scholarly journals The role of oral anticoagulant therapy in patients with acute coronary syndrome

2017 ◽  
Vol 8 (12) ◽  
pp. 353-366 ◽  
Author(s):  
Jae Youn Moon ◽  
Deepa Nagaraju ◽  
Francesco Franchi ◽  
Fabiana Rollini ◽  
Dominick J. Angiolillo
Keyword(s):  
Acute Coronary Syndrome ◽  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Thrombus Formation ◽  
Oral Anticoagulant Therapy ◽  
Ease Of Use ◽  
Coagulation Cascade ◽  
Bleeding Complications ◽  
Coronary Syndrome

Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 receptor antagonist represents the current standard of care to prevent atherothrombotic recurrences in patients with acute coronary syndrome (ACS). However, despite the use of DAPT, the recurrence rate of cardiovascular ischemic events still remains high. This persistent risk may be in part attributed to the sustained activation of the coagulation cascade leading to generation of thrombin, which may continue to play a key role in thrombus formation. The use of vitamin K antagonists (VKAs) as a strategy to reduce atherothrombotic recurrences after an ACS has been previously tested, leading to overall unfavorable outcomes due to the high risk of bleeding complications. The recent introduction of non-VKA oral anticoagulants (NOACs), characterized by a better safety profile and ease of use compared with VKA, has led to a reappraisal of the use of oral anticoagulant therapy for secondary prevention in ACS patients. The present article provides an overview of the rationale and prognostic role of oral anticoagulant therapy in ACS patients as well as recent updated clinical data, in particular with NOACs, in the field and future perspectives on this topic.

Bleeding complications to long-term oral anticoagulant therapy

1994 ◽  
Vol 1 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Annette Lemche Gull�v ◽  
Birgitte Gade Koefoed ◽  
Palle Petersen
Keyword(s):  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Oral Anticoagulant Therapy ◽  
Bleeding Complications

scholarly journals Comparison of the native prothrombin antigen and the prothrombin time for monitoring oral anticoagulant therapy

Blood ◽  
1984 ◽  
Vol 64 (2) ◽  
pp. 445-451 ◽  
Author(s):  
B Furie ◽  
HA Liebman ◽  
RA Blanchard ◽  
MS Coleman ◽  
SF Kruger ◽  
...  
Keyword(s):  
Prothrombin Time ◽  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Warfarin Therapy ◽  
Oral Anticoagulant Therapy ◽  
Bleeding Complications ◽  
Thromboembolic Complications ◽  
Serum Samples ◽  
Time Index ◽  
Patients At Risk

Abstract We have measured the fully carboxylated (native) prothrombin antigen and the undercarboxylated (abnormal) prothrombin antigen in patients treated with sodium warfarin using specific immunoassays to evaluate a new approach for monitoring oral anticoagulant therapy. Plasma and serum samples (391) were assayed for the prothrombin time, native prothrombin antigen, and abnormal prothrombin antigen. The results were correlated with the presence of bleeding or thromboembolic complications at the time of phlebotomy. The native prothrombin antigen correlated with the occurrence of complications in 95% of samples. Of 13 samples from patients with bleeding complications, 13/13 (100%) had a native prothrombin of 12 micrograms/mL or lower. Of seven samples from patients with thromboembolic complications, 6/7 (86%) had a native prothrombin of 24 micrograms/mL or greater. By comparison, a prothrombin time index of 1.5 to 2.5, 1.5 to 2.2, 1.5 to 2.0, or 1.3 to 1.8 identified 6/20 (30%), 9/20 (45%), 11/20 (55%), or 12/20 (60%) patients at risk, respectively. Although the prothrombin time index did correlate with the presence of bleeding complications, the native prothrombin antigen correlated closely with the presence of bleeding and thromboembolic complications. According to these results, the native prothrombin antigen, maintained in a range of 12 to 24 micrograms/mL by regular adjustment of the warfarin dosage, may be associated with a reduced risk of complications due to excessive or insufficient warfarin therapy. On the basis of these preliminary data, we recommend that the native prothrombin antigen be considered to monitor warfarin therapy.

scholarly journals Thrombocytopenia in Patients Receiving Oral Anticoagulant Therapy

