scholarly journals The Effects of Warfarin and Direct Oral Anticoagulants on Systemic Vascular Calcification: A Review

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 773
Author(s):  
Kalaimani Elango ◽  
Awad Javaid ◽  
Banveet K. Khetarpal ◽  
Sathishkumar Ramalingam ◽  
Krishna Prasad Kolandaivel ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Arterial Calcification ◽  
Frequent Monitoring ◽  
Cardiovascular Morbidity And Mortality ◽  
Retrospective Cohort Studies ◽  
History Of ◽  
The Cost

Warfarin has been utilized for decades as an effective anticoagulant in patients with a history of strong risk factors for venous thromboembolism (VTE). Established adverse effects include bleeding, skin necrosis, teratogenicity during pregnancy, cholesterol embolization, and nephropathy. One of the lesser-known long-term side effects of warfarin is an increase in systemic arterial calcification. This is significant due to the association between vascular calcification and cardiovascular morbidity and mortality. Direct oral anticoagulants (DOACs) have gained prominence in recent years, as they require less frequent monitoring and have a superior side effect profile to warfarin, specifically in relation to major bleeding. The cost and lack of data for DOACs in some disease processes have precluded universal use. Within the last four years, retrospective cohort studies, observational studies, and randomized trials have shown, through different imaging modalities, that multiple DOACs are associated with slower progression of vascular calcification than warfarin. This review highlights the pathophysiology and mechanisms behind vascular calcification due to warfarin and compares the effect of warfarin and DOACs on systemic vasculature.

Increasing Use of Anticoagulants in Germany and Its Impact on Hospitalization for Tooth Extraction

2021 ◽  
Author(s):  
Olga von Beckerath ◽  
Knut Kröger ◽  
Frans Santosa ◽  
Ayat Nasef ◽  
Bernd Kowall ◽  
...  
Keyword(s):  
Tooth Extraction ◽  
Hospital Admissions ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Annual Number ◽  
Hospitalization Rates ◽  
Defined Daily Doses ◽  
Hospital Referral ◽  
History Of

Abstract Objectives This article aimed to compare nationwide time trends of oral anticoagulant prescriptions with the time trend of hospitalization for tooth extraction (TE) in Germany from 2006 through 2017. Patients and Methods We derived the annual number of hospital admissions for TE from the Nationwide Hospital Referral File of the Federal Bureau of Statistics and defined daily doses (DDD) of prescribed anticoagulants in outpatients from reports of the drug information system of the statutory health insurance. Results From 2005 to 2017, annual oral anticoagulation (OAC) treatment rates increased by 143.7%. In 2017, direct oral anticoagulants (DOACs) represented 57.1% of all OAC treatments. The number of cases hospitalized for TE increased by 28.0 only. From all the cases hospitalized for TE in Germany in 2006, 14.2% had a documented history of long-term use of OACs. This proportion increased to 19.6% in 2017. Age-standardized hospitalization rates for all TE cases with long-term use of OACs increased from 6.6 in 2006 to 10.5 cases per 100,000 person-years in 2014 and remained almost unchanged thereafter. Conclusion Our comparison showed that the large increase in OAC treatment rates in general from 2006 to 2017 had only a small impact on hospitalized TE cases with long-term use of OAC which flattens since 2014.

scholarly journals Direct oral anticoagulant and AKI: apixaban-induced acute interstitial nephritis

2019 ◽  
Vol 12 (6) ◽  
pp. e230371 ◽  
Author(s):  
Christina DiMaria ◽  
Wael Hanna ◽  
Julie Murone ◽  
James Reichart
Keyword(s):  
Clinical Practice ◽  
Interstitial Nephritis ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Acute Interstitial Nephritis ◽  
Direct Oral Anticoagulant ◽  
History Of ◽  
Proven Case ◽  
Short And Long Term

