certainly could have been worded better lol
October, 2015: Study finds 40% of Tissue Valve Recepients At Risk For A Stroke!
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4 days of warfarin treatment. That's a very unusual strategy by your doctors, given that it often takes longer than that to get 'in range', and that the warfarin you take today is usually reflected in your INR at least a couple of days later. I ,for example, had to keep my Heparin shots going for about 4 days after leaving the hospital, until my INR was in range. That's 7 days of taking warfarin before I was truly anticoagulated. It was two further weeks before I was consistently in range. It's hard to imagine why your doctor didn't just have you on heparin for the four days post surgery. I'm sure there was a reason though!
It might have been heparin - it was abdominal injections for four days of an "anticoagulant."
I was on Warfarin ACT for 90 days post surgery. So what is the bottom line for us tissue valvers? Do we need ACT or not?
pellicle
Professional Dingbat, Guru and Merkintologist
Hi
*Need* - probably not - *benefit from* - perhaps.
Interesting findings.
If you aren't suffering any symptoms then I would say perhaps not.
Well if this research is to be believed and if you are showing signs of valve leaflet stiffening then perhaps this would reverse that.skeptic49;n859141 said:
*Need* - probably not - *benefit from* - perhaps.
Interesting findings.
If you aren't suffering any symptoms then I would say perhaps not.
Warfarin can lead to calcification so does that sound a good idea to take it with tissue valve stiffening ?
cldlhd
Well-known member
I confess I didn't thoroughly read through all the info but it seemed to me that warfarin was used to treat limited leaflet motion and was helpful if it was due to clotting on the leaflet which makes sense to me since warfarin is an anti coagulant. I can't imagine warfarin would have a significant,if any , positive effect if the limited motion was due to calcification. First of all there is some research that shows warfarin MAY lead to calcification and also because there are a lot of patients out there who have stenosis/calcification and are on warfarin. If it improved that condition I think it would have been discovered by now.
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Exactly ! All patients with age related degererative calcification of the aortic valve (tri-leadlet) would be treated with warfarin and so avoid the need for AVR !cldlhd;n859146 said:
I'm sure it depends, yeah? My cardiologist has me on 325 mg aspirin with my native valve to lower stroke risk. Been on that for 12 years now.
pellicle
Professional Dingbat, Guru and Merkintologist
Hi
First time to hear this ... do you have any references? In fact normally I hear the exact opposite (that it contributed to decalcification, which has never been substantiated by subsequent studies)Paleogirl;n859145 said:
pellicle
Professional Dingbat, Guru and Merkintologist
Ok
so a bit of research turned up this:
http://www.ncbi.nlm.nih.gov/pubmed/9743228 Warfarin causes rapid calcification of the elastic lamellae in rat arteries and heart valves.
as always the devil is in the details. The article starts its abstract by saying:
ok ... so immediately none us are on "high doses", which makes it unlikely to be transferable to us.
How high is high? Well according to the methods:
For a 70Kg body weight that's dose of 1g of warfarin. (or 1,050mg - one thousand and fifty mg) twice a day
right.... hand's up here who takes that amount?
it then goes on to say:
which reflects the opposite of what people are saying is a fear in other threads: that being warfarin causes bone calcium loss. Perhaps its related to their point that there was co administration of sufficient Vitamin K that INR was NORMAL.
So in the contrived situation where you are on oodles of warfarin and pumping up with vitamin K to keep your INR as normal, then perhaps there is something to this. For the rest of us on quite small does (and I would love to know what those doses were relative to body weight) its likely a total non issue.
This next paper suggests something educating:
http://www.ncbi.nlm.nih.gov/pubmed/21298649 Association of warfarin use with valvular and vascular calcification: a review.
All righty then ... promote an alternative more expensive drug ... so I smell a rat here ... (pun intended) ... suddely you have to ask the question of "why is this topic newly focused when millions of guys like **** have been on warfarin for decades with no linkage to calcification of arteries, but lots of questions about osteoporosis?"
Could it be that makers of dabigatran and rivaroxaban have money making interests to serve?
Since those articles were published trials of dabigatran have been halted because too many people died.
My observations are that warfarin is undergoing a renasiance in administration because we now have a new tool, computerised monitoring. This brings more accurate dosage and minimisation of dose. So just like computerisation and electronics has made car engines more efficient in their use of fuel, these tools are being employed in drug administration to good effect.
I would recommend two things here:
so a bit of research turned up this:
http://www.ncbi.nlm.nih.gov/pubmed/9743228 Warfarin causes rapid calcification of the elastic lamellae in rat arteries and heart valves.
as always the devil is in the details. The article starts its abstract by saying:
ok ... so immediately none us are on "high doses", which makes it unlikely to be transferable to us.
How high is high? Well according to the methods:
... ok so multiply that x10 to make it Kg (normal discussion of doses are in mg/Kg bodyweight, but rats aren't so heavy) which means they gave 15mg per Kg twice a day ... high isn't it?
For a 70Kg body weight that's dose of 1g of warfarin. (or 1,050mg - one thousand and fifty mg) twice a day
right.... hand's up here who takes that amount?
it then goes on to say:
which reflects the opposite of what people are saying is a fear in other threads: that being warfarin causes bone calcium loss. Perhaps its related to their point that there was co administration of sufficient Vitamin K that INR was NORMAL.
So in the contrived situation where you are on oodles of warfarin and pumping up with vitamin K to keep your INR as normal, then perhaps there is something to this. For the rest of us on quite small does (and I would love to know what those doses were relative to body weight) its likely a total non issue.
