Atrial fibrillation (AF) is an important cause of ischemic stroke that often remains undetected until stroke occurs. Awareness of the risk factors and symptoms is important so that AF can be diagnosed and thromboprophylaxis given. However, the extent of public awareness of AF is uncertain. We assessed public awareness of AF across six continents and compared it with that of other thrombotic and non-thrombotic disorders.In collaboration with Ipsos-Reid, we conducted an internet-based, cross-sectional survey between September and October of 2016 in 10 countries: Argentina, Australia, Canada, Germany, Japan, Thailand, the Netherlands, Uganda, United Kingdom, and United States. Participants were selected from survey panels in weighted, age-stratified categories (40-60, 61-74, and ≥75 years). The survey included 11 questions about demographics and assessed awareness about AF, as well as that of other thrombotic and non-thrombotic disorders. Proportions and 95% confidence intervals (CI) were calculated.Of a total of 6312 respondents, overall awareness of AF was 48% (95% CI, 46-50%), which was lower than awareness about other thrombotic and non-thrombotic disorders except for deep vein thrombosis (awareness 43%, 95% CI, 41-45%). Awareness about AF ranged from 25% to 69% across countries, while awareness of the risk factors for AF ranged from 8% to 52%, and awareness that AF leads to stroke ranged from 36% to 46%. Among those reporting awareness of AF, 82% correctly identified palpitations as an AF symptom.Global public awareness of AF is low. Improving awareness may empower patients to seek timelier stroke preventive care.
Increased deposition and lysis of fibrin, associated with malignant tissue, has led to look for activators of both the coagulation and fibrinolytic systems produced by tumor cells. We report the evidences of a procoagblant activity (PA) in the extracts of intratumoral necrosis from two experimental breast adenocarcinomas in murine model (BALB/c). The tumors have different metastatic capacity (MC). M3 without MC and MM3 with high MC. The addition of the extracts to: 1- Normal Plasma, 2- Deficient substrates in coagulation factors, 3- Purified, fibrinogen (I), showed: 1- Shortening of the plasma recalcification time (PRT) and APTT, without ;modification on prothrombin time (PT), 2- Reduction of the PRT on deficient substrates in factors: VIII; VII; VII and X; V; V, VII and X; without modification on II deficient substrate, 3- No PA on I. Table: C: Control, s: seconds, m: minutes. The PA was not affected by heparin. The results suggest that the PA is independent of the presence of either factor VIII or factor VII (intrinsic or extrinsic pathway respectively), as well as presence of either factor V or factor X. Any effect was observed either on factor II deficient substrate or on I, so, there was no evidence of thrombin activity The PA could be act directly on factor II, suggesting that fibrin formation could be induced by a “non-classical” activation pathway. No significant differences (p>0.5) in PA were observed between both tumoral necrosis extracts. The necrotic area in M3 (37%) is bigger than in MM3 (18%). So, much more PA could be present in MM3 and this could play a role in the MC of this tumor.
The association between cancer and hypercoagulability states is well known. It usually presents as a complication of gastrointestinal tract adenocarcinomas. We present the case of patient diagnosed of prostatic adenocarcinoma who was admitted because of pain and inflammation in the left side of the neck. The ultrasound study showed a jugular vein thrombosis. In the bibliographic review (MEDLINE 1990-1995), we have not found any similar reports Jugular vein thrombosis is a rare complication and usually is secondary to central vein catheter insertion, although it has been also described with ovarian hyperstimulation syndrome, infections, head and neck tumors and rarely in other neoplastic diseases. The physiopathologic process is not well known, although it is known that neoplastic cells interact with the thrombin and plasmin generating systems and that there is also a decrease in coagulation inhibitors, all of which leads to prothrombin activation in the absence of the corresponding increases in thrombin inhibitor complexes.
Summary Hyperhomocysteinemia (HHcy), lupus anticoagulant (LA) and anticardiolipin antibodies (ACA) are independent risk factors for thrombosis. Even though risks are cumulative, the clinical impact of the association is unknown. Preliminary data suggested that HHcy might be associated with transient LA and ACA, disappearing after lowering HHcy. We prospectively evaluated the association of HHcy and LA/ACA, the effect of lowering HHcy with folic acid in LA behavior, and the correlation of the initial dRVVT with LA behavior after folic acid in 210 patients with thrombosis and adverse pregnancy outcomes. Prevalence of HHcy among patients with LA/ACA was 40%. Thirty-one patients exhibited only HHcy (15%; Group 1), 106 (50%; Group 2) had only LA/ACA, while 73 (35%; Group 3) had both. After therapy, 63% and 64% of LA/ACA remained positive in Group 3 and 2, respectively. We observed a trend towards a more positive dRVVT in persistent LA after lowering HHcy. No differences in clinical presentation or in outcomes after two years of followup were observed among the groups. Even though the association of HHcy and LA/ACA is common in patients with thrombosis, it might have no prognostic implications if Hcy levels are lowered. Currently, no laboratory findings correlate with LA behavior, which is independent of homocysteine levels and vitamin treatment.
The letter published in the November 1997 issue, regarding simultaneous occurrence of lupus anticoagulant (LA) and factor VIII inhibitors [1,2], is very interesting.We agree with Dr. D.A. Triplett that it is of critical importance to differentiate an LA from a factor VIII inhibitor.Strict observance of the criteria recommended by the SSC Subcommittee on Lupus Anticoagulant/Phospholipid-Dependent Antibodies [3] is essential for this purpose.More than one test, with different assay principles, is necessary to screen for an LA, mainly in patients with other simultaneous coagulation defects, such as a neutralizing inhibitor or a factor deficiency.In a recently published study of 170 consecutive hemophilia A patients, we found 36 hemophiliacs who fulfilled the criteria for the diagnosis of LA, 18 of them with a time-dependent effect.It is possible that subjects with a strong time-dependent effect may have both a factor VIII inhibitor and an LA (n ס 12) [4].LAs were diagnosed based mainly on diluted Russell viper venom time (dRVVT).The activated partial thromboplastin time (APTT) is affected by factor VIII inhibitors; however, the platelet neutralization procedure of the APTT showed similar results to those obtained for dRVVT, except in three patients with positive dRVVT, for whom the shortening of the PNP was not sufficient to be considered positive.In our study, the StaclotLA results agreed with those from dRVVT; 8/8 were positive on LAs and 3/3 were negative on factor VIII inhibitors.We believe that factor VIII inhibitors could be masked by LA and the misdiagnosis could delay the prescription of the appropriate therapy [5].The above evidence stresses the need to develop a specific test to identify factor VIII inhibitors without interference of LA, and vice versa.
guideline) showed an increased VWF ratio of >0.7 at 0.5-2(6) h after infusion (0.83-1.27), whilst VWF ratio in 4 cases (0.10-0.21) who had been diagnosed as type 2A VWD were still low of < 0.7 (0.23-0.68) during the time course.