included. Thus, it is still not determined about the risk factors for thrombotic complications in lymphoma patients. As a predictive model for cancer-associated thrombosis, Khorana risk score has been proposed including cancer type, body mass index (BMI), prechemotherapy white blood cell, hemoglobin, and platelet count. However, there is few data prospectively validating the role of this risk model in Asian lymphoma patients. Therefore, we explored risk factors influencing the occurrence of venous and arterial thrombotic complications in diffuse large B-cell lymphoma (DLBCL) patients who were uniformly treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone). Methods We analyzed the incidence of venous and arterial thrombotic complications from DLBCL patients enrolled in our prospective cohort study (NCT00822731). Patients were pathologically confirmed and treated with R-CHOP. Thrombotic complications defined as venous thrombosis including pulmonary thromboembolism (PTE) and deep vein thrombosis (DVT), and arterial thrombosis including stroke and infarction occurred after diagnosis. The thrombotic complications were diagnosed with radiologic imaging studies including CT scan and ultrasound imaging. Results 352 patients were enrolled between 2008 and 2011, and they were prospectively monitored regarding the occurrence of thrombotic complications with the median follow-up duration of 22. 6 months. The median age was 56 years old (range 16–86) and male to female ratio was 1. 3:1. Thrombotic complications occurred in 48 patients (crude incidence: 13. 6%) including venous thrombosis (n = 37, 10. 5%) and arterial thrombosis (n = 11, 3. 1%). Venous thrombosis including DVT and PE occurred within 6 months after diagnosis (32/37, 86. 5%), so the actuarial incidence of venous thrombosis at one year was 10. 1%. However, arterial thrombosis mainly occurred around 12 months after diagnosis. Among 37 cases of venous thrombosis, anticoagulation therapy was used for 22 patients with symptomatic DVT or PE. Incidental cases of DVT or PE which were found during imaging follow-up for evaluation of tumor response did not require therapy. There were two deaths-related with venous thrombosis including refractory hypoxemia due to PE and bleeding due to anticoagulation while no death was found in arterial thrombosis. Age older 60 years and poor performance status (≥ ECOG grade 2) were significantly associated with thrombotic complications. However, other host factors including co-morbidity, body mass index (BMI), and gender were not related (P > 0. 05). Disease-related factors representing high tumor burden such as elevated serum LDH, two or more than two extranodal involvements, and Ann Arbor stage III/IV were significantly associated with increased risk of thrombotic complications (P < 0. 05). However, a particular extranodal site including stomach, pancreas, intestine, and mediastinum did not influence the thrombotic complications. Khorana score-based risk model failed to predict the occurrence of thrombotic complications in our study population. Furthermore, each parameter such as the level of hemoglobin, white blood cell and platlet count before chemotherapy, and BMI did not show a significant association with venous and arterial thrombotic complications. In fact, the number of patient more than 35 kg/m2 BMI was extremely small in our population. As a result, the International Prognostic Index was predictive for the occurrence of thrombotic complications in diffuse large B-cell lymphoma patients treated with R-CHOP. Conclusions The incidence of venous and arterial thrombotic complications in our study population was significantly associated with the IPI rather than Khorana score model. These results may help better defining lymphoma patients at high risk of thrombotic complications in Asian lymphoma patients. Disclosures: No relevant conflicts of interest to declare.
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8

Miller, Mariel, Kamil K. Khanipov, Christopher Zahner, and George K. Golovko. "Increased Risk of Thrombosis in Patients with Polycystic Ovarian Syndrome." Blood 142, Supplement 1 (November 28, 2023): 5544. http://dx.doi.org/10.1182/blood-2023-190997.

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Polycystic Ovarian Syndrome (PCOS) is the most common endocrine-metabolic disorder in reproductive age women, with an estimated prevalence of 6-12% of assigned female at birth women in the US. We identified a pattern in our coagulation diagnostic management team, wherein women with PCOS had increased rates of and repeated histories of thrombotic events, such as strokes, heart attacks, pulmonary embolisms, and deep vein thromboses. However, clinical coagulation assays on these PCOS patients with repeated thrombotic events were all within the normal reference range. Our goal was to investigate the validity of this pattern and its occurrence in both local and national populations. This was accomplished by 1) Determining the incidence rate of thrombosis in PCOS and 2) Analyzing clinical presentations of thrombosis in PCOS. Methods/Study populations : Analyses on the rate of thrombotic events in PCOS patients locally at UTMB and in the US were performed on the TriNetX health research network. Using the incidence and prevalence and compared outcomes analytic functions on TriNetX, we determined the rate of thrombosis from 2013-2018 and explored patient characteristics. We further analyzed thrombosis in PCOS with the Symptom-Disease Pair Analysis of Diagnostic Error (SPADE) method. Through the compare outcomes analysis on the TriNetX platform, we looked at PCOS and control patients who experienced thrombotic events between 2013-2018 and analyzed clinical presentations that occurred in the 90 days prior to the index event. Patient queries included the diagnostic code for PCOS, ICD10 E28.2, women age 15-75, who had a clinical encounter since 2013. Exclusion criteria included inherited thrombotic disorders, smoking history, and human immunodeficiency virus. Events of interest included myocardial infarctions, cerebral infarctions, pulmonary embolisms, arterial embolisms and thrombosis, and portal vein thromboses. Statistical analysis: For evaluating statistical significance of the rate of thrombosis, we performed a compare outcome analysis on the UTMB network, with propensity score matching for current age. A Kaplan-Meier Analysis and a student's t-test were performed on the number of instances/events, and statistical significance was defined as a p-value &lt;0.0001. Results:Between 2013-2018, the incidence rate of thrombosis in PCOS patients was 4.35% with 5.36% prevalence, this was statistically significantly higher than the control cohort at 2.66% incidence and 3.5% prevalence. The incidence rate of thrombosis in PCOS increased dramatically in post-menopausal women. Of the 60 outcomes investigated, 24 were determined to be statistically significant between control and PCOS, 22 symptoms and 2 procedures. Discussion: This is the first study to analyze the rate of thrombotic events in PCOS. We identified significant presentations and gaps that could assist in the early detection of thrombotic events in PCOS. However, the mechanisms of thrombosis in PCOS are unknown and are poorly detected with current clinical assays. Future studies will examine clinical assays in the detection of thrombosis in PCOS and investigate thrombotic mechanisms in PCOS.
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Kreidy, Raghid. "Pathophysiology of Post-Thrombotic Syndrome: The Effect of Recurrent Venous Thrombosis and Inherited Thrombophilia." ISRN Vascular Medicine 2011 (November 9, 2011): 1–4. http://dx.doi.org/10.5402/2011/513503.

