Warfarin Is Bad to the Bone, Fracture Data Affirms

Is your doctor warning you about this and all these other rat poison(warfarin) side effects? 

• warfarin side effects (32)

 

Warfarin Is Bad to the Bone, Fracture Data Affirms

In U.S. claims analysis, fracture risk lower with DOACs

• by Nicole Lou, Staff Writer, MedPage Today November 25, 2019

Warfarin (Coumadin) may not be the best oral anticoagulant in atrial fibrillation (Afib) in terms of bone health, a retrospective study suggested.
On multivariable-adjusted, propensity score-matched analyses of insurance claims, new users of direct oral anticoagulants (DOACs) were at lower fracture risk over an average 16.9 months of follow-up compared with new warfarin users:

• Fractures requiring hospitalization: HR 0.87 (95% CI 0.79-0.96)
• All clinical fractures: HR 0.93 (95% CI 0.88-0.98)
• Hip fractures: HR 0.91 (95% CI 0.78-1.07)

The strongest effect estimates were observed when comparing apixaban (Eliquis) and warfarin, whereas head-to-head comparisons among DOACs showed similar fracture risk, Pamela Lutsey, PhD, of University of Minnesota School of Public Health in Minneapolis, and colleagues reported in JAMA Internal Medicine.
"Collectively, our findings support the notion that warfarin may be harmful to bone health," they concluded. They argued that the lack of statistical significance for the outcome of hip fracture may have to do with lower precision for this outcome.
Warfarin had been associated with higher fracture risk than dabigatran (Pradaxa) in a 2017 study from Hong Kong.
Recently, other groups have also reported fewer cases of poor osteoporotic outcomes when Afib patients took DOACs in lieu of the vitamin K antagonist.
"Vitamin K is important in posttranslational glutamination of osteocalcin, the major noncollagenous bone matrix protein. Warfarin interferes with this process and consequently inhibits the activation of bone matrix proteins," the investigators noted.
They recommended caution when prescribing warfarin to patients with Afib at high risk of fracture.
The study used MarketScan administrative claims databases for information on a commercially-insured population of people with non-valvular Afib who were prescribed oral anticoagulants in 2010-2015. These were new users without known prior exposure to oral anticoagulation.
Groups were categorized according to the first oral anticoagulant they were prescribed: dabigatran (18.9%), rivaroxaban (Xarelto, 21.1%), apixaban (10.6%), warfarin (49.4%).
In the end, 167,275 individuals were matched for comparison. Their average age was 68.9 years; 38.0% were women. Each DOAC user was matched to up to three warfarin recipients.
The subgroup of people diagnosed with osteoporosis especially benefited from DOACs over warfarin, according to Lutsey's team.
Potential confounding is an inherent limitation to such a retrospective analysis, the authors acknowledged. Even after matching, the warfarin and apixaban groups in this study were older and had higher CHA₂DS₂-VASC scores compared to the dabigatran and rivaroxaban groups.
Furthermore, the databases used for the analysis excluded people without insurance, and edoxaban (Savaysa) was excluded from the study because there were too few users of this DOAC in the dataset.

The study was supported by grants from the National Heart, Lung, and Blood Institute; the National Institute on Aging; and the American Heart Association.
Lutsey disclosed receiving NIH grants.

• Primary Source

  JAMA Internal Medicine

  Source Reference: Lutsey PL, et al "Association of anticoagulant therapy with risk of fracture among patients with atrial fibrillation" JAMA Intern Med 2019; DOI: 10.1001/jamainternmed.2019.5679.

Warfarin-induced skin necrosis within psoriatic plaques

You can check out these other warfarin side effects from taking rat poison. Luckily I had none and was only on it for a couple of months, now I'm on 325 aspirin and don't seem to have the bleeding side effects from that.

• warfarin side effects (31)

 

Warfarin-induced skin necrosis within psoriatic plaques 

Abstract 

A myriad of different phenomena exist in the dermatological literature which are based on the concept of locus minores resistentiae. The most commonly described phenomenon is the Koebner phenomenon, which is classically associated with the emergence of psoriatic lesions post trauma. Warfarin-induced skin necrosis (WISN) is a rare but severe side effect that leads to necrosis of the skin, predominantly on areas with increased subcutaneous fat. The presented case reports on WISN within psoriatic plaques.
Pictures at link.

