D.P.Gumby

I use 2 simple methods myself, since I have trouble remembering all the rules in the heat of the momemt at 3am (Though next time i'm calling bieber).

1) Are all the V leads concordant? (All positive or negative). If so.... prolly V-Tach

2) Is there right axis deviation? If so Prolly V-Tach

Consider thier "normal" rythm in this case. If they are a A-Fib look for regularity in your strip. Regular wide strip in a A-Fib patient strongly leans toward V-Tach.

If you are really unsure..... just use Amiodarone! Can`t go wrong

danger! danger will Robinson

amiodarone is used at your patients' peril in patients with Afib wpw. slowing the node in a patient with Ann accessory pathway can produce even nastier rhythms. This may or may not be the case here, but I think it bears remembering that amiodarone is not safe in all cases (and not effective in many)

There are several reports of the danger, but I think this is a good start:

http://www.cjem-online.ca/v7/n4/p262

Well, for starters, maybe trust the higher level of care and the experience he brings to the table and perhaps it isn't simply a case of withholding the O2.

Based on what is presented here, I'd say it sounds like a chronic COPD pt and lower O2 sats may be normal. What is more of the history - meds, past medical history, etc. How about physical findings such as lung sounds? Underlying rhythm on the ECG?

Remember, not all patients need 'VOMIT' = Vitals, O2, IV, Monitor, Transport. Also remember the saying of treat the patient and not the monitor. Based on the O2 sats, was it clinically significant? Do you have the possibility of disrupting the 'hypoxic drive' if she is a COPDer?

As others have indicated, try using it as a learning experience and ask what their thought process was. It's not fair to assume what was going through their mind and questioning their decision making. You would probably find that their was a logical thought process.

All of this seems reasonable, but I think the hypoxic drive comment deserves mention: it's been pretty thoroughly debunked. Only a portion of COPD'rs are chronic CO2 retainers who could even putatively adapt to chronic hypercarbia and loose any impetus to breathe besides hypoxic drive. Even among that subset, several studies (can't find the list of citations right now unfortunately) have failed to find a decrease in respiratory rate due to oxygen administration, although they have revealed an increasing acidosis, and I've yet to see any reliable reports of apnea due to O2. Simply put there is no evidence that the hypoxic drive takes over in these patients, results in a decreased respiratory drive when exposed to high FiO2, or explains any of the pathology seen in COPD.

Also the idea that cerebral chemoreceptors become totally “non-responsive” to rising levels of CO2 seems rather odd, as most other receptors/control systems will exhibit adaptation in the form of a changed “set-point” rather than complete abandonment of regulation. I do not believe any evidence exists to suggest that there is a loss of responsiveness of chemoreceptors to changes in CO2.

That said, there is evidence of hypercarbia and acidosis following O2 administration in COPD patients, but this has nothing to do with decreased respiratory rate due to "hypoxic drive." Similarly, there is now evidence of increased mortality due to over-oxygenation of COPD patients in the prehospital environment (http://www.bmj.com/content/341/bmj.c5462.abstract), so your concerns are perhaps correct, but not because of the hypoxic drive.

Some additional input on the epi issue. There is at least one study that has directly examined the use of racemic versus L-epinephrine for croup:

http://www.ncbi.nlm.nih.gov/pubmed/1734400

Although it is a RCT, unfortunately it is small and not of the best quality: I don't think it can confirm the non-superiority of racemic epi, but it probably does establish L-epi (the more readily available form) as a plausable treatment. A quick look didn't turn up any better literature, though it certianly may exist.

I think the summary above was good, and from what I've seen the proposed benefit of racemic epinephrine is indeed minimization of side effects. I have to say, I've never seen a good explanation of this purported benefit, and it doesn't seem to make too much sense.

As the L-epi form is generally considered the only active enantiomer (racemic epi is 50/50 of the L and R enantiomers), the idea that racemic epi would somehow minimize effects doesn't make sense. If R-epi is not physiologically active, it's inclusion in the administration should have no effect. If R-epi is active, presumably its action is similar to l-epi, and we would expect a similar side effect profile.

Super case study, thanks for having the cohunes to post it.

I'm not quite settled about the treatment choices, however. It seems like amiodarone is still on the list of options (as the default for wide/fast rythms).