2002 ◽  
Vol 8 (3) ◽  
pp. 213-215 ◽  
Author(s):  
Gianluca Sottilotta ◽  
Vincenzo Oriana ◽  
Caterina Latella ◽  
Vincenzo Trapani Lombardo
Keyword(s):  
Anticoagulant Therapy ◽  
Therapeutic Range ◽  
Oral Anticoagulant ◽  
Bleeding Complication ◽  
Oral Anticoagulant Therapy ◽  
Bleeding Complications

The aim of this report was to determine the frequency of thrombocytopenia in a cohort of 1,126 patients receiving oral anti- coagulant therapy (OAT), and to compare the grade of thrombocy- topenia and the severity of bleeding complications. Severe thrombo- cytopenia was observed in five patients, and moderate and light thrombocytopenia were observed in 208 patients. Thrombocytopenic patients receiving OAT presented five major and six minor hemor- rhages. The presence of hepatitis markers and autoantibodies was assessed. All parameters at the time of the bleeding complication were in the therapeutic range.

No Indication for APTT Screening in Patients on Oral Anticoagulant Therapy

1999 ◽  
Vol 81 (03) ◽  
pp. 364-366 ◽  
Author(s):  
Hans Vos ◽  
Frits Rosendaal ◽  
Felix van der Meer
Keyword(s):  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Oral Anticoagulant Therapy ◽  
Factor Ix ◽  
Bleeding Complications ◽  
Prolonged Aptt

SummaryPatients on oral anticoagulant therapy (OAT) may bleed due to a very low factor IX level caused by a mutation at Ala-10 in the propeptide region of the factor IX gene. We evaluated screening of patients on OAT with an APTT to detect patients with this abnormality. In 734 patients an APTT was assessed. Twenty-three patients had a disproportionately prolonged APTT. In these patients the factor IX level, the mutation at Ala-10 and the frequency of bleeding complications were assessed. No severely lowered factor IX levels were found (1 patient with 5% factor IX). No mutations at Ala-10 were found and bleeding complications were not more frequent in these patients. Conclusion: Routine APTT screening of patients on OAT is not useful to detect patients with increased bleeding or with the Ala-10 mutation in the factor IX gene.

scholarly journals Chronically Elevated Interleukin-6 Disturbs the Coagulation Cascade in Mice

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 2065-2065
Author(s):  
Tanja Knopp ◽  
Jeremy Lagrange ◽  
Rebecca Jung ◽  
Johannes Wild ◽  
Heidi Rossmann ◽  
...  
Keyword(s):  
Board Of Directors ◽  
Interleukin 6 ◽  
Thrombus Formation ◽  
Vena Cava ◽  
Coagulation Cascade ◽  
Bleeding Complications ◽  
Thrombin Inhibitor ◽  
Advisory Committees ◽  
Hemostatic System

Abstract Introduction: Pro-inflammatory cytokines play an essential role as activators of the hemostatic system and in the regulation of physiological antithrombotic mechanisms. Interleukin-6 (IL-6) influences platelet production and platelet activation. It was associated with accelerated clotting and intravascular coagulation in tissue factor (TF)-driven murine thrombosis models. However, the precise role of myeloid cell-derived IL-6 on thrombosis formation and the hemostatic system is still unknown. Methods and Results: To better understand the role of IL-6 in thrombosis and the hemostatic system, we developed a new mouse strain with Cre-recombinase driven constitutive IL-6 expression specifically in myeloid cells (LysM-IL-6 OE, Control mice: IL-6 OE). LysM-IL-6 OE mice had a prolonged tail bleeding time and lacked venous thrombus formation induced by inferior vena cava (IVC) stenosis. There were no differences in D-Dimer levels in LysM-IL-6 OE mice neither on baseline level nor after IVC ligation. However, we found unstoppable post-operative bleedings in LysM-IL-6 OE. They showed a prolonged aPTT, a significantly increased INR and a prolonged thrombin converting time. The Factor V and IX expression were reduced, but von Willebrand factor, antithrombin and fibrinogen expression were up-regulated and could not explain the missing thrombus formation. We found significantly elevated erythrocyte sedimentation in line with erythrocytes aggregates, which seemed to be mediated by IL-6 and α2M. Most importantly, hepatic levels of thrombin inhibitor α2 macroglobulin (α2M) mRNA and protein were increased in LysM-IL-6 OE/+ mice compared to control mice. In parallel, Platelet erythrocyte interaction seemed to be essential in the development of the bleeding phenotype. Conclusions: These findings show the role of chronically elevated IL-6 in driving the accumulation of A2m on the surface of erythrocytes, thereby mediating a phenotype of increased bleeding complications. This work was supported by the DFG KA4035/1-1 and by the German Ministry for Education and Research (BMBF 01EO1503) Disclosures Lämmle: Takeda: Membership on an entity's Board of Directors or advisory committees; Ablynx: Membership on an entity's Board of Directors or advisory committees, Other: Travel Support, Speakers Bureau; Baxter: Other: Travel Support, Speakers Bureau; Alexion: Other: Travel Support, Speakers Bureau; Siemens: Other: Travel Support, Speakers Bureau; Bayer: Other: Travel Support, Speakers Bureau; Roche: Other: Travel Support, Speakers Bureau; Sanofi: Other: Travel Support, Speakers Bureau. Ruf: ARCA bioscience: Consultancy, Patents & Royalties; ICONIC Therapeutics: Consultancy; MeruVasimmune: Current holder of individual stocks in a privately-held company.

