{"title":"Variation in Platelet Function Testing Has a Major Influence on Detection of Aspirin Resistance in Healthy Subjects","authors":"M. Božič-Mijovski, M. Rakuša, M. Stegnar","doi":"10.1159/000173727","DOIUrl":"https://doi.org/10.1159/000173727","url":null,"abstract":"Introduction: An increased demand for monitoring aspirin treatment by platelet function tests has been observed, but data on the biological variation of these tests are insufficient. The aim of this study was to assess the biological variation of optical platelet aggregometry and closure time in healthy subjects without aspirin and after aspirin ingestion. Subjects and Methods: In 20 healthy subjects, blood was sampled 4 times: on 2 consecutive mornings a day after aspirin ingestion (100 mg/daily) and on 2 consecutive days of no treatment. In all samples, arachidonic acid-, ADP- and collagen-induced optical platelet aggregation was measured, and closure times were determined by collagen/epinephrine (CEPI) and collagen/ADP (CADP) cartridges in a platelet function analyzer-100. Results: Aspirin significantly reduced arachidonic acid- and ADP-induced platelet aggregation and significantly prolonged CEPI closure time, but had no significant effect on collagen-induced platelet aggregation and CADP closure time. Aspirin increased both within- and between-subject coefficients of variation. Arachidonic acid-induced platelet aggregation was the most sensitive to aspirin and no aspirin-resistant subjects were detected on either day after aspirin. According to ADP-induced platelet aggregation or CEPI closure time, 25 and 30% of healthy subjects, respectively, changed from aspirin resistant to aspirin responsive or vice versa from one day to another. There was no agreement between platelet function tests in determining aspirin resistance. Conclusions: A significant variation in optical platelet aggregometry and closure time exists and is presumed to have a major effect on determination of aspirin resistance.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"84 - 90"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Upper-Extremity Deep Vein Thrombosis in a Patient on Clozapine Therapy Carrying the Prothrombin G20210A Mutation","authors":"A. Vayá, María López, G. Plumé, J. Ribes","doi":"10.1159/000173731","DOIUrl":"https://doi.org/10.1159/000173731","url":null,"abstract":"Clozapine treatment for resistant schizophrenic disorders has been associated to venous thromboembolic events. We report the case of a patient who developed upper-extremity deep vein thrombosis just 2 months after starting on clozapine in whom the thrombophilia work-up revealed the presence of the prothrombin G20210A mutation.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"105 - 107"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173731","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D. Imberti, M. Giorgi Pierfranceschi, M. Falciani, D. Prisco
{"title":"Venous Thromboembolism Prevention in Patients with Heart Failure: An Often Neglected Issue","authors":"D. Imberti, M. Giorgi Pierfranceschi, M. Falciani, D. Prisco","doi":"10.1159/000173724","DOIUrl":"https://doi.org/10.1159/000173724","url":null,"abstract":"Several epidemiological studies have shown a high prevalence of venous thromboembolism (VTE) complications in patients with acute heart failure; in addition, the level of risk associated with this disease is notable, ranging from 15 to 30%. Three large clinical trials have clearly demonstrated the efficacy and safety of pharmacological prophylaxis in internal medicine patients hospitalized for an acute medical disease; on the contrary, until now there are no studies which have evaluated antithrombotic prophylaxis in a selected population of patients with heart failure only. Moreover, discrepancies existing among recommendations reported in different guidelines may produce uncertainties in the management of VTE prevention in patients with heart failure and may contribute to an underuse of thromboprophylaxis in the daily clinical practice. The aim of this review is to analyze the existing evidence about VTE risk in patients with heart failure as well as the efficacy and safety of antithrombotic prevention, and to underline which are the most important unmet clinical issues for the optimal management of thromboprophylaxis in this particular clinical setting.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"69 - 74"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173724","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Sagastagoitia, Y. Sáez, M. Vacas, I. Narváez, J. P. Sáez de Lafuente, E. Molinero, Antonio Escobar, M. Lafita, J. Iriarte