Interaction between warfarin and cannabis

Be careful out there. I guess I may have to wait until I'm off warfarin after my next stroke before I start rehabbing with marijuana.

My 13 reasons for marijuana use post-stroke.  

Don't follow me, I'm not medically trained. 

 

Interaction between warfarin and cannabis

Per Damkier

Dorte Lassen

Mette Marie Hougaard Christensen

Kenneth Grønkjær Madsen

Maja Hellfritzsch

Anton Pottegård

First published: 16 October 2018

https://doi.org/10.1111/bcpt.13152

This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/bcpt.13152

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Abstract

Delta‐9‐tetrahydrocannabinol (THC), the main psychoactive cannabinoid in cannabis, may inhibit the cytochrome P450 enzyme CYP2C9. Consequently, cannabis use might infer a risk of drug‐drug interaction with substrates for this enzyme, which includes drugs known to have a narrow therapeutic window. In this study, we describe a case report of a 27‐year‐old man treated with warfarin due to mechanical heart valve replacement who presented with elevated international normalized ratio (INR) value (INR = 4.6) following recreational cannabis use. We conducted a review of the available literature, using the PubMed and EMBASE databases while following PRISMA guidelines. Following screening of 85 articles, three eligible articles were identified, including one in vitro study and two case reports. The in vitro study indicated that THC inhibits the CYP2C9‐mediated metabolism of warfarin. One case study reported of a man who on two occasions of increased marijuana use experienced INR values above 10 as well as bleeding. The other case study reported of a patient who initiated treatment with a liquid formulation of cannabidiol (CBD) for the management of epilepsy, ultimately necessitating a 30% reduction in warfarin dose to maintain therapeutic INR values. The available, although sparse, data suggest that use of cannabinoids increase INR values in patients receiving warfarin. Until further data are available, we suggest patients receiving warfarin be warned against cannabis smoking.
This article is protected by copyright. All rights reserved.

Omega-3 Fatty Acid Supplementation and Warfarin: A Lethal Combination in Traumatic Brain Injury

Consult with your doctor if you need to be concerned about this. How much fish oil causes this problem?
http://journals.lww.com/journaloftraumanursing/Abstract/2017/01000/Omega_3_Fatty_Acid_Supplementation_and_Warfarin__.4.aspx

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Journal of Trauma Nursing:

January/February 2017 - Volume 24 - Issue 1 - p 15–18

doi: 10.1097/JTN.0000000000000256

Case Study

Omega-3 Fatty Acid Supplementation and Warfarin: A Lethal Combination in Traumatic Brain Injury

Gross, Brian W. BS; Gillio, Maria BS; Rinehart, Cole D. BS; Lynch, Caitlin A. BS; Rogers, Frederick B. MD, MS, FACS

Abstract

Polyunsaturated fatty acids such as omega-3 eicosapentaenoic acid and omega-6 docosahexaenoic acid, found in over-the-counter fish oil supplements, are often consumed for their beneficial, prophylactic, anti-inflammatory effects. Although the mechanisms of action are not fully known, a diet rich in polyunsaturated fats may reduce the risk of hyperlipidemia, atherosclerosis, high low-density lipoprotein cholesterol levels, hypertension, and inflammatory diseases. Masked by its many benefits, the risks of omega-3 fatty acid supplementation are often underappreciated, particularly its ability to inhibit platelet aggregation and promote bleeding in patients taking anticoagulant medications. The following details the clinical case of an elderly patient taking warfarin and fish oil supplementation whose warfarin-induced coagulopathy could not be reversed after suffering blunt head trauma.

Association of Selective Serotonin Reuptake Inhibitors With the Risk for Spontaneous Intracranial Hemorrhage

This is where your doctor needs to tell you of the pros and cons of SSRIs. Recover better but take the chance of an ICH? Ask your doctor if oral anticoagulants means aspirin or warfarin.