This next paper suggests something educating:
http://www.ncbi.nlm.nih.gov/pubmed/21298649 Association of warfarin use with valvular and vascular calcification: a review.
All righty then ... promote an alternative more expensive drug ... so I smell a rat here ... (pun intended) ... suddely you have to ask the question of "why is this topic newly focused when millions of guys like **** have been on warfarin for decades with no linkage to calcification of arteries, but lots of questions about osteoporosis?"
Could it be that makers of dabigatran and rivaroxaban have money making interests to serve?
Since those articles were published trials of dabigatran have been halted because too many people died.
My observations are that warfarin is undergoing a renasiance in administration because we now have a new tool, computerised monitoring. This brings more accurate dosage and minimisation of dose. So just like computerisation and electronics has made car engines more efficient in their use of fuel, these tools are being employed in drug administration to good effect.
I would recommend two things here:
- if you are going to read scientific papers, be critical, read their methods and look for a slant. Papers are often written to promote the writing of another paper because in the academic world its three rules: publish - publish and publish
- do not waste your time doing this outside of academic interest. The sky is not falling and all is generally as it seems. Do not even consider changing what you do in your drug administration on the early results of papers which are in all likelyhood describing highly specific results which are not transferable to your situation
Fundy
Well-known member
I found this article interesting on the subject of bio-prothetic valves and thrombosis detection.
http://www.medscape.com/viewarticle/838221#vp_1
This article on bio-prothetic valve thrombosis finds an incidence of about 0.18% over 4000 valves studied, 3000 were porcine valves.
Its actually a transcript of the included audio interview.
Near the bottom of page 2 of that article there is a rather long answer to "How can we diagnose BPVT, and are there any specific echocardiographic findings that we should be looking for?"
" Dr Pislaru: This is the biggest challenge of all. The most important thing is to be aware that the condition exists. We looked at our series. We identified patients with BPVT based either on surgical data (they had surgery for one reason or another; and at pathology, there was confirmed thrombus on the valve) or on clinical grounds. The active cardiologist involved with the patient thought of the possibility, treated them with a vitamin-K antagonist, and the gradient across the valve decreased. But when you look back at our echocardiographic data in this 31-patient series, we notice that in only a minority of patients did the initial echocardiogram suggest the possibility of BPVT. All the echocardiographic reports described abnormal valves. The common findings are thickened leaflets and increased gradients. These are the two common findings on an echocardiogram report. When you see these, you need to be aware that BPVT is in the differential diagnosis. So what we suggested was to consider the possibility whenever the gradient is more than 50% above the baseline value or above the published reference value (if you do not have the postimplant data) and you have thickened leaflets. Whenever you see those findings, you probably should consider obtaining a transesophageal echocardiogram (TEE) as a confirmation test for BPVT.
That being said, even the TEE is not perfect, because imaging, especially of a bioprosthetic valve, is extremely challenging. You have to image across the valve ring, and that creates acoustic shadowing. In our series, nine out of 12 patients with thrombosed aortic valves had been diagnosed by TEE, but in three out of 12 we were not able to identify it, even if there was confirmation at pathology of the thrombus being present. So it is quite a challenge. We do not know how well CT fares, so CT is another possibility to look at this. Other modalities are unlikely to play a role in the diagnosis. "
http://www.medscape.com/viewarticle/838221#vp_1
This article on bio-prothetic valve thrombosis finds an incidence of about 0.18% over 4000 valves studied, 3000 were porcine valves.
Its actually a transcript of the included audio interview.
Near the bottom of page 2 of that article there is a rather long answer to "How can we diagnose BPVT, and are there any specific echocardiographic findings that we should be looking for?"
" Dr Pislaru: This is the biggest challenge of all. The most important thing is to be aware that the condition exists. We looked at our series. We identified patients with BPVT based either on surgical data (they had surgery for one reason or another; and at pathology, there was confirmed thrombus on the valve) or on clinical grounds. The active cardiologist involved with the patient thought of the possibility, treated them with a vitamin-K antagonist, and the gradient across the valve decreased. But when you look back at our echocardiographic data in this 31-patient series, we notice that in only a minority of patients did the initial echocardiogram suggest the possibility of BPVT. All the echocardiographic reports described abnormal valves. The common findings are thickened leaflets and increased gradients. These are the two common findings on an echocardiogram report. When you see these, you need to be aware that BPVT is in the differential diagnosis. So what we suggested was to consider the possibility whenever the gradient is more than 50% above the baseline value or above the published reference value (if you do not have the postimplant data) and you have thickened leaflets. Whenever you see those findings, you probably should consider obtaining a transesophageal echocardiogram (TEE) as a confirmation test for BPVT.
That being said, even the TEE is not perfect, because imaging, especially of a bioprosthetic valve, is extremely challenging. You have to image across the valve ring, and that creates acoustic shadowing. In our series, nine out of 12 patients with thrombosed aortic valves had been diagnosed by TEE, but in three out of 12 we were not able to identify it, even if there was confirmation at pathology of the thrombus being present. So it is quite a challenge. We do not know how well CT fares, so CT is another possibility to look at this. Other modalities are unlikely to play a role in the diagnosis. "
Agian
Well-known member
So Pel,
These rats were given high doses of rat poison and survived to get calcium in their arteries.
:Scared:
These rats were given high doses of rat poison and survived to get calcium in their arteries.
:Scared:
pellicle
Professional Dingbat, Guru and Merkintologist
Agian;n859174 said:
Without the co-administration of such insane levels of vitamin K it would have been lethal doses
They died saying "witness me"
And they will ride eternal shiny and chrome.