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Post-thrombotic syndrome is an important chronic complication of deep vein thrombosis. This syndrome can be debilitating to patients and has a major economic impact on health care services. The pathophysiology of post-thrombotic syndrome is currently incompletely understood. Because therapeutic options for post-thrombotic syndrome are extremely limited and results are often disappointing, recognizing of the pathophysiology and risk factors of this syndrome is essential to prevent the disabling consequences of this disease. The present paper focuses on risk determinants of post-thrombotic syndrome after deep vein thrombosis. The contribution of recurrent venous thrombosis and inherited thrombophilia to the pathogenesis of this syndrome is reviewed and discussed in details.
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Park, D. J., S. E. Choi, H. Xu, J. H. Kang, and S. S. Lee. "AB0442 RISK FACTORS ASSOCIATED WITH THROMBOTIC EVENTS IN KOREAN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1519.3–1520. http://dx.doi.org/10.1136/annrheumdis-2020-eular.1674.

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Background:Objectives:Up to 30~40% of all patients with systemic lupus erythematosus (SLE) experience thrombosis, presenting as stroke and myocardial infarction, and these thrombotic events cause substantial morbidity and mortality in SLE. We explored the risk factors associated with the occurrence of thrombotic events in SLE patients.Methods:This study enrolled 259 SLE patients (mean age, 34.0 ± 13.7; 239 females) with available clinical data at the time of SLE onset from the lupus cohort at Chonnam National University Hospital. Sociodemographic, clinical, and laboratory data, and history of concomitant diseases were obtained. Thrombotic events were defined as the presence of arterial or venous thrombosis. The multivariable Cox’s model was performed to investigate the possible risk factors for thrombotic events.Results:During a mean follow-up of 103.3 months (SD, 53.4), 27 patients (10.4%) developed thrombotic events: stroke in 15 patients, venous thrombosis in five patients, myocardial infarction in four patients, and angina in three patients. In the multivariable Cox’s regression analysis, hypertension (hazard ratio [HR], 16.946; P=0.031), antiphospholipid syndrome (APS) (HR, 18.348; P=0.001), cumulative prednisolone >5 mg/day (HR, 14.374; P<0.001), use of ACE inhibitors (ACEi) or angiotensin receptor blockers (ARB) (HR, 0.110; P=0.004), and Systemic Lupus International Collaborating Clinics Group (SLICC) damage index (HR, 1.972; P=0.004) were significant predictors of the development of thrombotic events in patients with SLE.Conclusion:Patients with SLE showed significant thrombotic events during the course of their disease. Risk factors associated with thrombotic complications were higher cumulative dose of prednisolone, diagnosis of APS, and higher SLICC damage index. On the other hand, the use of ACEi or ARBs was associated with a reduced risk of thrombotic complications in patients with SLE. Our results support the need for increased monitoring of thrombotic complications in SLE patients.Disclosure of Interests: :None declared
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Більше джерел

Дисертації з теми "Thrombotic risk"

1

De, Lange Margaretha Elisabeth. "A twin study of thrombotic aspects of insulin resistance syndrome : determination of genetic and environmental contribution to thrombotic risk." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406126.

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2

Khan, Abdullah Rubiat (Emon). "Microparticles and their role in thrombosis in Behçet's Syndrome and their potential as a biomarker for thrombotic risk." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/58996.

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Анотація:
Thrombosis is common in Behçet’s Syndrome (BS), and there is a clear need both for a better understanding of causation and for biomarkers to enable thrombotic risk assessment. I set out to determine whether plasma microparticles (MP), particularly tissue factor expressing (TF+ MP) were increased in BS. Additionally, I investigated whether MP expressing tissue factor pathway inhibitor (TFPI) were also evident. Finally, I investigated whether these MP had a functional consequence role. MP were prepared from 88 BS patients and 72 healthy controls. The BS group contained 21 patients with a history of thrombosis (Th+) and 67 without (Th-). MP were identified by size and annexin V binding using flow cytometry, and were further analysed with antibodies to surface antigens. Assays used to assess the function of MP were an in-house coagulation lysis assay, calibrated automated thrombin generation assay and Factor Xa generation assay. Total MP numbers were increased in BS compared to HC, as were MP expressing TF and TFPI (all p < 0.001). Amongst BS patients, the Th+ group had increased total and TF positive MP (both p < 0.001) compared to the Th- group, but a lower proportion of TFPI positive MPs (p < 0.05). Consequently, the ratio of TFPI to TF MP counts (TFPI/TF) was significantly lower in Th+ versus Th- BS patients (p < 0.001), with no history of clinical thrombosis in BS patients with a TFPI/TF MP ratio > 0.7. Functional assays revealed no correlation with MP count. I conclude that MP expressing TF are increased in BS, more so in patients with thrombosis. An imbalance between microparticulate TF and TFPI may be pathophysiologically important for thrombosis in BS and may allow improved identification and appropriate treatment of thrombotic risk.
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3

Singh, Indu, and indu singh@rmit edu au. "The influence of antioxidants on thrombotic risk factors in healthy population." RMIT University. Medical Sciences, 2008. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20081205.121719.