Pros:

Antidepressants may help people recover from stroke even if they are not depressed Jan. 2013

 

Cons:

Association of Selective Serotonin Reuptake Inhibitors With the Risk for Spontaneous Intracranial Hemorrhage

Christel Renoux, MD, PhD^1,2,3; Sarah Vahey, MSc¹; Sophie Dell’Aniello, MSc¹; et al Jean-François Boivin, MD, ScD^1,3

Author Affiliations

JAMA Neurol. Published online December 5, 2016. doi:10.1001/jamaneurol.2016.4529

editorial comment icon

Editorial

Comment

• Editorial
  SSRIs and Intracranial Hemorrhage
  J. Claude Hemphill III, MD, MAS

Key Points

Question  What is the risk for intracranial hemorrhage associated with selective serotonin reuptake inhibitors and with antidepressants according to the strength of the inhibition of serotonin reuptake?
Findings  In this population-based cohort study, the use of selective serotonin reuptake inhibitors and more generally of antidepressants that are strong inhibitors of serotonin reuptake were associated with an increased risk for intracranial hemorrhage compared with tricyclic antidepressants, particularly in the first 30 days of use. Concomitant use of oral anticoagulants further increased this risk.
Meaning  Antidepressants with strong serotonin reuptake inhibition properties increase the risk for intracranial hemorrhage, and caution must be exerted with concomitant use of anticoagulants.

Abstract

Importance  Selective serotonin reuptake inhibitors (SSRIs) may increase the risk for spontaneous intracranial hemorrhage (ICH), an effect that is in theory linked to the strength of inhibition of serotonin reuptake of an antidepressant. However, whether antidepressants that are strong inhibitors of serotonin reuptake actually increase the risk for ICH and the effect of concomitant use of antithrombotics are unknown.
Objectives  To assess the risk for ICH associated with the use of SSRIs compared with tricyclic antidepressants (TCAs) among new users of antidepressants and according to the relative affinity of the antidepressant for the serotonin transporter and to assess whether concomitant use of antithrombotics modifies this risk.
Design, Setting, and Participants  This population-based cohort study included new users of antidepressants 18 years or older from January 1, 1995, to June 30, 2014. More than 650 general practices in the United Kingdom contributing to the Clinical Practice Research Datalink enrolled patients. with use of a nested case-control approach, each case of a first ICH identified during follow-up was matched with as many as 30 control individuals by age, sex, calendar time, and duration of follow-up. Follow-up was completed on October 31, 2014.
Interventions  Current use of SSRIs compared with TCAs and strong compared with weak serotonin reuptake inhibitors.
Main Outcomes and Measures  Incidence rate ratios (RRs) of ICH.
Results  Among a cohort of 1 363 990 incident users of antidepressants (36.8% male; 63.2% female; mean [SD] age, 47.9 [18.5] years), 3036 cases of ICH were identified during follow-up and matched to 89 702 controls. Current SSRI use was associated with an increased risk for ICH (RR, 1.17; 95% CI, 1.02-1.35) relative to TCAs, highest during the first 30 days of use (RR, 1.44; 95% CI, 1.04-1.99), and translating in very few additional events. Similarly, the risk was increased by 25% with strong inhibitors (RR, 1.25; 95% CI, 1.01-1.54) and highest during the first 30 days of use (RR, 1.68; 95% CI, 0.90-3.12). Concomitant use of anticoagulants may increase the risk substantially (RR, 1.73; 95% CI, 0.89-3.39).
Conclusions and Relevance  The use of SSRIs and more generally of antidepressants with strong inhibition of serotonin reuptake are associated with an increased risk for ICH, particularly in the first 30 days of use and when used concomitantly with oral anticoagulants.