{"title":"Acute versus Chronic Myocardial Ischemia: A Differential Biological Profile Study","authors":"J. Sagastagoitia, Y. Sáez, M. Vacas, I. Narváez, J. P. Sáez de Lafuente, E. Molinero, Antonio Escobar, M. Lafita, J. Iriarte","doi":"10.1159/000173728","DOIUrl":"https://doi.org/10.1159/000173728","url":null,"abstract":"Objective: To determine the possible differences in lipid, thrombogenic and inflammatory marker concentrations and the presence of chronic and acute coronary artery disease (stable and unstable angina, respectively), comparing them with a group of control patients with normal coronary arteries. Material and Methods: This prospective cohort study included 125 patients with unstable angina, 189 with stable angina and a control group of 83 patients with normal coronary arteries. Marker concentrations were measured in all 3 groups. Logistic regression analysis was performed to determine whether such factors could predict unstable or stable angina. Results: Lipid parameter concentrations were similar in the 2 coronary disease groups and significantly lower than in controls. Haemostatic and inflammatory marker concentrations were higher in patients with coronary disease, but were statistically significant only when comparing unstable angina patients with normal controls. Unstable angina patients had significantly higher levels of lipoprotein (a) [Lp(a)], fibrinogen, C-reactive protein (CRP) and leucocytes. Multiple logistic regression analysis showed that CRP (OR 2.635, 95% CI 1.417–4.898), smoking (OR 3.416, 95% CI 1.773–6.584), leucocytes (OR 2.034, 95% CI 1.079–3.836) and Lp(a) (OR 2.269, 95% CI 1.188–4.334) were independent risk factors of unstable versus stable angina. Conclusions: Patients with unstable angina present a more atherogenic profile than patients with stable angina. Together with smoking, elevated Lp(a), CRP and leucocyte concentrations proved to be associated with the presence of unstable angina.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"91 - 97"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173728","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Solá, A. Vayá, P. Villa, F. España, A. Estellés, Katherinne García, A. Hernández-Mijares
{"title":"Obesity and Activated Protein C Resistance","authors":"E. Solá, A. Vayá, P. Villa, F. España, A. Estellés, Katherinne García, A. Hernández-Mijares","doi":"10.1159/000173723","DOIUrl":"https://doi.org/10.1159/000173723","url":null,"abstract":"It has been reported that obesity may be associated with activated protein C resistance, which could increase the thrombotic risk in these patients. The aim of our study was to evaluate this parameter in obese patients and controls, as well as the effect of weight loss on this parameter. In 63 severely or morbidly obese patients and in 65 healthy volunteers, an anthropometric and analytical evaluation (activated protein C resistance and prothrombin fragment F1 + 2) was performed at baseline and after 3 months of diet. Obese patients showed higher levels of F1 + 2 than controls, whereas activated protein C sensitivity ratios showed no differences. After weight loss, prothrombin fragment F1 + 2 was reduced, but no differences were found in activated protein C sensitivity. We did not find an activated protein C-resistant phenotype in obese subjects.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"64 - 68"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173723","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Guler, O. Yapıcı, D. Erdem, G. Oǧur, D. Ozatli, T. Bakır
{"title":"Acute Complete Splenic Infarction in a Patient with Hirschsprung’s Disease and Literature Review of Complete Splenic Infarction","authors":"N. Guler, O. Yapıcı, D. Erdem, G. Oǧur, D. Ozatli, T. Bakır","doi":"10.1159/000173730","DOIUrl":"https://doi.org/10.1159/000173730","url":null,"abstract":"Here we report a case of Hirschsprung’s disease presenting with acute complete splenic infarction due to thrombus in the splenic vena. MTHFR C677T (methylenetetrahydrofolate) gene homozygote mutation was a risk factor for thrombosis. According to our knowledge, this is the first report for a Hirschsprung’s disease patient with acute complete splenic infarct due to isolated splenic vein thrombosis accompanied by MTHFR C677T gene homozygote mutation.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"102 - 104"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173730","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Successful Protein C Concentrate Administration during Initiation of Oral Anticoagulation in Adult Patients with Severe Congenital Protein C Deficiency: Report of Two Cases","authors":"D. Imberti, M. Giorgi Pierfranceschi","doi":"10.1159/000173721","DOIUrl":"https://doi.org/10.1159/000173721","url":null,"abstract":"Protein C (PC) is a vitamin K-dependent proenzyme with anticoagulant activity, and patients with congenital PC deficiency are at high risk for thrombotic episodes. In patients with PC deficiency, starting treatment with oral anticoagulant drugs is associated with a transient hypercoagulable state and clinically overt thromboembolic complications before reaching a full anticoagulant effect. This report describes a successful supplementation with PC concentrate in two adult patients with moderately severe PC deficiency during the initiation of oral anticoagulation and a course of therapeutic dose of low-molecular-weight heparin for acute venous thromboembolism. Plasma PC levels above 50% were observed in both patients and maintained during the entire supplementation treatment period with PC concentrate until a stable therapeutic anticoagulation level has been reached. These results have been obtained within a short time, thus allowing a safe administration of a loading dose of warfarin. No adverse reactions to the PC concentrate, i.e. skin necrosis and other thromboembolic complications, bleedings or allergic reactions, were observed. We conclude that PC concentrate seems to be effective for the prevention of thromboembolic complications and safe in patients with congenital PC deficiency while initiating oral anticoagulants.