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Oxidative damage has been suggested to play a key role in the pathogenesis of atherosclerosis and other cardiovascular disease. Increased free radical production induced by oxidative stress can oxidise low density lipoproteins, activates platelets, induces endothelial dysfunction and disturbs glucose transport by consuming endogenous antioxidants. Using a combination, of in vitro and in vivo experimental models, the primary aims of the studies undertaken for this thesis were to examine whether different antioxidants could negate risk factors leading to thrombosis, atherosclerosis and other cardiovascular diseases. The studies utilised the mechanisms involved in platelet activity and glucose uptake by skeletal muscle myotubes. The first study determined if olive leaf extract would attenuate platelet activity in healthy human subjects. Blood samples (n=11) were treated with five different concentrations of extract of Olea europaea L. leaves ranging from 5.4£gg/mL to 54£gg/mL. A significant reduction in platelet activity (pless than0.001) and ATP release from platelets (p=0.02) was observed with 54£gg/mL olive leaf extract. The next crossover study compared the effect of exercise and antioxidant supplementation on platelet function between trained and sedentary individuals. An acute bout of 1 hour exercise (sub maximal cycling at 70% of VO2max) was used to induce oxidative stress in 8 trained and 8 sedentary male subjects, before and after one week supplementation with 236 mg/day of cocoa polyphenols. Baseline platelet count and ATP release increased significantly (pless than0.05) after exercise in all subjects. Baseline platelet numbers in the trained were higher than in the sedentary (235¡Ó37 vs. 208¡Ó34 x109/L, p less than 0.05), whereas platelet activation in trained subjects was lower than sedentary individuals (51¡Ó6 vs. 59¡Ó5%, p less than0.05). Seven days of cocoa polyphenol supplementation did not change platelet activity compared to the placebo group. The third study determined the effect of 5 weeks of either 100mg/day £^-Tocopherol (n=14), 200mg/d £^-Tocopherol (n=13) or placebo (n=12) on platelet function, lipid profile and the inflammatory marker C-reactive protein. Blood £^-tocopherol concentrations increased significantly (pless than0.05) relative to dose. Both doses attenuated platelet activation (pless than0.05). LDL cholesterol, platelet aggregation and mean platelet volume were decreased by 100mg/d £^-tocopherol (all pless than0.05). The final study determined the effect of glucose oxidase induced oxidative stress and £^-tocopherol treatment on glucose transport and insulin signalling in cultured rat L6 muscle cells. One hour treatment with 100mU/mL glucose oxidase significantly decreased glucose uptake both with and without 100nM insulin stimulation (pless than0.05). Pre-treatment with 100ƒÝM and 200ƒÝM £^-tocopherol partially protected cells from the effect of glucose oxidase, whereas 200ƒÝM £^-tocopherol restored both basal and insulin stimulated glucose transport to control levels. Glucose oxidase-induced oxidative stress did not impair basal or insulin stimulated phosphorylation of Akt or AS160, but 200ƒÝM £^-tocopherol improved insulin-stimulated phosphorylation of these proteins. In summary, the results from the studies undertaken for this thesis provide evidence that antioxidant supplementation maintains normal platelet function, exerts a positive effect on blood lipid profile and improves glucose uptake in normal healthy asymptomatic population as well as under conditions of induced oxidative stress. Antioxidants including foods rich in cocoa, olive and gamma tocopherol have the potential to combat oxidative stress induced risk factors leading to cardiovascular diseases.
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4

Sharma, Sumeet. "Thrombotic risk assessment in end stage renal disease patients on renal replacement therapy." Thesis, University of Hertfordshire, 2015. http://hdl.handle.net/2299/17114.

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Анотація:
End stage renal disease (ESRD) patients have an excess cardiovascular risk, above that predicted by traditional risk factor models. Despite the advances in both Cardiovascular disease (CVD) management and renal replacement therapy (RRT), there still is a major burden of cardiovascular mortality and morbidity in the chronic kidney disease (CKD) population. Declining renal function itself represents a continuum of cardiovascular risk and in those individuals who survive to reach ESRD, the risk of suffering a cardiac event is uncomfortably and unacceptably high. Pro-thrombotic status may contribute to this increased risk. Global thrombotic status assessment, including measurement of occlusion time (OT) the time taken to form an occlusive platelet rich thrombus and thrombolytic status (time taken to lyse such thrombus) as assessed by measuring Lysis Time (LT), may identify vulnerable patients. The aim of this study was to assess overall thrombotic status in ESRD and relate this to cardiovascular and peripheral thrombotic risk. Small sub studies were also planned to establish the effect of RRT modality on the thrombotic status.
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5

Wright, Joy Rhiannon. "Variation in the haemostatic response and thrombotic risk : interplay between haemostatic factors, platelets and monocytes." Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/10075.

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The haemostatic response comprises the interaction of coagulation factors and peripheral blood cells which play a vital role in maintaining vascular integrity. This study begins with the finding that plasma from premature MI subjects has increased endogenous thrombotic potential linked to higher levels of circulating Tissue Factor (TF), suggesting these individuals may have a hypercoagulable phenotype. This study seeks to further understand how cellular interaction, in particular platelet-monocyte interaction, modulates the haemostatic response. Throughout the study, TF and Tissue Factor Pathway Inhibitor (TFPI) were studied as representing the procoagulant and anticoagulant response, respectively. Study of the effects of activated platelets on monocytes found that whereas direct platelet or platelet-microparticle adhesion to monocytes, and release of platelet soluble mediators induced monocyte gene expression of TF, induction of TFPI was driven solely by platelet soluble mediators. Extension of these studies using gene expression microarray technology found that whereas activation of monocytes via PSGL-1 generates a pro-angiogenic expression profile, platelet soluble mediators significantly enhanced this profile, enabling monocytes to interact with ECM components involved in the wound healing environment of the thrombus, and additionally induced anti-inflammatory, and anti-atherothrombotic genes. Whether cells within a thrombus act simply as structural and secretory components, or play a more active role involving gene expression is unclear, therefore gene expression array analysis was carried out on thrombi generated in vitro. Genes demonstrating significant time-dependent increases included those encoding chemotactic proteins (IL8, CCL2, CXCL1, CXCL2), cell adhesion (ITGAV, ITGA5, ITGB1), regulation of coagulation (THBD, PLAU, SERPINE1), wound-healing (ENDG, SPP1, LAMB3), and regulatory transcription factors (FOS, EGR1, PPARG). Whereas initiation of thrombosis is driven by plasma proteins and facilitated by the platelet surface, this study provides evidence that thrombus resolution may be driven by changes in gene expression within the thrombus that regulate the haemostatic response, thrombus growth, and facilitate wound-healing. These findings could have implications for individuals at risk of plaque rupture, where variation in gene expression may affect not just the formation of an occlusive thrombus but also the rate of resolution.
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Webster, Danielle L. M. D. "Higher Volume Hypertonic Saline and Increased Thrombotic Risk Without Improved Survival in Pediatric Traumatic Brain Injury." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406810346.

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7

Kundur, Avinash Reddy. "An Investigation into Gilbert’s Syndrome: Understanding the Role of Unconjugated Bilirubin in Targeting Platelet and Haemostatic Mechanisms Associated with Thrombotic Risk Factors." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/368189.

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Gilbert’s syndrome (GS) is a common genetic condition associated with mildly elevated unconjugated bilirubin (UCB) concentrations and increased protection against development of cardiovascular disease (CVD). Mutation in the uridine diphosphate glucuronosyltransferase (UGT1A1) gene causing a reduction in UGT1A1 enzyme activity that is responsible for conjugation and elimination of UCB, is considered as the cause for GS. Numerous studies have shown that elevated levels of UCB are negatively associated with risk of developing CVD. While, several in vitro and in vivo trials have shown that UCB at physiological concentrations can improve endothelial function, lipid profile and reduce vascular inflammation, thereby imparting its cardiovascular protection. Cardiovascular disease is a major cause of death globally, an estimated 17.3 million CVD related deaths are reported annually by the World Health Organization (WHO), making it the largest cause of human mortality. Furthermore, several studies have predicted that these numbers would continue rising in the coming years, due to factors such as aging, life style choices and environmental changes.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Björklund, Erik. "Early risk stratification, treatment and outcome in ST-elevation myocardial infarction /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6050.