Direct oral anticoagulants (DOACs)—dabigatran, rivaroxaban, apixaban and edoxaban—are changing the landscape of clinical practice for patients requiring short and long-term anticoagulation. We report a patient with no history of kidney disease developing acute interstitial nephritis (AIN) after starting a DOAC, apixaban. To date, this is the first biopsy proven case of apixaban-induced AIN.

scholarly journals Use of Anticoagulants in Patients with Pulmonary Hypertension

2020 ◽  
Vol 40 (03) ◽  
pp. 348-355
Author(s):  
Laurent Bertoletti ◽  
Valentine Mismetti ◽  
George Giannakoulas
Keyword(s):  
Pulmonary Hypertension ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Treatment Strategies ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Thromboembolic Pulmonary Hypertension ◽  
History Of ◽  
Potential Risks ◽  
Pulmonary Arterial

AbstractSince the earliest works on the understanding of different forms of pulmonary hypertension, thrombosis has been involved in the pathophysiology of the disease, both in pulmonary arterial hypertension (PAH) and in chronic thromboembolic pulmonary hypertension (CTEPH). Autopsy and then pathophysiological data paved the way for the use of anticoagulants as a treatment for PAH and CTEPH. In PAH their role has diminished with the advent of specific targeted therapies, but they are still prescribed in more than half of PAH patients, because of concomitant venous thromboembolism or atrial fibrillation. In CTEPH long-term anticoagulant therapy is the cornerstone of the management. The recent development of direct oral anticoagulants (DOACs) raises the question of the best anticoagulation strategy, both in patients with PAH and in patients with CTEPH. In this review, we present an overview of the history of anticoagulants in the management of patients suffering from PAH or CTEPH, an update of the available data on the underlying rationale of their use in these subjects, an alert on the potential risks of using DOACs in these poorly explored situations, and the setting up of dedicated trials to evaluate the best anticoagulant treatment strategies in patients suffering from PAH or CTEPH.

scholarly journals Indoxyl Sulfate and p-Cresyl Sulfate Promote Vascular Calcification and Associate with Glucose Intolerance

2019 ◽  
Vol 30 (5) ◽  
pp. 751-766 ◽  
Author(s):  
Britt Opdebeeck ◽  
Stuart Maudsley ◽  
Abdelkrim Azmi ◽  
Annelies De Maré ◽  
Wout De Leger ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Vascular Calcification ◽  
Serum Levels ◽  
Indoxyl Sulfate ◽  
Arterial Calcification ◽  
Molecular Signaling ◽  
Short Term ◽  
Short Term Exposure ◽  
Cardiovascular Morbidity And Mortality

BackgroundProtein-bound uremic toxins indoxyl sulfate (IS) and p-cresyl sulfate (PCS) have been associated with cardiovascular morbidity and mortality in patients with CKD. However, direct evidence for a role of these toxins in CKD-related vascular calcification has not been reported.MethodsTo study early and late vascular alterations by toxin exposure, we exposed CKD rats to vehicle, IS (150 mg/kg per day), or PCS (150 mg/kg per day) for either 4 days (short-term exposure) or 7 weeks (long-term exposure). We also performed unbiased proteomic analyses of arterial samples coupled to functional bioinformatic annotation analyses to investigate molecular signaling events associated with toxin-mediated arterial calcification.ResultsLong-term exposure to either toxin at serum levels similar to those experienced by patients with CKD significantly increased calcification in the aorta and peripheral arteries. Our analyses revealed an association between calcification events, acute-phase response signaling, and coagulation and glucometabolic signaling pathways, whereas escape from toxin-induced calcification was linked with liver X receptors and farnesoid X/liver X receptor signaling pathways. Additional metabolic linkage to these pathways revealed that IS and PCS exposure engendered a prodiabetic state evidenced by elevated resting glucose and reduced GLUT1 expression. Short-term exposure to IS and PCS (before calcification had been established) showed activation of inflammation and coagulation signaling pathways in the aorta, demonstrating that these signaling pathways are causally implicated in toxin-induced arterial calcification.ConclusionsIn CKD, both IS and PCS directly promote vascular calcification via activation of inflammation and coagulation pathways and were strongly associated with impaired glucose homeostasis.