Amiodarone has been associated with some less than stellar results in patients with WPW and atrial fibrillation in several case reports, and there doesn't seem to be any evidence that it works or is safe in WPW-afib, and several sources I've seen recommend proving Edison right about the safety of DC.

reviews of the case reports and lack of evidence here:

http://www.ncbi.nlm.nih/pubmed/20437113

http://www.ncbi.nlm.nih.gov/pubmed/17355684

This case isn't quite the same. If I'm understanding correctly, the initial rhythm was likely atrial flutter with WPW. I can find no evidence whatsoever about treating such a condition. All the same, I have to say that I've pretty much scared myself away from trying any pharmacology in a patient like this.

What is the perspective on this from the experienced smart brain trust? Is there really a role for amiodarone in this case?

ACLS considers cardioversion *more* invasive, which is why it is reserved for only the sickest of patients.

Why is that so? ( I ask of ignorance, not attempting to be a provocateur). By "more invasive" does the AHA really mean "more dangerous?" Especially in a case like this where the rhythm identification is difficult, I would have thought that there is more danger in administering medications that may cause harm if the ECG interpretation is incorrect.

[...]

Also, I'm a little confused about that ETCO2 reading. As I recall (and mind you, I'm sick so maybe I'm more confused than I realize), it would be hyperventilation that would cause that ETCO2 to be low, whereas hypoventilation would cause it to rise from the patient retaining so much CO2. So I'm a little baffled as to why his ETCO2 is only 31. I would expect him to be in respiratory acidosis, but that reading suggests the opposite. Though I guess bronchospasm or pulmonary embolism could cause low readings. So on that route, has he been bed bound for a while? Recent surgeries/trips or other PE risk factors? Any signs of a DVT? Also, do we have waveform with our ETCO2 and if so what waveform are we seeing?

I’ll take a whack at the low ETCO2 reading issue.

Two of the causes of poor concordance between PaCO2 and ETCO2 you mentioned: bronchospasm and PE (I suspect due to V/Q mismatch). However, COPD itself can also cause poor concordance, due to the already mentioned bronchospasm partially, but also due to an increase in deadspace and increasing V/Q mismatch.

This study of 118 COPD patients in the ED(I don’t have access to the full text, so I have to trust the abstract)

http://www.ncbi.nlm.nih.gov/pubmed/20224417

found:

“Mean arterial PCO2 levels were 43.24+/-14.73 and mean ETCO2 levels were 34.23+/-10.86 mmHg. Agreement between PCO2 and ETCO2 measurements was 8.4 mmHg and a precision of 11.1 mmHg.As there is only a moderate correlation between PCO2 and ETCO2 levels in COPD patients, ETCO2 measurement should not be considered as a part of the decision-making process to predict PaCO2 level in COPD patients.”

Similarly, this study (again, no full text for me) apparently found worsening concordance between PaCO2 and ETCO2 as degree of obstruction worsened:

http://www.ncbi.nlm.nih.gov/pubmed/18758420

There are several other similar but older studies with similar findings, all suggesting that ETCO2 cannot be trusted as an analogue of PaCO2 in those with cardiorespiratory disease.

One more, notably focused on prospective out of hospital use (though in Austria):

http://www.ncbi.nlm.nih.gov/pubmed/20224417

This all makes intuitive sense to me as well. We probably expect some degree of respiratory acidosis in COPD patients (especially the subset of “CO2 retainers”), and if these patients have systemic acidosis/hypercapnea due to inability to ventilate CO2, it makes sense that the level of CO2 escaping the pulmonary circulation and leaving the lungs to actually reach our ETCO2 detector could be lower than levels seen arterially.

I don’t think that low ETCO2 should necessarily increase our suspicion of PE without other indications, although I think your questions down that path are appropriate. Low ETCO2 readings are expected in COPD without other co-morbidities, and I don’t think that low ETCO2 is a particularly specific indicator of PE, at least not so much that my (inexperienced and very possibly wrong….) PE antenna go up with this patient. I think it’s far more likely that bronchospasm and mismatch/deadspace are the root of the lower than expected capnography readings.

Just a couple of pennies to add, hopefully the quotes all come out OK...

[...super discussion that I can only sit back and learn from, nothing productive to add...]

Firstly a most excellent find and thanks you, but just to split hairs I stated: I have yet to see any protocol that does NOT state use supplementary O2 for any CP or SOB. perhaps in the documented COPD patients a "target SP02" will be used, in future in EMS (although in the study that was Target SP02 was not identified clearly) That said as an RRT in hospital even back in the dark ages our "written" protocols for COPD was titrate 02 to KEEP SP02 88 to 92 %. Yes I certainly hope that this study finds its way into all EMS .. BUT I hope that the very old school limit(s) O2 flow to less than 4 lpm because all COPDers are hypoxic drive. (just not the case)

Fair enough. I don't think I could get any closer than a protocol which suggest titration.

