Talk:Myocardial infarction

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Here are some tasks you can do:
  • Requests: Sort out information that belongs elsewhere (under acute coronary syndrome, for example) to off-load the article. Be sure to leave stub explanations that create sufficient content for the readers who want to know exclusively about this topic.
  • Expand: External links, but be sure to strictly follow WP:EL.
    Sources for the unreferenced sections is top priority!
  • Stubs: Some of the terms in the "see also" section probably should be mentioned somewhere. First aid section is still stubbish.
  • Update: *The talk page and archives provide insight in the answers readers come looking for, so most of these things should be inserted. Also some excellent review articles are suggested.
  • Other: Once all the references are provided, this article should easily pass Good article review, and could move to WP:RFC. The ultimate goal is of course WP:FA.
    Please improve this "to do"-box.

Contents

[edit] Merge First Aid and Treatment

Has anyone given thought to merging the "first aid" and "treatment" sections? We could divide it up into immediate care and hospital care, or something like that. Thanks! Scope2776 21:09, 5 March 2007 (UTC)

[edit] Categories

What's up with the categories at the bottom of the page? I belive this article has plenty of sources, and I tried to remove the tags but could not find the code. Scope2776 09:46, 5 March 2007 (UTC)

[edit] FA status

Think this is good enough? TheKillerAngel 21:19, 12 July 2006 (UTC)

This article still lacks a lot of relevant information - epidemiological trends, modification of risk factors etc. It is relatively poor on references, given that MI is one of the most heavily researched subjects in modern medical science. JFW | T@lk 22:43, 26 July 2006 (UTC)

It would be a good idea to include some statistics on mortality rate from myocardial infarctions, with and without treatment.

Should the effects of personality types (Type A or hostile, easily-angered), psychological stress, catecholamines such as adrenaline etc., cortisol, and contraction band lesions be discussed as risk factors for heart attacks? H Padleckas 07:36, 27 July 2006 (UTC)

The actual evidence for personality types is deeply rubbish. A type C (depressed/dependable) was recently given much more prominence. It's science that has long been discredited. Same with stress and peptic ulcer (unless we're talking a stress ulcer, seen in intensive care). JFW | T@lk 22:58, 27 July 2006 (UTC)

[edit] History

Gene Braunwald sums up some important paradigms in MI research in a 1993 editorial here. JFW | T@lk 22:43, 26 July 2006 (UTC)

[edit] Choice of antiplatelet drug

The cite below just got reverted. Noting the complaints about the lack on numbers on the project page, this cite gives some valuable and reassuring nummbers about bleeding during antiplatelet drug prophylaxis as well as the relative cost of aspirin verses more expensive treatment. All-in-all, a very interesting matter, since so many persons are on antiplatelet treatment. IMHO it would get lost over on aspirin. Perhaps it could be set up as a separate page, but that seems an unecessary complication.

  • "Choice of Antiplatelet drug: A recent review [1] states: "....low-dose aspirin increases the risk of major bleeding 2-fold compared with placebo. However, the annual incidence of major bleeding due to low-dose aspirin is modest—only 1.3 patients per thousand higher than what is observed with placebo treatment. Treatment of approximately 800 patients with low-dose aspirin annually for cardiovascular prophylaxis will result in only 1 additional major bleeding episode." Further, "...the cost to prevent one major GI bleeding episode from aspirin in 1 year by substituting clopidogrel therapy would be $1,216,180..." Pprotctor (talk • contribs)
I removed that, and the reason is that (1) it is germane to all indications for aspirin, hence belongs on aspirin or antiplatelet drug, (2) leaving it here would overload the article - imagine if we listed the side-effects of ACEi, β-blockers, potassium-sparing diuretics? In a major disease like MI I'd prefer references either to official guidelines (which are based on systematic reviews) or to studies that have looked specifically at MI. JFW | T@lk 07:11, 4 September 2006 (UTC)

[edit] Pericarditus

I just redirected the entry on Pericarditus here. If someone wants expand that article, please feel free to, I just didn't consider the one-line article ("This is a type of condition in which the sac arond the heart becomes inflamed. It is usually associated with a acute-heart attack, but it really isnt.") encyclopedic enough to keep. ~ trialsanderrors 18:04, 21 September 2006 (UTC)

Erm, I think it's a mis-spelling of Pericarditis and needs deleting. --John24601 18:11, 21 September 2006 (UTC)
Thanks, I simply changed the redirect. No need to delete if it's a possible misspelling. ~ trialsanderrors 18:14, 21 September 2006 (UTC)

[edit] Self help in case of attack ?