Empowering and Directive Leadership: The Cost of Changing Styles

2021 ◽  
pp. 227853372110083
Author(s):  
Smita Mukherjee ◽  
Zubin R. Mulla
Keyword(s):  
Laboratory Experiment ◽  
Leadership Styles ◽  
Leadership Style ◽  
Affective Commitment ◽  
Team Outcomes ◽  
History Of ◽  
Satisfaction With The Leader ◽  
The Cost ◽  
First Time

We examine the cost of leaders changing between empowering and directive leadership styles on team outcomes. In a laboratory experiment, we collected data from 240 participants in 80 teams. Confederates enacted different leadership styles and led teams of participants in performing a series of tasks. When leaders changed their style from directive to empowering, teams took time to respond in terms of higher satisfaction with leader and affective commitment. However, when leaders changed their style from empowering to directive, the deterioration of satisfaction with leader and reduction in affective commitment were immediate. Moreover, teams of leaders who had been consistently directive showed higher affective commitment as compared to teams of leaders who had a history of being empowering but later shifted to being directive. First time managers can get inputs on how they should enact their leadership style and be aware that switching between styles may impose long-term costs on the team’s affective commitment and satisfaction with the leader.

Management of Oral Anticoagulation Therapy After Gastrointestinal Bleeding: Whether to, When to, and How to Restart an Anticoagulation Therapy

2017 ◽  
Vol 51 (11) ◽  
pp. 1000-1007 ◽  
Author(s):  
Kazuhiko Kido ◽  
Michael J. Scalese
Keyword(s):  
Gastrointestinal Bleeding ◽  
Cohort Studies ◽  
Oral Anticoagulation ◽  
Retrospective Cohort ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Anticoagulation Therapy ◽  
Cochrane Library ◽  
Oral Anticoagulation Therapy ◽  
Retrospective Cohort Studies

Objective: To evaluate current clinical evidence for management of oral anticoagulation therapy after gastrointestinal bleeding (GIB) with an emphasis on whether to, when to, and how to resume an anticoagulation therapy. Data Sources: Relevant articles from MEDLINE, Cochrane Library, and EMBASE databases were identified from 1946 through May 20, 2017, using the keywords: gastrointestinal hemorrhage or gastrointestinal bleeding and antithrombotic therapy or anticoagulation therapy or warfarin or dabigatran or rivaroxaban or apixaban or edoxaban.Study Selection and Data Extraction: All English-language studies assessing management of oral anticoagulation therapy after GIB were evaluated. Data Synthesis: A total of 9 studies were identified. Four retrospective cohort studies showed that resuming anticoagulation therapy was associated with significantly lower rate of thromboembolism (TE) in the general population. Meta-analyses and prospective cohort studies also supported this finding. Two retrospective cohort studies indicated an increase in GIB when anticoagulation reinitiation occurred in less than 7 days without a decrease in TE. Resuming therapy between 7 and 15 days did not demonstrate a significant increase in GIB or TE. A large retrospective study showed that apixaban was associated with the significantly lowest risk of GIB compared with both rivaroxaban and dabigatran. Conclusion: Anticoagulation therapy resumption is recommended, with resumption being considered between 7 and 14 days following GIB regardless of the therapy chosen. Data for warfarin management after GIB should be applied with caution to direct oral anticoagulants (DOACs) because of the quicker onset and experimental nature of reversal agents. Apixaban may be a preferred option when restarting a DOAC therapy.