Widely used heart drug tied to dementia risk - Warfarin

You'll have to grill your doctor on this to see if the risk is acceptable to you.
http://www.upi.com/Health_News/2016/05/05/Widely-used-heart-drug-tied-to-dementia-risk/2171462482024/
People with the heart rhythm disorder atrial fibrillation may have a heightened risk of developing dementia -- and the quality of their drug treatment may play a role, a new study hints.
Specifically, researchers found, patients on the clot-preventing drug warfarin showed a higher dementia risk if their blood levels of the medication were frequently too high or too low.
And that was true not only for people with atrial fibrillation, but also for those using warfarin for other reasons.
Dr. Jared Bunch, the lead researcher on the study, said the findings uncover two potential concerns: People with atrial fibrillation may face an increased risk of dementia, independent of warfarin use, but warfarin might also contribute to dementia if the doses are not optimal.
"If people's levels of warfarin were erratic, their dementia risk was higher, whether they had AF or not," said Bunch, who was scheduled to present his findings Thursday at the Heart Rhythm Society's annual meeting, in San Francisco.
The results do not prove that either atrial fibrillation or warfarin are to blame, according to Bunch, a cardiologist at Intermountain Medical Center, in Murray, Utah.
But, he said, there is reason to believe that both could contribute to dementia -- in part because of effects on blood flow to the brain.
Atrial fibrillation is a common arrhythmia, affecting about 3 million U.S. adults, according to the Heart Rhythm Society. In it, the upper chambers of the heart quiver instead of contracting efficiently. The condition is not immediately life-threatening, but it can cause blood clots to form in the heart. If a clot breaks free and lodges in an artery supplying the brain, that can trigger a stroke.
Because of that, people with atrial fibrillation often take medications that cut the risk of blood clots. Those include aspirin or anticoagulants such as warfarin (Coumadin).
Warfarin is a tricky drug to take, Bunch explained: People need regular blood tests to make sure their warfarin levels are in the "therapeutic range" -- high enough to prevent clots, but low enough to avoid internal bleeding. The doses typically have to be changed over time.
According to Bunch, it's possible that patients with erratic warfarin levels are more prone to "small clots" or "small bleeds" that could affect the brain.
The findings are based on records from over 10,000 patients who were on warfarin for atrial fibrillation or to prevent blood clots from other causes.
Over six to eight years, almost 6 percent of the atrial fib patients developed dementia, including Alzheimer's disease -- versus less than 2 percent of other warfarin patients.
People with atrial fib were generally older and in poorer health. But even after Bunch's team accounted for that, the atrial fib patients had more than double the risk of dementia than that other patients.
The quality of warfarin treatment also seemed to matter, whether patients had atrial fibrillation or not.
Compared with patients whose warfarin was in therapeutic range more than 75 percent of the time, those who were usually out of range had 2.5 to four times the odds of developing dementia.
However, there are many reasons a patient could be out of therapeutic range, said Dr. Gordon Tomaselli, chief of cardiology at Johns Hopkins University in Baltimore, and a past president of the American Heart Association.
So it's hard to pin the blame on warfarin management, according to Tomaselli, who was not involved in the study.
Still, he said it is plausible that both atrial fibrillation and erratic warfarin levels contribute to dementia.
A study that compared warfarin patients to those on newer anticoagulant drugs could help sort out the medication's role, Tomaselli said.
For now, Bunch had some advice for patients. "If you're doing well on warfarin, there's no reason to worry," he said.
In other cases, he added, closer monitoring and better management might help patients keep their warfarin levels in range.

Brain bleed risk from warfarin may be higher than thought

Also known as rat poison.  I  was on this for 6 months and  my ex hated having to haul me in every week to get my blood tested. Luckily I had no side effects, not even purple toe.
http://www.upi.com/Health_News/2016/03/09/Brain-bleed-risk-from-warfarin-may-be-higher-than-thought/8131457553581/
The widely used blood thinner warfarin -- also known as Coumadin -- may raise the risk of severe bleeding inside the skull by much more than previously thought, a new study suggests.
Researchers examined data from nearly 32,000 U.S. veterans, aged 75 and older, with a common heart rhythm disorder called atrial fibrillation. The investigators found that almost one in three suffered an "intracranial" bleed while taking warfarin for the condition.
"Atrial fibrillation ("a-fib") is a common heart rhythm disorder in elderly patients. And in patients with a-fib, treatment with the blood thinner warfarin reduces the risk of stroke by nearly two-thirds," explained study lead author Dr. John Dodson.

Dementia and Stroke Rates Were Lower Among Patients Receiving Long-term Anticoagulation Therapy With Novel Oral Anticoagulants Compared to Warfarin

Just in case you need to know about this for your post stroke interventions.
http://circ.ahajournals.org/content/132/Suppl_3/A11919.short

1. Victoria Jacobs1;
2. Heidi T May1;
3. Tami L Bair1;
4. Jeffrey L Anderson2;
5. Brian G Crandall1;
6. Michael Cutler1;
7. John D Day1;
8. Charles D Mallender1;
9. Jeffrey S Osborn1;
10. Scott M Stevens1;
11. J P Weiss1;
12. Scott C Woller1;
13. T J Bunch1

+ Author Affiliations

1. ¹Intermountain Heart Institute, Intermountain Med Cntr, Murray, UT
2. ²Intermountain Heart Institute, Intermountain Med Cntr, Univ of Utah, Murray, UT

Abstract

Introduction: Patients with atrial fibrillation (AF) are at an increased risk of developing dementia, and this risk appears sensitive to quality of warfarin control. Longstanding warfarin use predisposes AF patients to the development of microbleeds if they are over-anticoagulated and microemboli if they are under-anticoagulated. The novel oral anticoagulants (NOACs) offer an alternative to warfarin with a predictable anticoagulant effect, and comparatively favorable intracranial bleeding and thrombosis rates which may lower the risk of dementia.

