For around ten years I have had AF (latest report said 74% of the time) and also chronic inflammatory joint and muscle pain; both have been satisfactorily controlled (AF by PM and Bisoprolol) (inflammation by Diclofenac) and I have functioned and worked fully (if a little slowly at times!) and painless, until a recent TIA - following which I was warned off Diclofenac as it has been linked to "an increased risk of major cardiovascular events such as heart attack and stroke". Meloxicam and Celocoxib have been tried but are not as effective, and two doctors have both said that I may want to go back to Diclofenac.
My question is - has anyone actually quantified the increased risk? I ask because for instance Aspirin was quoted as giving a 45% increase of a stroke compared to using Warfarin BUT when you realise that this means an increase from 1.6% to 2.3% it puts things in a different perspective....
SO does anyone know the answer to my question?
PS before someone asks - following the TIA am also now on Edoxaban and Omeprazole
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quanglewangle
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Doh! I followed up on the link I sent and found the BMJ published report - and found that the increased risk is 50% of a MACE - BUT the whole study was based on people that did not have a pre-existing relevant condition so the baseline is irrelevant to anyone that already has AF.
NB the study shows that starting a course Ibuprofen, paracetamol and naproxen all showed a very similar increased risk of MACE of 20-30% - BUT nothing in the study established a causal relationship with AF for any of these medications or tells us what the baseline risk of MACE is for people with AF
Here is some info I googled, only parts of it as it was lengthy , I included the conclusion as it made the most sense . I have annoying arthritis pain and took naproxen for years until a fib hit. Now cardiologist says no, if having bad pain maybe twice a week. I don’t touch any nsaids now, when desperate I would slip a couple in but found I retained fluid and it jacked my blood pressure up the next day.
Intended for healthcare professionals
The BMJ logo
Research
Diclofenac use and cardiovascular risks: series of nationwide cohort studies
Morten Schmidt, registrar1 2, Henrik Toft Sørensen, professor1 3, Lars Pedersen, professor1
Author affiliations
Correspondence to: M Schmidt morten.schmidt@clin.au.dk
Accepted 19 July 2018
Abstract
Objective To examine the cardiovascular risks of diclofenac initiation compared with initiation of other traditional non-steroidal anti-inflammatory drugs, initiation of paracetamol, and no initiation.
Design Series of 252 nationwide cohort studies, each mimicking the strict design criteria of a clinical trial (emulated trial design).
Setting Danish, nationwide, population based health registries (1996-2016).
Conclusions and implications
Our study provides an overview of the spectrum and magnitude of cardiovascular risks related to initiation of diclofenac. We also showed that diclofenac initiators had an upper gastrointestinal bleeding risk similar to that of naproxen initiators and more than twice the risk of ibuprofen initiators. Treatment of pain and inflammation with NSAIDs may be worthwhile for some patients to improve quality of life despite potential side effects. Considering its cardiovascular and gastrointestinal risks, however, there is little justification to initiate diclofenac treatment before other traditional NSAIDs.40
It is time to acknowledge the potential health risk of diclofenac and to reduce its use. Diclofenac should not be available over the counter, and when prescribed, should be accompanied by an appropriate front package warning about its potential risks. Moreover, the choice to use diclofenac as the reference group to provide evidence of safety of selective COX-2 inhibitors represents a potential flaw in safety trials.414243 Future trials should instead use low dose ibuprofen (≤1200 mg/day) or naproxen (≤500 mg/day) as comparators.4 In conclusion, our data support that initiation of diclofenac poses a cardiovascular health risk, both compared with no use, paracetamol use, and use of other traditional NSAIDs.
What is already known on this topic
Diclofenac is the most commonly used non-steroidal anti-inflammatory drug (NSAID) in low, middle, and high income countries
Its cardiovascular risks compared with other traditional NSAIDs have never been examined in a randomised controlled trial, and current concerns about these risks make such a trial unethical to conduct
A series of Danish nationwide cohort studies, each mimicking the strict design criteria of a clinical trial (emulated trial design), included 1 370 832 initiators of diclofenac, 3 878 454 initiators of ibuprofen, 291 490 initiators of naproxen, 764 781 healthcare seeking initiators of paracetamol (matched by propensity score), and 1 303 209 healthcare seeking NSAID non-initiators (matched by propensity score)
What this study adds
The incidence rate ratio of major adverse cardiovascular events at 30 days among diclofenac initiators increased by 50% versus non-initiators, by 20% versus ibuprofen or paracetamol initiators, and by 30% versus naproxen initiators
The increased risk was observed for atrial fibrillation or flutter, ischaemic stroke, heart failure, myocardial infarction, and cardiac death; both sexes of all ages; and even at low doses of diclofenac.
Risk of upper gastrointestinal bleeding at 30 days with diclofenac was similar to that of naproxen, but considerably higher than for no NSAID initiation, paracetamol, and ibuprofen
The way I read the post it seemed quite clear that the pain has been an issue for a long time prior to the TIA - which was when anti-coagulant was initiated.
I think you raise an interesting point regarding relative and quantifiable risk, however, for me the numbers are not as important as my individual risk/benefit QOL scale and only I can quantify that as it is totally subjective.
Interestingly - many, many years ago - I worked for a pharmaceutical company which introduced an anti-inflammatory drug and my job was to collate and file the clinical studies. Only thing I can say is it really put me off taking any anti-inflammatory for life as the adverse affects seemed to far outweigh the benefits with only 40% efficacy overall.
I tend to use lots of anti-inflammatory foods instead of pharmaceuticals and some herbal remedies such as Astragalus - but with the help and support of nutritionist & herbalist.
Do not assume anything - it’s a herb from the pea family and can be just as potent as a pharmaceutical drug so you should always only take after professional consultation and with the OK of your Pharmacist and Doctor. It has a powerful anti-inflammatory affect by suppressing the immune system. It does not have a place in treating AF.
The PPI if taken long term will reduce your absorption of magnesium and vit B 12. Have you ever looked into why you are suffering from chronic inflammatory pain?
Not at all strange - low magnesium or any other electrolyte imbalance will cause Af. Have you looked at taking a magnesium supplement? Again talk to your doctor beforehand but also you may find the Doctor Gupta’s video on Magnesium helpful - youtu.be/Ckdcr-cp9w8
Good point about the PPI - I am adding magnesium and B12 to my daily plateful!
I started the Diclofenac so long ago that I don't remember why, but have been aware of joint pain if I missed a dose - so carried on taking it until my recent TIA when I was warned off it. In no time at all I had top to toe muscle and joint pain, so we have been trying out other antiinflammatories. Noticing that my AF seems diminished confirms (for me) that Diclofenac was the agravator if not the initiator of the AF. The improved well-being prompted me to check my BP for the first time in years and find that instead of my usual 115/70 I am running at up to 200/125 (still at my usual 60bpm) so am dropping off the celecoxib to see what happens.....
In answer to the other question - I have cut out cows' milk (no change) and am asking my GP to investigate possible causes.....
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