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9

Mooe, Thomas. "Left ventricular thrombus and stroke after acute myocardial infarction." Doctoral thesis, Umeå universitet, Medicin, 1997. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-100547.

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A left ventricular thrombus develops in approximately 40% of patients following an anterior myocardial infarction. Embolization from these thrombi has been regarded as the most important cause of stroke following a myocardial infarction. The occurrence and characteristics of left ventricular thrombi and stroke after anterior myocardial infarction may, however, have changed after the introduction of aspirin and thrombolytics as standard therapy. The occurrence of left ventricular thrombi was examined in 99 patients with an acute anterior myocardial infarction, 74 of whom were treated with streptokinase. Thrombi were equally common in the thrombolysis group (46%, 95% confidence interval [Cl], 35-57%) as in the non-thrombolysis group (40%, 95% Cl, 21-59%). The risk of thrombus formation was related to the degree of left ventricular segmental dysfunction. Using serial echocardiographic examinations, the formation and resolution of thrombi was found to be highly dynamic. The majority of thrombi diagnosed during the hospital stay had resolved at follow-up one month later, irrespective of treatment with streptokinase or anticoagulants. The development of new thrombi was, however, observed at every follow-up examination interval. One-hundred-and-twenty-four patients suffering a stroke within 28 days of an acute myocardial infarction were identified in the northern Sweden MONICA stroke registry between 1985 and 1994. The overall event rate of ischemic myocardial infarction-related stroke was 1.07%. The risk of a stroke was highest duringt he first 5 days after the infarction. Only approximately half the strokes were preceded by an anterior myocardial infarction. In a case-control analysis, atrial fibrillation (chronic or new onset), ST elevation and a history of a previous stroke were found to be independent predictors of stroke. There was a long-term trend towards a lower incidence and event rate for myocardial infarction-related stroke. Clinical stroke characteristics were examined in 103 patients with a first-ever stroke within 28 days of a myocardial infarction and compared with stroke characteristics in 206 control subjects without a recent myocardial infarction. The sudden onset of neurological symptoms, an impairment of consciousness, a progression in neurological deficits and a stroke of the total anterior circulation infarction subclass were more common in cases than in controls. The risk of a recurrent stroke during one year of follow-up was not influenced by a recent myocardial infarction, but patients who had suffered a myocardial infarction had markedly higher mortality. To conclude, thrombolytic treatment does not reduce the occurrence of left ventricular thrombi after a myocardial infarction. The risk of thrombus formation is related to the extent of the myocardial injury. The development and resolution of thrombi is a highly dynamic process. There is a long-term trend towards a lower incidence and event rate of ischemic stroke after a myocardial infarction. Although the clinical stroke characteristics differ, they are not specific enough to differentiate between patients with and without a recent myocardial infarction.

S. 1-84: sammanfattning, s. 85-136: 5 uppsatser


digitalisering@umu
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Heijden, Jeroen Frank van der. "Risk factors for bleeding during treatment with anti-thrombotics." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/75796.

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Книги з теми "Thrombotic risk"

1

Morganroth, Joel, and E. Neil Moore, eds. Risk/Benefit Analysis for the Use and Approval of Thrombolytic, Antiarrhythmic, and Hypolipidemic Agents. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1605-3.

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2

Autar, Atmaram. Nursing assessment of clients at risk of deep vein thrombosis (DVT): Developing the Autar DVT scale. Birmingham: University of Central England in Birmingham, 1994.

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Autar, A. R. Advancing clinical practice in the management of Deep Vein Thrombosis (DVT): Development, application and evaluation of the Autar DVT risk assessment scale. Leicester: De Montfort University, 2002.

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4

Eric, Kasner Scott, and Gorelick Philip B, eds. Prevention and treatment of ischemic stroke. Philadelphia: Butterworth-Heinemann, 2004.

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5

Jørgen, Jespersen, Bertina Rogier M, Haverkate F. 1931-, European Concerted Action on Thrombosis and Disabilities (Committee), and Commission of the European Communities., eds. ECAT assay procedures: A manual of laboratory techniques. Dordrecht: Kluwer Academic Publishers, 1992.

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6

Symposium on New Drugs and Devices (9th 1988 Philadelphia, Pa.). Risk/benefit analysis for the use and approval of thrombolytic, antiarrhythmic, and hypolipidemic agents: Proceedings of the Ninth Annual Symposium on New Drugs & Devices, October 27 & 28, 1988. Boston: Kluwer Academic Publishers, 1989.

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7

Hendriks, Herman G. D., and Joost T. M. de Wolf. Haematological and coagulation disorders and anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0084.

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This chapter covers the principal haematological disorders and their implications for anaesthesia. Haemoglobin concentration is the main determinant of oxygen delivery to the tissues making anaemia a potential concern for the anaesthetist. In deciding whether to correct anaemia with a red blood cell transfusion, the anaesthetist must consider the nature of the surgery and the underling cause of the anaemia as well as the haemoglobin concentration. Techniques to limit the need for blood transfusion and the complications of transfusion are discussed. Perfect haemostasis means control of bleeding without the occurrence of thrombotic events. Coagulation management requires an understanding of this balance and the knowledge that altered coagulation activity may result in clinically relevant bleeding or, in contrast, thrombosis. Therefore, the key in haemostasis is an understanding that every anticoagulant action enhances the risk of bleeding and every procoagulant action enhances the risk of thrombosis. If a specific defect in the haemostatic system is known, treatment is tailored to restore this defect. However, tests to predict surgical bleeding do not exist, as it is for test to predict thrombotic events. The strengths and limitations of coagulation tests should be appreciated before they are used to assist clinical decision-making in the perioperative period. An excellent coagulation test is the clinical field (i.e. the surgical wound). If there are abnormalities in the coagulation tests without clinical bleeding, a correction is hardly necessary. In patients taking anticoagulant medication, consideration must be given on an individual patient basis, to the relative risks of continuing (bleeding) or stopping (thrombotic events) the medication.
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8

Alikhan, Raza. Prothrombotic conditions. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0285.

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The term thrombophilia is used to describe an individual who has a tendency to develop thrombosis. Arterial thrombosis is usually linked with classical risk factors such as age, smoking, hypertension, hyperlipidaemia, or diabetes; a thrombophilia assessment and workup is not usually considered in cases of arterial thrombosis. A clinically useful approach to the diagnosis and management of a patient with a venous thrombotic process is to categorize the disorder as either a primary (inherited) or secondary (acquired) hypercoagulable state. This topic addresses the diagnosis and management of prothrombotic conditions.
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Haemostasis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0010.