Hypothesis: The use of NOACs will be associated with a lower risk of stroke, TIA, and dementia compared to warfarin.

Methods: Patients receiving long-term anticoagulation therapy with either warfarin or a single NOAC for thromboembolism prevention were studied (June 2010-December 2014). NOAC and warfarin patients were matched 1:1 by index date (± 6 months) and propensity score (±0.01). Multivariable Cox hazard regression was performed to evaluate the association of NOAC compared to warfarin use for the composite outcome of dementia, stroke, and TIA.

Results: A total of 5,254 (2,627 per group) patients were studied, and those receiving NOACs included: apixaban= 590 (22.5%), dabigatran=583 (22.2%), and rivaroxaban=1,454 (55.3%). Average age was 72.4±10.9 and 59.0% were male. The majority of patients were receiving long-term anticoagulation for AF (warfarin: 96.5% vs. NOAC: 92.7%, p<0.0001). History of a prior stroke/TIA were similar between the groups (warfarin: 10.7% vs. NOAC: 10.8%, p=0.89). Dementia incidence alone was lower in the NOAC group compared to the warfarin group (0.3% vs. 1.6%, p<0.0001). The composite outcome of dementia, stroke, and TIA occurred in 4.7% of warfarin patients and 1.8% of NOAC patients (p<0.0001). After adjustment, patients taking NOACs had a 51% decreased risk of dementia incidence or subsequent stroke or TIA compared to patients taking warfarin (HR=0.49 (0.35, 0.69), p<0.0001).

Conclusions: This study shows the use of NOACs in a community setting to be superior to that of warfarin for the composite outcome of dementia, stroke, and TIA among patients receiving long-term oral anticoagulation.

Abstract 17525: Warfarin Promotes Progressive Coronary Arterial Calcification: Insights From Serial Intravascular Ultrasound

This should spark immediate research because warfarin is used extensively post-stroke and calcification of arteries sounds dangerous. But that won't occur because stroke has NO strategy and NO leadership.
http://circ.ahajournals.org/content/132/Suppl_3/A17525.short

1. Jordan Andrews1;
2. Ozgur Bayturan2;
3. Mingyuan Shao3;
4. Brian Stegman3;
5. Mohamed Elshazly3;
6. Samir Kapadia4;
7. E. Murat Tuzcu4;
8. Steven Nissen3;
9. Stephen Nicholls1;
10. Rishi Puri5

+ Author Affiliations

1. ¹Heart Health Theme, South Australian Health and Med Rsch Institute, Adelaide, Australia
2. ²Cardiology, Celal Bayar Univ Sch of Medicine, Manisa, Turkey
3. ³Cardiology, Cleveland Clinic, Cleveland, OH
4. ⁴cardiology, cleveland Clinic, cleveland, OH
5. ⁵Cardiology, Qubec Heart and Lung Institute, Quebec City, Canada

Abstract

Background: Warfarin blocks the synthesis and activity of matrix Gla protein (MGP), a vitamin K-dependent inhibitor of arterial calcification. The impact of warfarin on coronary arterial calcification in vivo is unknown. This study compared serial changes in coronary percent atheroma volume (PAV) and calcium index (CaI) in patients treated with and without warfarin.

Hypothesis: Serial changes in coronary CaI are greater in warfarin-treated patients compared with those not on warfarin, independent of changes in PAV

Methods: In a patient-level analysis of 8 prospective randomized trials using serial coronary intravascular ultrasound, we compared changes in PAV and CaI in matched arterial segments in patients with coronary artery disease treated with (n=171) and without (n=4129) warfarin during an 18-24-month period.