I received an email about what to do if you have a heart attack and help is not immediately available. Basicaly it says that you should take a deep breath and (strongly) cough out the air, every 2 seconds. Does that really help or is this a hoax ? xerces8, --213.253.102.145 08:20, 7 November 2006 (UTC)

Umm... Kinda a hoax, based on a rare occurrence. If your heart were to stop completely you will pass out in about five seconds. If you were to know exactly when your heart stopped (for instance, if you were on a telemetry monitor that someone was watching), they could prompt you to cough to presumably create some cardiac output while waiting for your heart to restart. This is only really useful in a controlled setting in which someone was with you while you are on telemetry in a hospital or doctor's office. Particularly useful if there is a prolonged pause after the administration of adenosine or in a cardiac cath lab or EP lab when asystole or ventricular fibrillation is induced. Ksheka 16:56, 25 November 2006 (UTC)

"Cough CPR" does work in a controlled environment like the cath lab, but I agree it was a hoax. Cough CPR is for the supine patient on the cardiac monitor who is being coached by medical professionals to buy a little time while they attach and charge up the defibrillator. In other words, they see VF on the monitor and coach you to cough. How would you know you were in VF? By the time you figured it out you would be unconscious, especially if you were standing up. MoodyGroove 16:21, 23 December 2006 (UTC)MoodyGroove

[edit] Omega-3 and VF

The following provide a counterpoint to the reference I added:

  • Brouwer I, Zock P, Camm A, Böcker D, Hauer R, Wever E, Dullemeijer C, Ronden J, Katan M, Lubinski A, Buschler H, Schouten E (2006). "Effect of fish oil on ventricular tachyarrhythmia and death in patients with implantable cardioverter defibrillators: the Study on Omega-3 Fatty Acids and Ventricular Arrhythmia (SOFA) randomized trial". JAMA 295 (22): 2613-9. PMID 16772624. 
  • Raitt M, Connor W, Morris C, Kron J, Halperin B, Chugh S, McClelland J, Cook J, MacMurdy K, Swenson R, Connor S, Gerhard G, Kraemer D, Oseran D, Marchant C, Calhoun D, Shnider R, McAnulty J (2005). "Fish oil supplementation and risk of ventricular tachycardia and ventricular fibrillation in patients with implantable defibrillators: a randomized controlled trial". JAMA 293 (23): 2884-91. PMID 15956633. 

Fvasconcellos 20:39, 26 November 2006 (UTC)

[edit] AMI vs MI

Why the lead says that AMI is equal with MI ? — Indon (reply) — 11:01, 27 November 2006 (UTC)

Because chronic myocardial infarction exists, but is very rare, I guess.--Steven Fruitsmaak (Reply) 13:02, 27 November 2006 (UTC)
Correction: AMI is what is generally considered under MI; look at the ICD-10 classification and you will see how AMI and chronic ischemic heart disease are organised.--Steven Fruitsmaak (Reply) 16:24, 27 November 2006 (UTC)
When you talk about myocardial infarction, it must have been acute at some point. There is no such thing as a "chronic" myocardial infarction (implying progressive death of myocardium over weeks to months due to an occlusion of a coronary artery). "Acute" just means recent in this setting. If someone has a history of an acute myocardial infarction in the past, we just say they have a history of an MI. Ventricular remodeling after a myocardial infarction with subsequent cell death is a totally different animal. Ksheka 15:23, 28 November 2006 (UTC)

[edit] Statins

I removed the following bit from the article:

