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Aspirin -proven in cardiac care to save lives


Just Plain Ruff

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Ok, I have not had the time to research this so I'm not sure if the statement is completely true or not but I hope to have references back soon. Maybe we can have a great discussion.

What I'd like to start is to have people begin to give the generic drug flash card information on Aspirin.

And on with the show.

Was in the cadaver lab up in Dayton Ohio last week and a cardiologist said this in our cardiac station.

"Aspirin is the only drug that we give pre-hospital that has a proven life saving benefit in an MI" I think I got the quote right, if not BEorP and Anthony can give their version of the quote.

The physician said that of any medication in our arsenal to treat Acute Myocardial Infarction or Chest pain, Only aspirin has been proven to provide a life saving benefit to the patient. Not Nitro, Not morphine, not beta blockers, not our ALS drugs, but little old Aspirin is the one.

So he went on to say, IF you are going to give only one drug to a patient in an AMI, give aspirin.

I'd like to see where this discussion goes.

Thanks

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All I have to add is we had a local Dr. come into our station and talk to us about what to do if someone is having chest pain and it confirmed that it is cardiac chest pain.

The Dr. said that giving ASA is more beneficial to the patient then giving Nitro, and sooner we give ASA the better.

Sorry not very informative. I know ASA is a anticoagulant or (clott buster) and thats why it is important to be giving the ASA sooner than later. Our protocol states to give 0.4mg of Nitro followed by 2 chewable ASA

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No arguments. The ISIS and GUSTO studies demonstrated clearly the benefit of ASA in ACS. Morphine may worsen outcomes (although I have grave doubts about the conclusions and methodology of the CRUSADE study), Beta-blockers are a definite no go, clopidogrel causes more harm than good (in fact causes no good at all I believe), nitro might be nice for some symptom relief but doesn't alter outcomes and oxygen probably causes more harm than good unless the pt is actually hypoxemic.

Aspirin would definitely be my Desert Island Drug.

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My wording may be off, as it's been awhile since I read through the information, but ASA is the only drug that has been shown to increase out-of-hospital survival rates in AMI patients.

I asked the doctor that question more to prompt conversation about the topic in a round about way. But I think I heard it at EMTCity first a bit ago...

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No arguments. The ISIS and GUSTO studies demonstrated clearly the benefit of ASA in ACS. Morphine may worsen outcomes (although I have grave doubts about the conclusions and methodology of the CRUSADE study), Beta-blockers are a definite no go, clopidogrel causes more harm than good (in fact causes no good at all I believe), nitro might be nice for some symptom relief but doesn't alter outcomes and oxygen probably causes more harm than good unless the pt is actually hypoxemic.

Aspirin would definitely be my Desert Island Drug.

...and unfortunately (albeit I haven't reviewed the studies) all of those is still taught as the standard of care.

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I know ASA is a anticoagulant or (clott buster) and thats why it is important to be giving the ASA sooner than later.

The effects of aspirin are twofold. The most beneficial effect is the anti-platelet aggregation effect which stops further clots from forming and prevents the problem clot/s from increasing in size. The other effect of benefit is it's anti-inflammatory effect on the already ischemic areas of the heart. What it is not, is a clot buster (technically)! A clot buster would be a fibrinolytic agent that actually breaks down the clot such as streptokinase, tPA, alteplase, reteplase etc.

Morphine may worsen outcomes (although I have grave doubts about the conclusions and methodology of the CRUSADE study),

My understanding of the CRUSADE study is that Morphine worsens outcome in patients with CHF but it is still the preferred drug for ACS (without CHF). I like to give Fentanyl in ACS but it there has not been a study comparing Fentanyl to Morphine in ACS as far as I am aware. So at the moment AHA recommends Morphine for chest pain in ACS.

AHA guidelines do recommend starting oral beta-blockers in stable patients in the first 24 hours after presentation.

I wouldn't be so quick to say that beta-blockers are a "no-go". Rather that they may not indicated in the early, unstable phase of an ACS. Since there seems to be a number of studies saying that they are beneficial I think that the question of there benefit:risk is still undecided at this stage.

"Even if beta-blockers have no immediate effect on mortality," Dr. Fonarow explained, "it is still worthwhile where it is safe, well tolerated, and given appropriately, to start them early, since many patients with MI may only spend 2 or 3 days total in the hospital. When you start therapy early in hospitalization, it's more apt to be continued and remembered at discharge and patients are more likely to continue on it long term." http://www.thedoctorschannel.com/video/2866.html?specialty=8

Paramagic would you mind posting the studies that show clopidogrel causes more harm than good? I would be interested in reading them.

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Paramagic would you mind posting the studies that show clopidogrel causes more harm than good? I would be interested in reading them.

Been staking here fora while, and I figured I ought to contribute something. I've heard this claim about plavix as well, and got curious and I did some digging. I suspect that paramagic is referring primarily to the three big (drug company funded) clinical trials:

In NSTEMI:

The CURE trial, found here: http://www.nejm.org/...56/NEJMoa010746

On first glance it does seem to indicate benefit with the use of plavix in NSTEMI ACS, but if you read it carefully I think the claim of "no benefit" might be close.