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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Angela Theodoulou. Haemostasis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0010_update_001.

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Анотація:
Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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Частини книг з теми "Thrombotic risk"

1

Price, Erika Leemann, and Tracy Minichiello. "Thrombotic Risk Factors." In The Coagulation Consult, 185–202. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9560-4_12.

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2

Schindler, Adolf E. "Hormonal Contraceptives: Progestogen and Thrombotic Risk." In ISGE Series, 69–75. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-09662-9_8.

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3

Angelo Claudio, Molinari, and Paola Saracco. "The Thrombotic Risk of the Newborn." In Neonatology, 1–15. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-18159-2_239-1.

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Claudio, Molinari Angelo, and Paola Saracco. "The Thrombotic Risk of the Newborn." In Neonatology, 1455–69. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-29489-6_239.

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5

Mariani, G., G. D. Di Nucci, A. Chistolini, M. Motta, and F. Mandelli. "On the Evaluation of the Thrombotic Risk." In Advances in Hemostasis and Thrombosis, 129–40. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-9424-6_13.

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6

Debbie Jiang, M. D., and M. D. Alfred Ian Lee. "Thrombotic Risk from Chemotherapy and Other Cancer Therapies." In Thrombosis and Hemostasis in Cancer, 87–101. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-20315-3_6.

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7

Mammen, Eberhard F. "Oral Contraceptives and Thrombotic Risk: A Critical Overview." In Sex Steroids and the Cardiovascular System, 65–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-662-02764-6_5.

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8

Esplugas, E. "Contrast media effect of thrombotic risk during coronary angioplasty." In Abrupt closure during coronary angioplasty, 35–40. Paris: Springer Paris, 1991. http://dx.doi.org/10.1007/978-2-8178-0877-2_5.

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9

Siegemund, A., T. Siegemund, U. Scholz, S. Petros, and L. Engelmann. "Different Thrombotic Risk Factors — Contribution to the Endogenous Thrombin Potential." In 33rd Hemophilia Symposium, 257–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18260-0_41.

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10

Cianciaruso, B., G. di Minno, P. Ames, V. Bellizzi, and G. Bovi. "Thrombotic Risk During r-EPO Therapy in Hemodialyzed Patients. A New Hypothesys." In New Therapeutic Strategies in Nephrology, 349–51. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3884-4_102.

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Тези доповідей конференцій з теми "Thrombotic risk"

1

Broekmans, A. W., F. J. M. der Meer, and K. Briët. "TREATMENT OF CONGENITAL THROMBOTIC SYNDROMES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643718.

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Hereditary antithrombin III deficiency,protein C deficiency, and protein S deficiency predispose to the occurrence of venous thrombotic disease at a relatively youngage and often without an apparent cause. These disorders inherit as an autosomal dominant trait. Heterozygotes are at risk fosuperficial thrombophlebitis, thrombosis atnearly every venous site, and pulmonary embolism. Homozygous protein C deficiency may present itself with a purpura fulminans syndrome shortly after birth.In the acute phase of venous thromboembolism heparin is effective for preventing extension of the thrombotic process, and pulmonary embolism. In patients with antithrombin III deficiency the concomittant useof antithrombin III concentrate is controversial, although some patients may requirehigher doses of heparin.Substitution therapy is only indicated in homozygous protein C deficient patientswith purpura fulminans. Fresh frozen plasma i.v. is the treatment of choice, in a dosage of 10 ml/kg once or twice daily. The current prothrombin complex concentrates may induce new skin lesions and disseminated intravascular coagulation. After the lesions have been healed(mostly in 4 to6 weeks)coumarin therapy may effectively prevent new episodes of purpura fulminans, provided the prothrombin time is kept within 2,5 - 4,0 INR. Heparin is ineffective for preventing purpura fulminans due to homozygous protein C deficiency.The thrombotic manifestations in heterozygotes are effectively prevented by coumarin therapy. This is supported by the observation that patients may remain free of thrombosis during long-term treatment and may have recurrences shortly after the withdrawal of the coumarin drug. The therapeutic range for the prothrombin time should be within 2,0 - 4,0 INR, target value 3,0 INR. In the initial phase of oral anticoagulant therapy protein C deficient patients are prone to the development of coumarin induced hemorrhagic skin (tissue) necrosis.In the patients studied in Leiden, it occurred in about 3% of the treated patients. Heparin appears to be ineffective for the prevention of coumarin-induced skin necrosis; high loading doses of coumarin should be avoided and the prothrombin timeshouldbe checked dialy during the initial phase of oral anticoagulant treatment. Tissue necrosis may contribute to bleeding complications after fibrinolytic therapy, ashas been observed in two protein C deficient patients.In clinical situations with an increased risk for thrombosis such as surgery and pregnancy, heparin (in-low-doses) alone orin combination with coumarins have been used succesfully for the prevention of thrombosis. The need for antithrombin III concentrates in patients with hereditary antithrombin III deficiency in such situations is not substantiated.Although anabolic steroids are capable to increase the plasma concentrations of antithrombin III and of protein C in the respective deficiency states, its efficacy in preventing thrombotic episodes remains to be established.An optimal strategy for preventing thrombosis in congenital thrombotic syndromes is to identify still asymptomatic patients. In case of antithrombin III, protein C, and protein S deficiency this search is feasible. During risk situations for thrombosis patients are to be protected against the development of thrombosis.In Leiden pregnant women with one of the deficiencies are treated from the 14th week of pregnancy, initially with a shortacting coumarin drug, after the 34th week withheparin s.c. b.i.d. at therapeutic dosages,and after delivery coumarin therapy is reTnstituted during 6 weeks. The use of oralcontraceptives should be avoided, unlesspatients are under coumarin treatment. As long as deficient patients remain asymptomatic no antithrombotic treatment is indicated. After the first documented thromboticincident patients are treated indefinitelywith oral anticoagulants.
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Rouvier, J., H. Vidal, J. Gallino, M. Boccia, A. Scazziota, and R. Altman. "ACUTE INTERRUPTION OF ORAL ANTICOAGULANT THERAPY: A THROMBOTIC RISK?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643265.