Results: Patients (age 57.9±9.2 yrs; male 73%; prior and concomitant statin use: 73 and 97% respectively) demonstrated an overall increase in PAV by 0.18±0.06% (p=0.003 compared with baseline) and CaI [median (IQR)] by 0.04 (0.00, 0.11) (p <0.001 compared with baseline). Following propensity-weighted adjustment for clinical trial, clinical characteristics and laboratory parameters, there was no difference in annualized ΔPAV in the presence and absence of warfarin treatment (0.08±0.05 vs. 0.13±0.04%, p=0.41). Following adjustment for PAV, a greater annualized increase in CaI was observed in warfarin treated patients [median (IQR) 0.03 (0.0-0.08) vs. no-warfarin: 0.02 (0.0-0.06) p<0.001)]. In a sensitivity analysis evaluating a 1:1 matched cohort (n=164 per group), significantly greater annualized changes in CaI were also observed in warfarin-treated patients. In a multivariable model, warfarin independently associated with an increasing CaI [Odds Ratio (95% confidence interval) 1.12 (1.01, 1.24), p=0.027].

Conclusion: Warfarin therapy associates with progressive coronary atheroma calcification, independent of changes in atheroma volume. The impact of these changes on plaque stability and cardiovascular outcomes require further investigation.

Over-Anticoagulation Linked to Dementia in Patients With Atrial Fibrillation

Something to talk to your doctors about.
http://dgnews.docguide.com/over-anticoagulation-linked-dementia-patients-atrial-fibrillation?overlay=2&
Patients who receive anticoagulation with warfarin and anti-platelet agents such as aspirin appear to be at in increased risk of developing dementia if they are over-anticoagulated more than 25% of the time, researchers reported here at the 2014 Annual Meeting of the American Heart Association (AHA).
“There are multiple hypotheses for how over-anticoagulation can cause dementia, possibly because over anti-coagulation might cause some micro-bleeds into the brain,” said Jared Bunch, MD, Intermountain Health System, Salt Lake City, Utah.
Patients who were chronically over-anticoagulated -- more than 25% of the time having an International Normalized Ratio (INR) >3 -- had a 5.8% risk of developing dementia during a median of 4 years.

More at link.

Vitamin K status and cognitive function in healthy older adults

I would think if we had any smart doctors or hospital administrators they would be using this to make sure the meals in the hospital post-stroke were cognitive friendly. Unless you are on Warfarin  and need to stay away from vitamin K.
But I can almost 100% guarantee that absolutely nothing will be done to help your stroke recovery in this regard. Because we have shit for stroke associations and lead-assed inertia for doctors and stroke centers.
But thats just my reasoned opinion, if you have some proof otherwise please respond.
http://www.neurobiologyofaging.org/article/S0197-4580%2813%2900244-3/abstract

• Nancy Presse
,
• Sylvie Belleville
,
• Pierrette Gaudreau
,
• Carol E. Greenwood
,
• Marie-Jeanne Kergoat
,
• Jose A. Morais
,
• Hélène Payette
,
• Bryna Shatenstein
,
• Guylaine Ferland

Received 19 December 2012; received in revised form 22 April 2013; accepted 30 May 2013. published online 15 July 2013.

• Abstract
• Full Text
• PDF
• Images
• References
• Supplemental Materials

Abstract 

Evidence is accumulating that vitamin K could have a role in cognition, especially in aging. Using data from the Québec Longitudinal Study on Nutrition and Successful Aging (NuAge), a cross-sectional analysis was conducted to examine the associations between vitamin K status, measured as serum phylloquinone concentrations, and performance in verbal and non-verbal episodic memory, executive functions, and speed of processing. The sample included 320 men and women aged 70 to 85 years who were free of cognitive impairment. After adjustment for covariates, higher serum phylloquinone concentration (log-transformed) was associated with better verbal episodic memory performances (F = 2.43, p = 0.048); specifically with the scores (Z-transformed) on the second (β = 0.47; 95% confidence interval [CI] = 0.13–0.82), third (β = 0.41; 95% CI = 0.06–0.75), and 20-minute delayed (β = 0.47; 95% CI = 0.12–0.82) free recall trials of the RL/RI-16 Free and Cued Recall Task. No associations were found with non-verbal episodic memory, executive functions, and speed of processing. Our study adds evidence to the possible role of vitamin K in cognition during aging, specifically in the consolidation of the memory trace.

Warfarin increases risk of stroke among atrial fibrillation patients in first 30 days of use

 Is your doctor informing you of this?

