Vascular Calcification, Vitamin K and Warfarin Therapy – Possible or Plausible Connection?

Siltari, Aino; Vapaatalo, Heikki

doi:10.1111/bcpt.12834

Cited by 28 publications

(23 citation statements)

References 54 publications

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“… 7 It has been also suggested that warfarin therapy may be associated with an increase in arterial stiffness. 8 – 10 Therefore, development of direct oral anticoagulant (DOAC) drugs offers potential benefits for patients requiring anticoagulant therapy.…”

Section: Introductionmentioning

confidence: 99%

Patient satisfaction after switching from warfarin to apixaban in patients with nonvalvular atrial fibrillation: AGAIN study

Koretsune¹,

Ikeda²,

Kozuma³

et al. 2017

PPA

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PurposePatients treated with warfarin must adhere to frequent monitoring, dietary restrictions, and complicated dose adjustments. Apixaban, a direct factor Xa inhibitor, is an alternative to warfarin that may reduce patient burdens associated with warfarin therapy. However, there is limited evidence pertaining to patient satisfaction with anticoagulant therapies in Japanese patients. The purpose of this observational study was to investigate changes in patient satisfaction after switching from warfarin to apixaban.Patients and methodsNonvalvular atrial fibrillation (NVAF) patients who were scheduled to switch anticoagulants from warfarin to apixaban were enrolled and treated with apixaban for 12 weeks. Patient satisfaction was assessed before the change in medication and after 12 weeks of treatment with apixaban using the Anti-Clot Treatment Scale (ACTS), a patient-reported instrument for measuring satisfaction with anticoagulation treatment. The ACTS includes a 12-item burden scale (maximum 60 points) and a 3-item benefit scale (maximum 15 points).ResultsAmong 732 NVAF patients enrolled, the full analysis set consisted of 697 patients who completed two ACTS assessments (one before the medication change and one 12 weeks after the change). Mean (±standard deviation) patient age was 76.2±9.1 years and mean CHADS2 score was 2.5±1.3. There were no significant changes in ACTS benefit scores. However, ACTS burden scores showed significant improvements at Week 12 compared to baseline (55.6±5.3 at Week 12 and 49.7±8.7 at baseline; P<0.0001). Factors associated with changes in ACTS burden scores from the multiple logistic regression analysis were age ≥70 years (odds ratio [OR]: 1.86; 95% confidence interval [CI]: 1.12–3.10; P=0.0169), baseline ACTS burden score (OR: 0.79; 95% CI: 0.75–0.82; P<0.0001), and use of non-steroidal anti-inflammatory drugs/antiplatelet drugs (OR: 0.60; 95% CI: 0.36–1.00; P=0.0499).ConclusionSwitching from warfarin to apixaban improved patient satisfaction with anticoagulant therapy in Japanese patients with NVAF by reducing burden of treatment.

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Section: Introductionmentioning

confidence: 99%

Patient satisfaction after switching from warfarin to apixaban in patients with nonvalvular atrial fibrillation: AGAIN study

Koretsune¹,

Ikeda²,

Kozuma³

et al. 2017

PPA

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“…MGP binds calcium phosphate by chelating calcium and phosphate ions, as well as crystals (46). When vitamin K levels are reduced or absent, MGP remains inactive, as do other clotting factors such as prothrombin and factors VII, IX, and X (48,49). The vitamin K antagonist warfarin (Coumadin; Bristol-Myers Squibb) inhibits vitamin K activation by inhibiting the vitamin K epoxide reductase complex 1.…”

Section: Osteocalcinmentioning

confidence: 99%

Vascular Calcification: The Evolving Relationship of Vascular Calcification to Major Acute Coronary Events

et al. 2019

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Learning Objectives: On successful completion of this activity, participants should be able to (1) describe the pathogenesis of atherosclerosis; (2) understand the importance of the necrotic core in the genesis of microcalcification in the atheroma; and (3) distinguish between the prognostic importance of dense calcification and multiple small foci of calcification adjacent to lipid lakes. Financial Disclosure: The authors of this article have indicated no relevant relationships that could be perceived as a real or apparent conflict of interest. CME Credit: SNMMI is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to sponsor continuing education for physicians. SNMMI designates each JNM continuing education article for a maximum of 2.0 AMA PRA Category 1 Credits. Physicians should claim only credit commensurate with the extent of their participation in the activity. For CE credit, SAM, and other credit types, participants can access this activity through the SNMMI website (http://www.snmmilearningcenter.org) through September 2022.

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“…Atherosclerosis represents the process by which fibrous plaques are formed in the arterial wall with a subsequent increase in its rigidity, diminished blood flow, with an increase in systolic blood pressure, leading to critical cardiovascular events such as stroke and myocardial infarction [1]. Several reports have illustrated that vitamin K as well as vitamin K antagonists have an important impact in the pathogenic processes that occur during the atherosclerotic plaque formation [2].…”

Section: Introductionmentioning

confidence: 99%

CYP4F2 and VKORC1 Polymorphisms Amplify the Risk of Carotid Plaque Formation

Vesa

Vlaicu

Văcăraș

et al. 2020

Genes

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Introduction: Atherosclerosis represents the process by which fibrous plaques are formed in the arterial wall, increasing its rigidity with a subsequent decrease in blood flow which can lead to several cardiovascular events. Seeing as vitamin K antagonists are involved in the pathogenesis of atherosclerosis, we decided to investigate whether polymorphisms in genes that influence vitamin K metabolism might have an impact in modulating the risk of plaque formation. Patients and Methods: In the current study we included adult patients admitted in the Clinical Municipal Hospital of Cluj-Napoca without any carotid or femoral plaques clinically visible at the initial investigation, and a five year follow-up was subsequently performed. We recorded the following patient characteristics: age at inclusion, gender, area of living, smoking, presence of carotid and/or femoral plaques at five years, ischemic heart disease, arterial hypertension, atrial fibrillation, heart failure, diabetes mellitus, obesity, dyslipidemia, drug (oral anticoagulants, antihypertensives, hypolipidemic, anti-diabetic) use and status for the following gene polymorphisms: VKORC1 1639 G>A, CYP4F2 1347 G>T and GGCX 12970 C>G. Results: We observed that the major predictor of both carotid and femoral plaque formation is represented by ischemic cardiac disease. VKORC1 and CYP4F2 polymorphisms did not predict plaque formation, except for VKORC1 homozygous mutants. Nonetheless, both VKORC1 and CYP4F2 interacted with ischemic cardiac disease, increasing the risk of developing a carotid plaque, while only CYP4F2, but not VKORC1, interacted with ischemic cardiac disease to increase the risk of femoral plaque formation. Conclusions: We documented that CYP4F2 and VKORC1 polymorphisms boost the proinflammatory plaque environment (observed indirectly through the presence of ischemic heart disease), increasing the risk of plaque development.

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Vascular Calcification, Vitamin K and Warfarin Therapy – Possible or Plausible Connection?

Cited by 28 publications

References 54 publications

Patient satisfaction after switching from warfarin to apixaban in patients with nonvalvular atrial fibrillation: AGAIN study

Patient satisfaction after switching from warfarin to apixaban in patients with nonvalvular atrial fibrillation: AGAIN study

Vascular Calcification: The Evolving Relationship of Vascular Calcification to Major Acute Coronary Events

CYP4F2 and VKORC1 Polymorphisms Amplify the Risk of Carotid Plaque Formation

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