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It is still on discussion how oral anticoagulant therapy must be interrupted. A progressive diminution of drug intake have been proposed in order to avoid a MreboundM of vitamin K-dependent procoagulant factors. At the present, it is well known that coumarin drugs affect not only the biologic activity of factors II, VII, IX and X but also Protein C (PC), an inhibitor of coagulation kinetics, and their cofactor Protein S. With the aim to determine the recovery level of PC in relation with the others vitamin K-dependent factors, the effect of suppression of anticoagulant therapy in patients under chronic treatment with acenocoumarin was studied.Quick time, functional factors II, VII, X (one stage methods), functional PC (Francis method) and immunological Factor II and Protein C (Laurell) were determined before and 36 hours after suspension of acenocoumarin administration.Results showed that: 1) Recovery levels of functional Protein C (increased from 28.55% ±2.57 to 72.64% ±5.9) were significantly higer than functional Factor II (22.09% ±2.34 to 30.73% ±8.64), Factor VII (22.55% ±2.01 to 40.73% ±4.85) and Factor X (23.27% ±2.66 to 39.18% ±3.19). Statistical analysis (Newmann-Keuls test) showed at least a p<0.01 between PC increase and factors II, VII or X increment.2) No significant differences were seen between immunological levels of Factor II before and after suspension of acenocoumarin.3) Levels of immunological PC in patients under anticoagulant therapy were higer than functional PC. After acenocoumarin suppression, not correlation was seen between immunological and functional Protein C recovery.It is concluded that acute suppression of acenocoumarin does not induce a thrombotic tendency because the recuperation of functional Protein C is more important than factors II, VII and X recovery.
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Hill, Samuel J., Alistair Young, Ronak Rajani, and Adelaide De Vecchi. "Assessment of Thrombotic Risk following Transcatheter Mitral Valve Replacement." In 2021 Computing in Cardiology (CinC). IEEE, 2021. http://dx.doi.org/10.23919/cinc53138.2021.9662855.

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4

Bertaggia, D., A. Aliotta, and L. Alberio. "A New Laboratory Tool to Detect Hypercoagulation and Thrombotic Risk." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680254.

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Wilson, J., P. J. Grant, M. Boothby, J. A. Davis, and C. R. M. Prentice. "ENDOGENOUS VASOPRESSIN RELEASE CONTRIBUTES TO THE THROMBOTIC RISK OF HIP SURGERY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643695.

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Vasopressin (aVP) infusions in man that simulate physiological concentrations in plasma produce increases inboth factor VIII and plasminogen activator activity (PAA) and we have found evidence that aVP release contributes to the activation of coagulation during abdominal surgery. The aimof this study was to investigate whether aVP has a similar role in theregulation of haemostasis during hipsurgery. Venous blood samples were taken for FVIII:C, FVIII RiCof, vWF:Ag,fibrinopeptide A (FPA), ECLT, platelet aggregation in whole blood andaVPfrom separate venepuncture sites in 7 patients undergoing elective hip surgery. Samples were taken pre-operatively, post induction of anaesthesia, at skin incision, during divisionof the femoral neck, reaming of the acetabulum, cementing of the prosthesisand on thefirst post-operative day. FVIII:C increased during the operation from a geometric mean of 70%pre-operativelyto 109% (p < 0.05) post-operativgly.vWF:Ag and FVIII RiCof rose in a similar manner. PAA (106 /ECLT2) rose significantly from 12 units pre-operatively to a peak value of 167 units(p< 0.001) at prosthesis cementing,andpost-operatively fell to subnoral levels. FPA concentrations followed a similar pattern rising from13 pmol/ml to 58 psmol/ml (p < 0.02)atprosthesis cementing, and falling to9pmol/ml post-operatively. PlasmaaVP rosefrom 0.5pg/ml pre-operatively to 40pg/ml (p < 0.01) at division of the femoral neck, and returned to0.5 pg/ml post-operatively. There were no changes in platelet aggregation in whole blood using a single doseof 1.5 μM ADP. These results are similarto those we have observed duringabdominal surgery. They confirm thaduring surgery, thrombin generation occurs with increased PAA,both of which are preceded by a risein aVP. This isconsistent with the hypothesisthat aVP is an important mediatorof changes in haemostatic function occurringduring surgery, and we are now investigating the relationship between intra-operative changesin haemostaticfunctionand risk of post-operative DVT.
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Schwartz, R., E. Kavanagh, K. Bauer, R. Rosenberg, J. Ballard, J. Latino, V. Strother, M. Mosesson, W. Haire, and M. DeLeo. "ANTITHROMBIN III CONCENTRATE (AT-III) FOR PROPHYLAXIS ANDTREATMENT OF CONGENITAL AND ACQUIREDAT-III DEFCIENCY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643678.

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An investigation has been undertakenin 13 patient studies to determine the efficacy of AT-III in prevention and treatment of thrombosis in patients with congenital (cong.) and acquired (acq.) AT-III deficiency. The mean in vivo incremental recovery of 17 infusions of AT-III in 7 patientswith cong. AT-III deficiency (2 kinetic studies, 5 prophylaxis) was 1.4%/U/kg (functional assay) administered. The mean in vivo recovery of 38 infusions in 4 non-bleeding patients(3 cong., 1 acq.) treated for thrombosis or pulmonary embolism (P.E.) with heparin was 1.33%/U/kg which was not significantly different. The half-life determined in an earlier study exceeded 2.5 days. All patients treated prophylactically or therapeutically received a loading dose to increase plasma AT-III to 120%, and then received maintenance doses, generally every 24 hours, to maintain plasma AT-III levels in the general range 80-120%. AT-III levels were monitored every 12 hours initially and doses and intervals modified accordingly. None of 5 patients with cong. deficiency treated prophylactically for high risk situations (surgery, delivery, catheterization) developed a thrombotic complication. Six patients (3 cong., 2 acq., 1 probably acq.) were treated for thrombosis/P.E., two of whom were pregnant. Heparin resistance was reversed in two, both pregnant. One patient with superior mesenteric-portal vein thrombosis (cong. deficiency) and another with superior mesenteric artery-aortic occlusion (acq. deficiency) survived without further progression of thrombosis. DIC resolved in one patient treated with AT-III and benefit was observed in a 2nd patient as well. AT-III was well tolerated, with but a single mild reaction in 176 infusions. We conclude AT-III may be beneficialas prophylaxis in patients with cong.AT-III deficiency during high thrombotic risk situations, as well as anadjunct to heparin in treatment for thrombotic complications in congenital and acquired AT-III deficiency.
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7

Borrell, M., J. Fontcuberta, E. Muñiz, E. Grau, and A. Oliver. "FIBRINOLYTIC ACTIVITY AND OTHER COAGULATION PROTEINS IN PATIENTS WITH LUPUS ANTICOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644237.