\http://www.alphagalileo.org/ViewItem.aspx?ItemId=137513&CultureCode=en

Warfarin Induces Cardiovascular Damage in Mice

Damn, we're screwed either way, risk of stroke due to clotting or ruining our arteries. Which way the hell does your doctor equivocate on?
http://atvb.ahajournals.org/content/33/11/2618.abstract.html?etoc

Abstract

Objective—Vascular calcification is an independent risk factor for cardiovascular disease. Once thought to be a passive process, vascular calcification is now known to be actively prevented by proteins acting systemically (fetuin-A) or locally (matrix Gla protein). Warfarin is a vitamin K antagonist, widely prescribed to reduce coagulation by inhibiting vitamin K–dependent coagulation factors. Recently, it became clear that vitamin K antagonists also affect vascular calcification by inactivation of matrix Gla protein. Here, we investigated functional cardiovascular characteristics in a mouse model with warfarin-induced media calcification.

Approach and Results—DBA/2 mice received diets with variable concentrations of warfarin (0.03, 0.3, and 3 mg/g) with vitamin K1 at variable time intervals (1, 4, and 7 weeks). Von Kossa staining revealed that warfarin treatment induced calcified areas in both medial layer of aorta and heart in a dose- and time-dependent fashion, which could be inhibited by simultaneous vitamin K2 treatment. With ongoing calcification, matrix Gla protein mRNA expression decreased, and inactive matrix Gla protein expression increased. TdT-mediated dUTP-biotin nick end labeling–positive apoptosis increased, and vascular smooth muscle cell number was concomitantly reduced by warfarin treatment. On a functional level, warfarin treatment augmented aortic peak velocity, aortic valve–peak gradient, and carotid pulse-wave velocity.

Conclusion—Warfarin induced significant calcification with resulting functional cardiovascular damage in DBA/2 wild-type mice. The model would enable future researchers to decipher mechanisms of vascular calcification and may guide them in the development of new therapeutic strategies.

Warfarin Induces Cardiovascular Damage in Mice

When is the research coming that will test this out in humans? A great stroke association would start this immediately. Hopefully this can be explained by the rodent model in inflammation is not the same as humans.
----------------------------------------------------------------------------------------
http://atvb.ahajournals.org/content/early/2013/08/29/ATVBAHA.113.302244.abstract

Abstract

Objective—Vascular calcification is an independent risk factor for cardiovascular disease. Once thought to be a passive process, vascular calcification is now known to be actively prevented by proteins acting systemically (fetuin-A) or locally (matrix Gla protein). Warfarin is a vitamin K antagonist, widely prescribed to reduce coagulation by inhibiting vitamin K–dependent coagulation factors. Recently, it became clear that vitamin K antagonists also affect vascular calcification by inactivation of matrix Gla protein. Here, we investigated functional cardiovascular characteristics in a mouse model with warfarin-induced media calcification.

Approach and Results—DBA/2 mice received diets with variable concentrations of warfarin (0.03, 0.3, and 3 mg/g) with vitamin K1 at variable time intervals (1, 4, and 7 weeks). Von Kossa staining revealed that warfarin treatment induced calcified areas in both medial layer of aorta and heart in a dose- and time-dependent fashion, which could be inhibited by simultaneous vitamin K2 treatment. With ongoing calcification, matrix Gla protein mRNA expression decreased, and inactive matrix Gla protein expression increased. TdT-mediated dUTP-biotin nick end labeling–positive apoptosis increased, and vascular smooth muscle cell number was concomitantly reduced by warfarin treatment. On a functional level, warfarin treatment augmented aortic peak velocity, aortic valve–peak gradient, and carotid pulse-wave velocity.

Conclusion—Warfarin induced significant calcification with resulting functional cardiovascular damage in DBA/2 wild-type mice. The model would enable future researchers to decipher mechanisms of vascular calcification and may guide them in the development of new therapeutic strategies.

Gene Variant in Blacks Alters Warfarin Response

I'm sure your doctor will tell you about this before you bring it up to them.
http://www.medpagetoday.com/Cardiology/Strokes/39631?
The first genome-wide association study to focus on warfarin dose in African Americans found a genetic variant that explains their variable response to the blood thinner.
African Americans with one copy of the rs12777823 variant would need to reduce their warfarin dosage by 6.92 mg per week to obtain its full benefits, according to Julie Johnson, PharmD, of the Center for Pharmacogenomics at the University of Florida in Gainesville, and colleagues.
Those of African descent with two copies of this single-nucleotide polymorphism (SNP) would require a dose reduction of about 9 mg/week, a good portion of the 40 mg average weekly dose for African Americans, researchers reported online in The Lancet.