1) There was a demonstrated reduction in risk of a combined primary endpoint of MI, Stroke, Death and secondary of those three plus refractory ischemia. Small benefit was seen with this combined endpoint (especially a small reduction in subsequent MI or ischemia), but no decrease in death was found, though the study was not designed to detect a mortality difference.

2) This study only includes a small, very high risk, subset of potential ACS cases: those with elevated troponin levels or ECG changes. Initially patients over 60 with history of artery disease were included, but after the first 3000 patients with this criteria only harm was found, and the inclusion criteria was adjusted mid-study. The exclusion list was rather lengthy as well.

3) Harm was found: bleeding rates went up significantly. I'm not clear on the clinical significance of some of these events.

IN STEMI:

The CLARITY-TIMI study, examining addition of clopridogrel to ASA and Fibrinolytics in STEMI: http://www.ncbi.nlm....pubmed/15758000

Really this study is largely the same. Plavix caused a modest improvement in their primary and secondary outcomes, which again were composites of proposed surrogate markers of disease (better blood flow or re-occlusion) or death, and no difference in death was found, and the primary action seemed to be on the rate or re-occlusion. There was a slight trend towards increased mortality with plavix, but the study was underpowered to detect such a difference.

This study again had very strict exclusion criteria (half a column!) and the accompanying NEJM editorial suggests that they may have selected low risk patients this time: rate of death and MI were strangely low. The editorial raises other issue as well (no rapid PCI, exclusion issues, etc) and is a good read.

This study showed a lesser increase in bleeding rates than CURE, but in a different population, and I think there might be a trend towards more bleeding in the elderly. Truthfully I got a bit confused with the data interpretation, and don't have much else to say, but I think that's the fault of the study. Unfortunately numbers are a bit lacking (in my relatively uneducated opinion). There are few tables, mostly looking at odds ratios for benefit in different cohorts, but I don't find that tremendously useful. They only measured rates of bleeding within the first 8 days or until the day after angiography, and I would really like to know if there was a bleeding difference at other time points, especially before angiography (particularly since placebo randomized patients receiving stents were placed on plavix, and I"m not sure where they ended up in the analysis) . Again, I'm not sure of the clinical significance of the bleeding risk, and could be convinced either way.

The third big trial is the COMMIT trial (no the B-blocker part): http://www.ncbi.nlm....pubmed/16271642

I haven't read it yet, and don't have time to now, but it's big (well gigantic really) and purports to show a decrease in death in STEMI with plavix. Of course it is from China….

Not mentioned here is that there also seems to be a rebound effect when ending Plavix. I guess there is a cluster of clinical events which may be related to a hypercoaguable state within a week or so following cessation of treatment. That sort of harm would not be part of the analysis of these studies, if such harm exists, and a brief look didn't turn up great evidence.

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FDNY EMS BLS protocols allow EMTs to administer ASA for chest pain (unless allergy or other factors contra-indicates). We can also "assist" a patient in taking their own Nitro after assuring the "Rights". We do not carry Nitro, either pill, paste, or spray.

The FDNY EMS ALS protocols have the Paramedics carrying Nitro pills, for use by their patients under the ALS protocols.

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Hi Gumby. I must say that is an excellent post, it has covered exactly the issues there are with plavix, thank you.

It is interesting to note that in the CURE study the methodology was actually changed half way through the trial, because the only results they were getting were negative. They moved the parameters to look only at the really high risk patients to try and salvage some sales. Oops, I meant salvage some results...

I haven't finished with the COMMIT trail yet, but I haven't really seen anything that we don't already know from it: Small reduction in MI in high risk patients, coupled with reasonable risk of bleeding that pretty much outweighs the benefits. It's also difficult to say how much external validity the study has wth regards to the difference between western and eastern health care systems, in particular with respect to PCI vs. thrombolysis in infarct patients. (The use of PCI is something else that confounds Sabatine's trial as well)

The rebound effect from plavix certainly seems to be of concern. There has been a study published in JAMA in 2008 that was very compelling, showing adverse effects out to 90 days post cessation, but the authors recognize that further study is needed. It's certainly something that the cardiothoracic and general surgeons don't like.

Given the setting of the back of an ambulance (being on an EMS forum after all) beta-blockers are most definitely a no-go. They are also most likely a no-go after we get them to the hospital. Beta-blockers are a useful drug in patients with coronary artery disease, they have no place in the emergent treatment of evolving ACS, particularly in the back of an ambulance.

I think it was the COMMIT trial that had a list of exclusions for patients recieving beta-blockers, one of which was those with a high likelihood of devloping cardiogenic shock (or words to that effect - cardiogenic shock is what we give people when we give them beta-blockers). However one of the recommendations put forward is that beta-blockers should be given to patients with tachycardia. Now, what is a predictor of cardiogenic shock in ACS? That's right, tachycardia!

There is far too much evidence of harm and far too few beneficial effects to consider beta-blockers as a standard part of the treatment regimen for ACS.

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Not tooting my own horn but this exact discussion is why the city is so valuable to the EMS community.

Keep the discussion going.

I have another good question on the way for the weekend.

Sent from my SPH-D700 using Tapatalk

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