There is no evidence that LDL cholesterol reduction alone predicts the decrease in cardiovascular risk,[1] and emerging evidence suggests multiple beneficial effects of statins after a MI, for example via a decrease in C-reactive protein levels.[2]

  1. ^ Hayward RA, Hofer TP, Vijan S. "Narrative review: lack of evidence for recommended low-density lipoprotein treatment targets: a solvable problem." Ann Intern Med 2006;145(7):520-30. PMID 17015870
  2. ^ Ray KK, Cannon CP. "The potential relevance of the multiple lipid-independent (pleiotropic) effects of statins in the management of acute coronary syndromes." J Am Coll Cardiol 2005;46(8):1425-33. PMID 16226165

There is definitely something wrong about it (it's just not true), and it actually contradicts the previous line in the article. The bit about C-reactive protein is actually backwards. C-reactive protein (CRP) is a marker of inflammation. I don't believe there is any study that decreasing the CRP level itself (via plasmapheresis) is of benefit. Rather, decreasing inflammation is of benefit, and the decrease in inflammation is seen as a decrease in CRP levels. (This should be addressed in an article on coronary artery disease, and not in this article.) Ksheka 16:28, 29 November 2006 (UTC)

The first reference about (PMID 17015870) is a review article which doesn't really make much sense, since it is contradicted by a number of mega-trials (4S for instance). Ksheka 16:35, 29 November 2006 (UTC)
Of course statins are beneficial in MI, but the question is wether this is via LDL-c alone: there seems to be some research about other effects ("pleiotropic") too. Also, I saw some studies who just treated MI patients with statins and it reduced cardiovascular risk, without looking at the patients reduce in LDL: would you not say then, that it can be beneficial to all patients, even those with LDL, say, <130? The first reference, in my eyes, doesn't contradict 4S: the question is wether people with normal LDL-c could benefit from statins, no?--Steven Fruitsmaak (Reply) 16:47, 29 November 2006 (UTC)
Okay. This should be made more clear, then. Maybe mentioning that the effects of statins may be more than their LDL lowering effects and that general consensus is that statins have plaque stabilization and other pleiotropic effects that may prevent myocardial infarction. Ksheka 16:52, 29 November 2006 (UTC)
Okay. I put in a different sentence in the article. I'll reference it later if no one beats me to it. :-) Ksheka 17:01, 29 November 2006 (UTC)

[edit] Length warning

The article is now 64Kb! We should really try to keep it short and readable, certainly not above 64K! If stuff is covered in subtopic articles, it should be left out here. While comprehensiveness is important, citation seems to be a big priority too for the moment...--Steven Fruitsmaak (Reply) 19:40, 1 December 2006 (UTC)

I noticed earlier today about the size, and really wasn't sure what to make of it. We're about 12 printed pages not including references, with a lot of content still to be added (the reperfusion section is what I am working on now). The general guideline is that the text should not be more than 10 pages. I personally think we should ignore the guideline on this one and let it overflow, at least until the edits quiet down (I plan on working on this for another month). If, at that time, it seems too large, then break away parts into smaller articles (ie: an article on reperfusion during an acute MI could easily be 64k itself). Ksheka 22:21, 1 December 2006 (UTC)
Another reason to let the text get to be more than 64k is that we have a lot of well broken out sections, and each section is of manageable size. Ksheka 22:22, 1 December 2006 (UTC)
Another thing to note: Medical topics tend to run long. AIDS is a 108k article and 13 printed pages. And there is a lot more to talk about in myocardial infarction. So let's not worry about page length for now. And use more citations, not less. :-) If you want to delete some text to clean up the language, that's fine. Just please don't do it to keep the page length down. Ksheka 00:27, 2 December 2006 (UTC)
If you look closely, I'll hope you agree that I only removed things from the reperfusion section that were already mentioned elsewhere. I think a better strategy than writing first and splitting into new articles later, is just write stubs in the individual sections now, with the essentials, and expand on those in new articles later -but that's just my opinion. However, I agree that a featured article on this topic would be over 64Kb, more around 80Kb, if I compare with, for example, Bacteria.
About the references, maybe it's a better strategy to look for quality papers and guidelines and write starting from them, instead of writing from our basic knowledge and looking for references afterwards.--Steven Fruitsmaak (Reply) 13:33, 2 December 2006 (UTC)
The problem with writing to the guidelines is that the guidelines are always a bit behind current practice. A lot of the references I put in the article are the articles that the guidelines reference themselves. A lot of the other references should probably be changed in the future, once the rough text is all in place. I'll have to check about one of the larger paragraphs you deleted. Ksheka 14:30, 2 December 2006 (UTC)