Rest at link.

Warfarin-induced Skin Necrosis

Your doctor prescribing you Warfarin(rat poison) will have told you all the side effects to looks for. Purple toe, etc.
http://onlinelibrary.wiley.com/doi/10.1002/9781118618189.ch36/summary
Patients who are deficient in protein C and S are at most risk for this complication.
Because routine screening for protein C and S deficiency is not part of the standard of care
for warfarin therapy, detection of this subset of patients is often not possible

A Case of Cerebral Infarction in Atrial Fibrillation Caused by Interruption of Warfarin Therapy for Colonoscopy

Be careful out there.
http://scholar.google.com/scholar_url?hl=en&q=http://arrhythmia.medimedia.co.kr/archive/archive/43/PDF/A_Case_of_Cerebral_Infarction_in_Atrial_Fibrillation_Caused_by_Interruption_of_Warfarin_Therapy_for_Colonoscopy.pdf&sa=X&scisig=AAGBfm1Mx1myx9piXAT4f0wbKD08S_1kTQ&oi=scholaralrt

Warfarin-induced Venous Limb Gangrene

Ask your doctor what the early symptoms are for this so you can get it treated in time. I'm sure your doctor already warned you about this.
http://europepmc.org/abstract/MED/23198012/reload=0;jsessionid=dP6xnwKxPxeSA8XDQVn9.2
Warfarin is a commonly used anticoagulant that has been associated with several significant cutaneous side effects, most notably warfarin-induced skin necrosis. A lesser known adverse reaction to warfarin is warfarin-induced venous limb gangrene. Both cutaneous adverse effects share the same pathophysiology, but are clinically quite different. The majority of cases of warfarin-induced venous limb gangrene has been in patients with cancer or heparin-induced thrombocytopenia. However, other hypercoagulable disease states, such as the antiphospholipid antibody syndrome, can be associated with venous limb gangrene. In order to increase recognition of this important condition, the authors report a case of warfarin-induced venous limb gangrene in a patient with presumed antiphospholipid antibody syndrome and review the literature on warfarin-induced venous limb gangrene.

A case of severe embolic complications due to warfarin withdrawal

Beware, your doctor should know all about this.
http://www.ncbi.nlm.nih.gov/pubmed/23362770

Abstract

We report a case of three severe embolic complications due to warfarin withdrawal. An 83-year-old man with hypertension, angina pectoris and atrial fibrillation underwent bladder biopsy under spinal anesthesia after 13 days of warfarin withdrawal. On the second postoperative day, the patient complained of chest pain and was diagnosed as acute myocardial infarction. Embolus was successfully removed by suctioning. Warfarin and heparin therapy was started after that. On the 6th postoperative day, the patient complained of abdominal pain and was diagnosed as superior mesenteric artery embolism. After suctioning of the thrombus and monteplase injection, symptoms disappeared. On the 9th postoperative day, paralysis on the right side of his body and aphasia appeared. Stroke was suspected. Coma advanced day by day and he died due to brain herniation on the 16th postoperative day. In this patient we should have assessed the risk of the thromboembolic complication and planned the appropriate anticoagulation with closer cooperation with his attending physicians.

Gastric ulcer with hemorrhage due to concomitant use of aspirin and warfarin

Be careful out there.
http://www.cadrj.com/qikan/epaper/zhaiyao.asp?bsid=17701

Abstract  

A 62-year-old male patient received combined therapy with aspirin 0.1 g once daily and warfarin 3.0 mg once daily for prevention of thrombosis after undergoing aortic valve replacement. On day 5 of treatment, he presented with vague pain in the upper abdomen. On day 14, his abdominal pain worsened and, on day 15, he presented with melena. Laboratory tests showed the following values: red blood cell count 2.2×1012/L, hemoglobin 65 g/L, prothrombin time (PT) 45.9 s, international normalized ratio (INR) 3.7, fecal occult blood (++). Gastroscopy revealed gastric ulcer with hemorrhage. Aspirin and warfarin were withdrawn, and then the patient was given hemostatic and symptomatic treatment. On day 2, the patient’s abdominal pain was relieved and hemorrhage ceased. His PT decreased to 12.8 s and his INR decreased to 1.1 one week later. The patient resumed the anticoagulation treatment with warfarin.