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Patients with lupus anticoagulant (LA) is a group with recognised risk of thrombosis. In order to study the possible causes of this tendency, we have studied the fibrinolytic activity and some other coagulation parameters considered as thrombotic markers in a group of 12 patients with LA. Half of them had presented thrombotic disease and/or recurrent abortions. 3 patients presented systemic lupus erythematosus and in the other 9 we couldn't detect any connective tissue disorder. The following tests were performed: tissue plasminogen activator (t-PA) activity, t-PA antigen, t-PA inhibitor, fibrin plates with and without kaolin, -antiplasmin, plasminogen, prekallikrein, antithrombin III, protein C, protein S. The results were analysed comparing the values obtained in LA group with respect to normal values, and among the LA group between patients who had suffered from thrombotic disease and those who did not.The results obtained did not show significant differences between control group and LA patients except in t-PA activity which was found decreased in LA group: 1.86±0.89 versus 3.0±0.94 in control group (meantstandard deviation). Among this group there were no differences between patients who had suffered from thrombotic disease and those who didn’t.From these results we suggest that unpaired t-PA activity may contribute but not be the only responsible factor for the dvelopment of thrombosis in these patients.
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8

Konig, Maximillian F., Jessica Li, and Michelle Petri. "O1 Hydroxychloroquine blood levels and risk of thrombotic events in systemic lupus erythematous." In 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.15.

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9

Finke, U., J. Schneider, E. Friderichs, L. Flohé, and H. Giertz. "MYOCARDIAL SALVAGE BY COMBINED TREATMENT WITH RECOMBINANT SINGLE-CHAIN UROKINASE-TYPE PLASMINOGEN ACTIVATOR AND RECOMBINANT HUMAN SUPEROXIDE DISMUTASE IN A CANINE CORONARY THROMBOSIS MODEL*." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643570.

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Recanalization of thrombotic coronary occlusion with fibrinolytic treatment is a promising approach to salvage jeopardized ischemic myocardium. However, the success of thrombolytic treatment of myocardial infarction may be curtailed by the risk inherent to reperfusion. Cell damage upon reoxygenation after an ischemic period is tentatively attributed to the formation of oxygen-derived free radicals. Improved myocardial salvage is therefore expected from coadministration of a free radical scavenger and fibrinolytic treatment. We tested this hypothesis in a canine model of left anterior circumflex coronary artery (LCX) thrombosis. Thrombolysis was achieved with the fibrin- selective single-chain urokinase-type plasminogen activator of recombinant origin (r-scu-PA). As enzymatic scavenger of oxygen radicals recombinant human superoxide dismu-tase (r-HSOD) was used. The three experimental groups were: group I (n=4) did not receive any treatment after LCX thrombosis; in group II (n=9) at 100 min after LCX thrombosis r-scu-PA (20 μg/kg/min i.v. for 30 min) was infused; dogs in group III (n=8) received concomitant treatment with r-scu-PA and r-HSOD (10 mg/kg i.v. for 60 min). Infarct size as percent of the risk zone was 38.2 ± 4.1 in group I, 25.3 ± 3.7 in group II (p ≤ 0.05 vs group I) and 14.9 ± 3.2 in group III (p ≤ 0.05 vs group II). Incidence of reperfusion arrhythmias and increase in plasma CK were significantly diminished by r-HSOD when compared to dogs receiving r-scu-PA only. There were no significant differences in hemodynamic parameters between the groups. In conclusion, in terms of infarct size reduction, suppression of reperfusion arrhythmias and attenuation of intracellular enzyme release the combined treatment with r-scu-PA and r-HSOD yielded a significant higher myocardial salvage versus thrombolytic treatment alone in a canine LCX thrombosis model.* This work is part of the doctoral dissertation of Miss U. Fincke
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10

Dautzenberg, M. D., F. Monge, A. M. Fischer, R. Girot, and P. Cornu. "COAGULATION AND FIBRINOLYSIS IN SICKLE CELL DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643056.

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Sickled erythocytes appear to be primarily responsible for occlusion of microvasculature in patients with homozygous sickle cell disease (SCD), but it is unknown whether the activation of the coagulation pathway is also contributory to these vaso-occlusive crisis and other complications as leg ulcers, aseptic necrosis of bone, strokes. Thus, we studied coagulation and fibrinolysis parameters in 12 patients (ages 2 to 26 years with SCD, in steady-state, far from thrombotic events which occurred in 3 of them) to determine if it would be possible to detect a high-risk group for thrombosis. We were surprised to observe that all the vitamin K dependent factors levels (II, VII+X, IX, protein C) were found next to the lowest values of the normal range.But in 3 out of 12 patients, protein C was significantly lower and 2 of them have had thrombotic events (stroke, leg ulcers). Factor V level was in the normal range except for 3 patients with low levels. As other authors, we observed normal fibrinogen, plasminogen and a 2 antiplasmin values and always very high factor VIII levels. Antithrombin III activity was normal or even high contrasting with the lower levels of the other factors synthesized in the liver. However all these abnormalities seem to balance since the thrombin generation test performed in the patients plasmas are in the normal range. As a marker of high-risk group for thrombosis, fibrin-D-Dimer levels (using a latex bead agglutination assay) were measured and found to be positive in 4 patients, 3 of them having suffered from thrombosis associated in two cases with a protein C deficiency. Thus, if the hemostatic modifications observed are involved in the mechanism of thrombosis, fibrin-D-Dimer and protein C seem to be the most significant parameters in this study.
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Звіти організацій з теми "Thrombotic risk"

1

Chan, Benjamin, Ayodele Odutayo, Peter Juni, Nathan M. Stall, Pavlos Bobos, Adalsteinn D. Brown, Allan Grill, et al. Risk of Vaccine-Induced Thrombotic Thrombocytopenia (VITT) following the AstraZeneca/COVISHIELD Adenovirus Vector COVID-19 Vaccines. Ontario COVID-19 Science Advisory Table, May 2021. http://dx.doi.org/10.47326/ocsat.2021.02.28.1.0.

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Published estimates of the risk of vaccine-induced thrombotic thrombocytopenia (VITT) from countries with moderate to high data quality range from 1 case per 26,500 to 1 case per 127,300 first doses of AstraZeneca/COVISHIELD administered (Table 1). The risk of VITT in Canada as of May 8, 2021 has been estimated to be approximately 1 per 55,000 doses, but several presumptive cases are still under investigation.
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2

Shi, Guoxin, and Wen Zhao. Risk factors for deep venous thrombosis in patients with stroke: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0045.

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3

Xiong, Yuchen, Weiwei Wu, and Shanzi Yu. Different spine tumor pathology and risk of venous thrombosis : systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0121.