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"53 - 57"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173721","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Major and Potential Prothrombotic Genotypes in Patients with Venous Thrombosis and in Healthy Subjects from Slovenia","authors":"M. Bedenčič, M. Božič, P. Peternel, M. Stegnar","doi":"10.1159/000173722","DOIUrl":"https://doi.org/10.1159/000173722","url":null,"abstract":"The objective of our study was to investigate the prevalence of the polymorphisms factor V Leiden (FVL), prothrombin G20210A (PT G20210A), methylenetetrahydrofolate reductase C677T (MTHFR C677T), plasminogen activator inhibitor type 1 –675 4G/5G (PAI-1 4G/5G) and factor XII –4 C/T (FXII –4 C/T) in 295 Slovenian patients with venous thrombosis (VT) and 223 healthy controls in order to establish their contribution to the risk for VT. The major genetic risk factor was FVL, while PT G20210A, MTHFR 677 C/T, PAI-1 4G/5G and FXII –4 C/T polymorphisms were not. However, PT G20210A increased the risk of recurrent VT, MTHFR C677T increased the risk in older patients, while the FXII –4 T allele suggested a possible protective effect in younger patients. The risk of VT increased with increasing number of genetic defects.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"58 - 63"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173722","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adenosine Diphosphate-Induced Platelet Aggregation Correlates with Platelet Activation Identified with the Use of Flow Cytometry","authors":"Milagros García, D. Schneider","doi":"10.1159/000173725","DOIUrl":"https://doi.org/10.1159/000173725","url":null,"abstract":"Background: Assessment of the likelihood of platelet activation (i.e. platelet reactivity) identifies patients at high and low risk of subsequent thrombotic events. Turbidometric platelet aggregation has been used to assess platelet function for more than 4 decades. We have developed a method to assess individual components of platelet activation with the use of flow cytometry that is performed in minimally altered whole blood. Aims: To compare assessment of platelet reactivity determined with the use of aggregometry and flow cytometry. Material and Methods: Twenty adult patients with atherosclerotic vascular disease were included in this study. Blood from each patient was used to determine turbidometric platelet aggregation and to assess platelet activation by flow cytometry. ADP was used as the agonist. Values are means ± SEM. Comparison was performed with the use of Student’s t test and correlation was assessed with the use of Pearson’s correlation analysis. Results: Both maximal aggregation and the slope of aggregation correlate with the percentage of platelets that bound fibrinogen in response to 0.2 μM ADP. The best correlation was seen between the slope of aggregation induced by 0.2 or 1 μM ADP and the percentage of platelets that bound fibrinogen in response to 0.2 μM ADP (for 0.2 μM r = 0.62, p = 0.038; for 1 μM r = 0.71, p = 0.025). Conclusion: The binding of fibrinogen to activated platelets assessed with the use of flow cytometry correlates best with the slope of turbidometric aggregation and appears to reflect the propensity of platelets to activate.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"84 1","pages":"75 - 79"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173725","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of Iron Therapy on Platelet Function among Iron-Deficient Women with Unexplained Menorrhagia","authors":"O. Akay, Enver Akin, F. Mutlu, Z. Gulbaş","doi":"10.1159/000173726","DOIUrl":"https://doi.org/10.1159/000173726","url":null,"abstract":"This study was performed to evaluate the effect of iron therapy on platelet function among women with unexplained menorrhagia in order to better understand possible interactions between iron deficiency anemia and platelet behavior and menorrhagia. Platelet aggregation and adenosine triphosphate (ATP) release induced by 5.0 mM adenosine diphosphate (ADP), 0.5 mM arachidonic acid (AA), 1.0 mg/ml ristocetin and 2 μg/ml collagen were studied by whole-blood platelet lumi-aggregometer in 50 menorrhagic women before and after oral iron therapy and in 22 women of the control group. There was a significant increase in AA- induced platelet aggregation (p < 0.05) and a decrease in ristocetin-induced platelet aggregation (p < 0.01) after treatment. Pre- and posttreatment platelet aggregation responses to ADP and collagen were not significantly different (p > 0.05). Pre- and posttreatment platelet secretion responses to all agonists disclosed no significant difference (p > 0.05). There was no significant difference between the study group after treatment and the control group in respect to platelet aggregation and ATP secretion values induced by all agonists (p > 0.05). We conclude that iron deficiency anemia in women causes AA-induced platelet dysfunction, which may give rise to increased menstrual blood loss and can be reversed by iron repletion.","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"80 - 83"},"PeriodicalIF":0.0,"publicationDate":"2007-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000173726","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65094614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}