Point 2: Then again yes O2 can relieve the feeling of SOB as possibly in this case of Pulmonary Hypertension this is a completely different pathology, in fact SOB i.e. shortness of breath is a complaint from the patient not a sign like say cyanosis, nor can SOB be quantified, moreover it is a symptom. If you follow my drift, please lets not scare the bejesus out of LadyBug because with her "post" as she states that despite SP02 readings her Heart Rate comes down, not an apple an orange (but I will let others take a stab at the explanation first ... why as to not be a show off)

Totally concur, I wasn't suggesting that the role of O2 in COPD was anything like the role of O2 in pulmonary hypertension - as you say totally different. As for the mechanism of decreased tachycardia in pulmonary hypertension, I think someone somewhere threw out the idea of release of hypoxic pulmonary vasoconstriction, and that makes sense to me, although I haven't done my research and as such have no evidence supporting that guess.

You did find in the "documented known COPD cases" that high flow was detrimental in regards to mortality morbidity, that was linked to PFTs and previous diagnosis (there is lots walking around undiagnosed, I believe it is becoming more "trendy" with the CHF patient as well to titrate O2 to SPO2 as to just blow back ones hair @ NRM 15 lpm.

Point 3: Way back in 2008 even supplemental 02 (low flow) and link quoted that the post operative geriatric patient (with no prior COPD PMHX) also had an increase in morbidity mortality when low flow O2 was used hypotheses being Staff equated Low SP02 to hypoxia when it was Ventilatory Failure (high PaCo2s)

I don't think I've seen that post-op paper, looks like a good read thanks. Also, you mentioned in another thread that there was evidence supporting a mortality (?) benefit with titrated O2 in CHF, and I a similar idea here. I did some looking but was only able to find one recent article, and it was a very small pilot study looking at oxygen in chronic left ventricular systolic dysfunction. I turned up some older studies (still working on reading them) which were more specific to oxygen in CHF/APE, but nothing newer. Is this new trend based on new evidence that I couldn't find, or old research, or....?

[...]

Again how can one in the field "Quantify" please note that in Kevkie attachment on the use of thromblytic protocol the target SPO2 ie Keep Sats > 92%. I have yet to see any protocol that does not state use supplementary O2 for any CP or SOB. A better question could be can one PROVE that Oxygen in the field is detrimental, just saying

[...]

Why, yes, in one setting involving SOB I believe I can prove that "high flow" O2 can be detrimental, and quantify the detriment even!

http://www.ncbi.nlm....pubmed/20959284

(ok, maybe not prove, but "support such a claim with evidence" perhaps...)

Edit: when I saw my post I realized the post I was quoting was....eh...rather old. This study wasn't even published in 2009. Apologies!

This is a great site where I've found a lot of interesting research on various practices in EMS. I haven't gone through and examined all of the studies just yet, but if someone wants to highlight one in particular feel free.

http://emergency.med...otocols/toc.cfm

If you haven't heard of it, the Cochrane library maintains a similar database for many medical topics, although it is not EMS focused. I am sort of jealous of that Canadian document, though. Maybe I should have moved up there, I hear the skiing is good too....

Creating a compendium like that is a huge undertaking, I suspect you'll have more success with smaller steps, going through individual topics. Why don't you start off the discussion - pick a topic that interests you and tell us what you think of the evidence. I'd be happy to play along with a more manageable activity like that, and maybe some of smart experienced people could give some more specific input with a start like that.

I worship daily at the alter of Dave Schriger and Mel Herbet for bringing clarity and common sense to the world of medical literature!

You are right about some of the trials having dodgy methodolgy, and it's not just in the IIb/IIIa studies. I can't remember which one off the top of my head, but one of them was comparing plavix AND aspirin against plavix alone and against no treatment and then saying "Wow! look how good plavix is!" Well of course it's better than nothing, that's not really the point! My understanding is simply that on further examination of the data canny clinicans confirmend they had been conned (there's some nice alliteration for this hour of the day!) and simply haven't taken to

I haven't read this one yet, but my suspicion is that it is industry funded? In which case it probably read like an advert because it is an advert! It's very common for these sorts of studies to have lots of "slices" of data looked at in an attempt to come up with something that will sell the drugs. Strange endpoints, conclusions that aren't actually drawn from the data: it's all designed to get the product moving. The trouble is, it works. I suspect that most of us (and I am certainly guilty of this) grab a study, read the abstract and conclusion and say "Neato! We should be using this!" Actually burrowing through the data is time consuming and often very difficult, particularly for those of us without much of a mathematical bent (like me) so we take the easy way out.