Anticoagulation in the Management of Non-ST-Segment Elevation Acute Coronary Syndrome

2010 ◽  
Vol 23 (4) ◽  
pp. 324-334
Author(s):  
Paul P. Dobesh ◽  
Toby C. Trujillo
Keyword(s):  
Acute Coronary Syndrome ◽  
Anticoagulant Therapy ◽  
Plaque Rupture ◽  
Thrombus Formation ◽  
The United States ◽  
Detailed Examination ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
St Segment ◽  
Elevation Acute Coronary Syndrome

There are currently over 1 million patients admitted to hospitals in the United States with the diagnosis of non-ST-segment elevation acute coronary syndrome (NSTE ACS). Due to the significant morbidity and mortality associated with NSTE ACS, appropriate use of the numerous medications employed is critical in ensuring optimal outcomes. Because atherosclerotic plaque rupture and thrombus formation are the central pathophysiologic process in patients with NSTE ACS, it is important to utilize effective and safe combinations of antiplatelet and anticoagulant drug therapy. There are a number of different anticoagulant agents available for use in patients with NSTE ACS, but it is essential to have an in-depth knowledge of the setting in which these agents have been investigated, what current consensus guidelines recommend, as well as an appreciation for the treatment approach and philosophy of the institution for management of patients with NSTE ACS. In this review manuscript, the reader will find an evaluation of the current guidelines concerning the use of anticoagulant therapy in patients with NSTE ACS, as well as a detailed examination of the literature with critical analysis on issues that should be considered when deciding on the appropriate implementation of anticoagulant therapy in protocols for NSTE ACS patients.

Antithrombotic therapy for acute coronary syndrome: Past, present and future

2017 ◽  
Vol 117 (07) ◽  
pp. 1240-1248 ◽  
Author(s):  
Dirk Sibbing ◽  
Dominick J. Angiolillo ◽  
Kurt Huber
Keyword(s):  
Acute Coronary Syndrome ◽  
Thrombus Formation ◽  
Blood Platelets ◽  
Treatment Strategies ◽  
Coagulation Cascade ◽  
Current Guideline ◽  
Antithrombotic Treatment ◽  
Coronary Syndrome ◽  
Research Activities ◽  
Number Of Patients

SummaryPlaque erosions and ruptures are the histopathological hallmarks of arterial thrombus formation in the coronary arteries. The clinical condition associated with this process is usually referred to as acute coronary syndrome (ACS). Importantly, both blood platelets and the coagulation cascade are key players for initiation, amplification and perpetuation of ACS. There has been great progress in ACS treatment in recent decades, both at the technical level of (percutaneous) revascularisation and at the level of antithrombotic treatment. Numerous trials have led to significant advancements in the development of effective anticoagulant and antiplatelet drugs. The large number of randomised controlled clinical trials (RCTs) and the huge number of patients enrolled in these RCTs, with mega trials including >10,000 patients, is unique in the history of medical research and also reflects the exceptional efforts associated with these huge research activities. The crucial issue, however, with respect to optimising treatment, relates to finding the delicate balance between the reduction of thrombotic events by effective drug treatment and the induction of bleeding that is linked to the use of potent or multiple antithrombotic agents. Interestingly, there is a gap in modern days between current guideline recommendations favouring potent platelet inhibition in ACS and the utilization of the respective drugs in clinical practice. In this review, we will summarise and discuss the past, present and future antithrombotic treatment for ACS patients with a focus on the development of optimised antiplatelet treatment strategies and their utilisation in the real world.

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