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4

Cheng, Fangqun, Biyun Ye, Ying Tang, Zhuo Xiao, Dan Liu, Ke Wang, Peiyu Cheng, and Jingping Zhang. Risk factors for deep vein thrombosis in patients with cerebral hemorrhage: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0068.

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Review question / Objective: To identify the risk factors of deep venous thrombosis in patients with cerebral hemorrhage. Eligibility criteria: Inclusion criteria: ①Comply with the “Guidelines for diagnosis of cerebral hemorrhage in China”[7] or “Guidelines for the management of spontaneous intracerebral hemorrhage in the United States”[37], or be diagnosed as ICH in combination with brain CT, MRI, and cerebral angiography; ②Age ≥18 years old; ③Ultrasonography or color polygraph Pler ultrasonography confirmed DVT; ④ The study type was cohort study or case-control study; ⑤ Newcastle-Ottawa Scale (NOS) [8] score ≥ 6 points; ⑥ The language was limited to Chinese and English. Exclusion criteria: ① Repeated publications; ② Studies without full text, incomplete information, or data extraction impossible.
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5

hou, xianbing, dandan chen, tongfei cheng, dan wang, xiaojun dai, yao wang, bixian cui, et al. Bleeding risk of anticoagulant therapy in patients with advanced cancer in palliative care settings：a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0064.

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Review question / Objective: The systematic review aim to provide synthesised and appraised evidence to assess the bleeding risk of anticoagulant therapy in patients with advanced cancer in palliative care settings. Condition being studied: Cancer is a recognized risk factor for venous thromboembolism (VTE). The main forms of thromboembolic disease include pulmonary embolism (PE) and deep vein thrombosis (DVT). Given their diagnosis and often poor physical status, patients with advanced cancer are at particularly high risk of developing VTE, resulting in reduced activity levels or even immobility. The exact incidence and prevalence of VTE in the population of cancer patients receiving hospice or palliative care has not been well investigated and few reports are available. Clinical studies have not yet determined whether such patients benefit from anticoagulant therapy and whether there is an increased risk of bleeding and death.
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6

Gong, Wei, Yongqi Li, Yu Tian, Jing Zhang, and Lei Li. Effects of cardiovascular disease and traditional cardiovascular risk factors on deep vein thrombosis in stroke patients: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0016.

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7

Saldanha, Ian J., Wangnan Cao, Justin M. Broyles, Gaelen P. Adam, Monika Reddy Bhuma, Shivani Mehta, Laura S. Dominici, Andrea L. Pusic, and Ethan M. Balk. Breast Reconstruction After Mastectomy: A Systematic Review and Meta-Analysis. Agency for Healthcare Research and Quality (AHRQ), July 2021. http://dx.doi.org/10.23970/ahrqepccer245.

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Objectives. This systematic review evaluates breast reconstruction options for women after mastectomy for breast cancer (or breast cancer prophylaxis). We addressed six Key Questions (KQs): (1) implant-based reconstruction (IBR) versus autologous reconstruction (AR), (2) timing of IBR and AR in relation to chemotherapy and radiation therapy, (3) comparisons of implant materials, (4) comparisons of anatomic planes for IBR, (5) use versus nonuse of human acellular dermal matrices (ADMs) during IBR, and (6) comparisons of AR flap types. Data sources and review methods. We searched Medline®, Embase®, Cochrane CENTRAL, CINAHL®, and ClinicalTrials.gov from inception to March 23, 2021, to identify comparative and single group studies. We extracted study data into the Systematic Review Data Repository Plus (SRDR+). We assessed the risk of bias and evaluated the strength of evidence (SoE) using standard methods. The protocol was registered in PROSPERO (registration number CRD42020193183). Results. We found 8 randomized controlled trials, 83 nonrandomized comparative studies, and 69 single group studies. Risk of bias was moderate to high for most studies. KQ1: Compared with IBR, AR is probably associated with clinically better patient satisfaction with breasts and sexual well-being but comparable general quality of life and psychosocial well-being (moderate SoE, all outcomes). AR probably poses a greater risk of deep vein thrombosis or pulmonary embolism (moderate SoE), but IBR probably poses a greater risk of reconstructive failure in the long term (1.5 to 4 years) (moderate SoE) and may pose a greater risk of breast seroma (low SoE). KQ 2: Conducting IBR either before or after radiation therapy may result in comparable physical well-being, psychosocial well-being, sexual well-being, and patient satisfaction with breasts (all low SoE), and probably results in comparable risks of implant failure/loss or need for explant surgery (moderate SoE). We found no evidence addressing timing of IBR or AR in relation to chemotherapy or timing of AR in relation to radiation therapy. KQ 3: Silicone and saline implants may result in clinically comparable patient satisfaction with breasts (low SoE). There is insufficient evidence regarding double lumen implants. KQ 4: Whether the implant is placed in the prepectoral or total submuscular plane may not be associated with risk of infections that are not explicitly implant related (low SoE). There is insufficient evidence addressing the comparisons between prepectoral and partial submuscular and between partial and total submuscular planes. KQ 5: The evidence is inconsistent regarding whether human ADM use during IBR impacts physical well-being, psychosocial well-being, or satisfaction with breasts. However, ADM use probably increases the risk of implant failure/loss or need for explant surgery (moderate SoE) and may increase the risk of infections not explicitly implant related (low SoE). Whether or not ADM is used probably is associated with comparable risks of seroma and unplanned repeat surgeries for revision (moderate SoE for both), and possibly necrosis (low SoE). KQ 6: AR with either transverse rectus abdominis (TRAM) or deep inferior epigastric perforator (DIEP) flaps may result in comparable patient satisfaction with breasts (low SoE), but TRAM flaps probably increase the risk of harms to the area of flap harvest (moderate SoE). AR with either DIEP or latissimus dorsi flaps may result in comparable patient satisfaction with breasts (low SoE), but there is insufficient evidence regarding thromboembolic events and no evidence regarding other surgical complications. Conclusion. Evidence regarding surgical breast reconstruction options is largely insufficient or of only low or moderate SoE. New high-quality research is needed, especially for timing of IBR and AR in relation to chemotherapy and radiation therapy, for comparisons of implant materials, and for comparisons of anatomic planes of implant placement.
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8

Significant risk of another thrombosis remains if anticoagulation is stopped. National Institute for Health Research, October 2019. http://dx.doi.org/10.3310/signal-000830.

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9

Continuing an anticoagulant at home after abdominal surgery cuts thrombosis risk. National Institute for Health Research, December 2019. http://dx.doi.org/10.3310/signal-000850.

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