They are certainly interesting outcome measures you mention in relation to that study. I struggle to see how ST segment changes are really a significant measure, given that they are dynamic in STEMI anyway. Does the drug help, or is it merely the natural progression of ST segments trending down (before skyrocketing up again!): a natural regression to the mean? Equally TIMI flow has shown to not necessarily correlate well with survival, so again, not sure how much use that is as a clinical endpoint.

May I ask what your background is? I assume sciences or mathematics? It is rare to find a paramedic student who is able to analyse data so effectively, but it is pleasing to see. Maybe there is hope for EMS after all!

Sorry for the delay, was enjoying vacation. I think I'll join you at the alter of the great doctors (and a few others). I really enjoy that Dr. Schriger does the Annals of Em Med journal club writeups. A lot of what he writes flies straight over my head (especially where statistics are involved), but his way of looking at information and medicine is inspiring clever and robust

As for plavix,The big studies are all indeed drug company funded infomerci...err..studies. I like your take on all of this, and couldn't say it any better, so I won't try. I do remember reading the abstract to that aspirin/plavix study, and I think that's one situation where the abstract is all you need to read

Thanks again for the flattery (although it may be misplaced). I wish I could say that my partial paramedic education taught me how to read research, but the truth is I have a BS, the earning of which included much interpretation of research. It causes me much angst and frustration that there isn't the barest of a mention of research methodology or learning how to read evidence in my medic classes - it's a skill that takes time and practice to learn, and it bothers me that everyone isn't getting the same opportunity that I had.

My background is in a basic science, so this clinical stuff is a bit outside of my training, but the thought processes are similar and this is proving good practice for me. This thread has sort of died, but it was a useful exercise for me so I'm going to work on B-blockade for the end of the week.

The glycoprotein inhibitors studies have produced some excellent sales... oops, there I go again, I mean results! I haven't had a look at them for the last year or so, but there were about 4 studies done, all of them industry sponsored. The patients were all at low risk of bleeding and at high risk from death due to infarct, so these are the patients we would expect to see good results in. There were none.

No reduction at all in the re-occurence of MI at 6 months or death at 6 months, yet a reasonably significant (0.8% or about 1 in 115) patients suffered from a significant complication (cerebral haemorrhage or bleeding requiring transfusion)

There was a reduction in the need for repeat angioplasty, but as this was separate from and did not effect death or MI, it's really a waste of an endpoint.

No benefit, significant harm. No brainer really. Mind you, I'm not aware of any EMS that uses IIb/IIIa inhibitors, so it may be a moot point for us anyway.

If there are any studies newer than a year or so old that anyone knows of, please let me know, I haven't been very diligent in keeping up with this lately.

I'm not ready for the B-blocker discussion yet, but I did try to do my reading for GPIIb/IIIa inhibitors.

I think you covered it for the big 4 for NSTEMI (If we're talking about the same 4: PRISM, PRISM-PLUS, PURSUIT, and GUSTO-IV). David Schriger and Mel Herbert wrote a nice review of this data almost 10 years ago that I think nicely cover the myriad of problems with taking those 4 as proof of safety and efficacy (and provides a great example of how to do really good analysis):

http://www.ncbi.nlm.nih.gov/pubmed/11524643

As for new stuff, there seems to be a huge volume of literature on these drugs, and some of the studies are new, but from what I can tell they tend to be smaller and are using multiple divergent combinations of medications in a wide variety of settings. The truth is the volume of literature and diversity of interventions proved a bit overwhelming to me and I have to admit I'm especially not clear on the role of glyc. inhibitors in STEMI, maybe someone could point me in some sort of direction? I've heard that really glycoprotein inhibitors are being somewhat abandoned in practice, but I'm not clear on why that is. I agree that the initial studies were not as conclusive as touted, but (I think) those big 4 did lead to the widespread adoption of the drugs. What is driving the move away from them (have they gone generic or something?)?

Since we're in EMS I do think it bears mention that there was a recent (2008) RCT looking at prehospital use of tirofiban prior to PCI in the setting of STEMI published in the Lancet:

On-TIME 2:

http://www.ncbi.nlm.nih.gov/pubmed/18707985

I feel like this is getting rather repetitive, but the analysis here is not greatly different than other antiplatlet meds.