scholarly journals ORAL ANTICOAGULANTS IN THE TREATMENT OF VENOUS THROMBOEMBOLIC COMPLICATIONS: FOCUS ON APIXABAN

2017 ◽  
pp. 56-62 ◽  
Author(s):  
M. Yu. Gilyarov ◽  
E. V. Konstantinova
Keyword(s):  
Vitamin K ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Factor Xa ◽  
Vitamin K Antagonist ◽  
Fixed Dose ◽  
Vein Thrombosis ◽  
Venous Thromboembolic ◽  
Deep Vein

Venous thromboembolism (VTE), comprising deep vein thrombosis and pulmonary embolism, is a common condition associated with a significant clinical and economic burden. Anticoagulant therapy is the mainstay of treatment for VTE. Current guidelines recommend the use of either low molecular weight heparins or fondaparinux overlapping with and followed by a vitamin K antagonist for the initial treatment of VTE, with the vitamin K antagonist continued when long-term anticoagulation is required. These traditional anticoagulants have practical limitations that have led to the development of direct oral anticoagulants that directly target either Factor Xa or thrombin and are administered at a fixed dose without the need for routine coagulation monitoring. The paper reviews results of the trials of apixaban application for treatment and/or long-term secondary prevention of VTE. The paper analyses effectiveness and safety of apixaban in different groups of patients, as well as features of apixaban application in every day practice.

Oral anticoagulant treatment: friend or foe in cardiovascular disease?

Blood ◽  
2004 ◽  
Vol 104 (10) ◽  
pp. 3231-3232 ◽  
Author(s):  
Leon J. Schurgers ◽  
Hermann Aebert ◽  
Cees Vermeer ◽  
Burkhard Bültmann ◽  
Jan Janzen
Keyword(s):  
Cardiovascular Disease ◽  
Vitamin K ◽  
Heart Valves ◽  
Vitamin K Antagonists ◽  
Oral Anticoagulants ◽  
Arterial Calcification ◽  
Adverse Side Effect ◽  
Oral Anticoagulant Treatment ◽  
Carboxyglutamic Acid

Abstract Calcification is a common complication in cardiovascular disease and may affect both arteries and heart valves. Matrix γ-carboxyglutamic acid (Gla) protein (MGP) is a potent inhibitor of vascular calcification, the activity of which is regulated by vitamin K. In animal models, vitamin K antagonists (oral anticoagulants [OACs]) were shown to induce arterial calcification. To investigate whether long-term OAC treatment may induce calcification in humans also, we have measured the grade of aortic valve calcification in patients with and without preoperative OAC treatment. OAC-treated subjects were matched with nontreated ones for age, sex, and disease. Calcifications in patients receiving preoperative OAC treatment were significantly (2-fold) larger than in nontreated patients. These observations suggest that OACs, which are widely used for antithrombotic therapy, may induce cardiovascular calcifications as an adverse side effect.

Resolution of warfarin-induced alopecia with conversion to apixaban

2021 ◽  
Vol 14 (3) ◽  
pp. e240579
Author(s):  
Katherine Leigh Hull ◽  
Richard Gooding ◽  
James O Burton
Keyword(s):  
Hair Loss ◽  
Warfarin Therapy ◽  
Negative Impact ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Hair Follicles ◽  
Dialysis Access ◽  
Close Monitoring ◽  
Patient Reported

Warfarin is frequently prescribed as a long-term anticoagulant in patients with end-stage kidney disease as direct oral anticoagulants undergo renal excretion. Anticoagulation is a rare cause of alopecia in adults and is thought to be due to the promotion of the ‘resting phase’ of hair follicles. In this case report, a prevalent haemodialysis female patient required long-term anticoagulation following a complex pulmonary embolus and dialysis access complications. After commencing warfarin therapy, the patient reported generalised loss and thinning of her hair. All other potential causes were excluded. Cessation of warfarin therapy and conversion to apixaban with close monitoring alleviated the hair loss. Warfarin therapy is a rare cause of alopecia but should be considered in patients on long-term anticoagulation when other diagnoses have been excluded. Hair loss has a profoundly negative impact on patient quality of life and should prompt investigation to determine the underlying cause.

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