This study randomized PCI candidates either to "placebo" (600mg Plavix + 500mg ASA + 5000IU heparin all IV) or placebo plus 25mcg/kg loading and 0.15 mcg/kg/min infusion of tirofiban. Primary endpoint was resolution of ST elevation, with a couple of composite endpoints including death, MI, urgent revascularization (TVR), or bail-out use of tirofiban. They also looked at TIMI graded flow. N was 984.

They did find a significant improvement in ST-elevation, of course its up to the reader to determine the clinical relevance of that endpoint. They also found an improvement in their composite clinical endpoint, but that was driven largely by bail-out use of tirofiban being higher in the placebo group, which I think is a pretty mediocre surrogate measure. When they looked at Death/MI/TVR there was a slight trend to benefit with tirofiban, but nowhere near significant. There was also a marginal benefit in TIMI rated flow prior to PCI. Again, there was a trend towards greater rates of major bleeding (4% versus 2.9% placebo, p=0.363) and minor bleeding (6.1% versus 4.4%, p=0.233).

This study actually irked me a bit, it really read like an advertisement. A brief list of my biggest objections: They designed the study to look at ECG endpoints, but threw in a heap of other clinical endpoints as well, reported nonsignifigant trends towards clinical improvement in these endpoints (especially TIMI outcomes) without noting that these trends weren't significant, and at the same time claimed that there was "no significant increase in the rate of bleeding" ignoring the trend.

Second, they used this odd composite endpoint including bail-out use of tirofiban in order to achieve significance and claim improved clinical outcome (and to imply a significant improvement in mortality) despite marginal benefits in other endpoints.

Finally, they threw in a paragraph long "meta-analysis" of this study and unpublished pilot data from a non RCT to support the claim of a mortality difference.

Ah, I feel better.

Minor quibbles aside, I'm not sure how this study fits into the other glycoprotein inhibitor literature as applied to STEMI, but color me unconvinced about field usage. Of course there are issue of external validity here, as this was not conducted in the US and often involved physician staffed ambulances.

That aside, I'm still a bit confused about the issue with these druges. I'd love to hear more about GPiia/iiib in STEMI, as well as the reason for the move away from using these antiplatelet agents.

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...

Thanks for the kind words, I enjoyed your thoughts as well.

I'm sure that sales had nothing to do with any of these studies [http://www.emtcity.com/uploads/emoticons/default_whistle.gif' alt=':whistle:'>]. Really I was pretty disappointed with the almost blatant salesmanship in some of the writing. As a more blatant example, look at the third paragraph of the CLARITY-TIMI trial: "Clopidogrel has been shown to prevent death AND [emphsis added] ischemic complications in patients with 1. symptomatic artherosclerotic disease, 2. patients who have undergone percutaneous coronary intervention, AND 3. PATIENTS WITH UNSTABLE ANGINA OR MYOCARDIAL INFARCTION WITHOUT ST-SEGMENT ELEVATION [numbers and emphasis added]."

No study has shown a "prevention of death" in NSTEMI, certianly not their flagship CURE trial. This is almost a blatant misrepresentation, but they cleverly list conditions for which a decrease in death has been found (I haven't read the other studies, so benefit of the doubt on that claim), and tack on NSTEMI on the end, implying to anyone not carefully reading that a mortality benefit was found in NSTEMI as well as in the other two. I'm sure the authors would claim they meant that in each of these three settings ischemic complications OR death were prevented, but this is really grammatical trickery. Is it fair to say that plavix prevents ischemic endpoints OR alien invasion?

I'm very new to this game, so I'm not sure how common nonsense like this is, but really, pretty disappointing.

[...]

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.

I haven't seen that study, I'll have to read it, thanks. This issue actually may have be a bit relevant to the EMS world as well, at least as far as diagnosis, as I wonder if a history of recently discontinued Plavix should maybe increase our suspicion of thrombotic issues (stroke PE etc). Something to keep in mind.

I had heard somewhere along the line about the surgeons objecting as well. I assume this is predominantly in patients requiring CABG? I think 5 days is the time for plavix to clear, but I also think the Plavix people claim it's not much of an issue. I can't seem to find where I read that claim, though.

[...]

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!

This is another trial I need to go re-read. I think you're right, but I have heard advocacy for retaining B blockers for some tachycardic patients (e.g. those with hypertension, good perfusion, clear lungs, no other s/s of failure/CHF), where maybe the goal of decreasing the myocardial oxygen demand down might outweigh the low chance of fialure. I'm not sure how the COMMIT data interacts with that proposal, or how well associated with failure tachycardia is, maybe you know more.

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.

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.