[edit] Copyright issues

While looking for references for the first aid section, I found a site (http://heart-disease.health-cares.net/survive-heart-attack.php) that apparently copied content from this article, so I reported it on Wikipedia:Mirrors_and_forks/Ghi#Health-cares.net. The original structure seems to have been introduced in this rewrite from JFW.--Steven Fruitsmaak (Reply) 21:00, 3 December 2006 (UTC)

[edit] Delay caused by ASA?

According to this website, people should call 911 prior to looking for an ASA. Probably correct, but could use some real pubmed references. :-)

You should not delay calling 9-1-1 to take an aspirin. Studies have shown that people sometimes delay seeking help if they take an aspirin (or other medicine). Emergency department personnel will give people experiencing a heart attack an aspirin as soon as they arrive. So, the best thing to do is to call 9-1-1 immediately and let the professionals give the aspirin.

Ksheka 00:26, 5 December 2006 (UTC)

Okay. I looked this up in the guidelines. It seems to be based on a single study, and the guidelines don't have an opinion on whether ASA should be administered before calling EMS. Ksheka 03:20, 5 December 2006 (UTC)

[edit] A one-sided affair?

The article is coming along nicely. There is only one problem: A lot of what we write, and the references we use, make it sound like things are certain. This is probably the way we should do it for this sort of article. Is there a benefit in giving other opinions on matters? As an example, I have a bunch of references I will (hopefully) add today to show that PCI is better than thrombolytics for treatment of an STEMI. However, this is the consensus opinion that has developed after a long series of studies have looked at the matter. And some of the studies (which I will likely not reference) showed that there was no benefit of PCI over thrombolytics.

Again, I think we are doing this the correct way, but was wondering if this will be a sticking point if we aim for feature article status in the future. Ksheka 14:23, 5 December 2006 (UTC)

I think there's no need for such nuances; we should inform about the highest forms of consensus, and disclose uncertainties were debate exists: if meta-analyses have shown that there is a general trend, that overrules the negative findings of some studies. As long as we are being objective, no-one can accuse us of favouring certain views, even if we do not mention things in the extreme detail.--Steven Fruitsmaak (Reply) 17:03, 5 December 2006 (UTC)

[edit] Most common presentation of IHD?

Looking at these statistics, I would suppose that MI is more frequent than angina. Of course, WHO groups coronary atherosclerosis under ischemic heart disease, and together with silent ischemia this may be very frequent, but not with symptoms. But this study says in the omitted table which I looked up, that of their 74 patients, 10 showed stable angina, 11 AMI, and 53 unstable angina. But then again, that first sentence was mainly ment to establish a link with the WHO data, to indicate that it's the nr. cause of death worldwide. And angina doesn't kill you, MI does.--Steven Fruitsmaak (Reply) 13:27, 7 December 2006 (UTC)

Yeah. I wasn't sure about the fact myself. I just thought that it would show up as true, based on other stuff I had read. Just goes to show you that really everything in this article has to be properly references. Most of the epidemiology facts I have relate more to CAD than to MI (I haven't put any of these in any article yet.):
  • The prevalence of CAD is higher in men than women at all ages.
  • CAD is the leading cause of death in the U.S. and Western Europe.
  • There is an epidemic increase in CAD in Eastern Europe, Far East, and Asia.
  • The prevalence of reversible risk factors are decreasing except DM.
  • Cardiovascular deaths are decreasing in men but not in women.
  • The incidence of MI is decreasing in men but increasing in women.
  • Health care makes up 15% of the GDP.
  • The incidence of CAD is decreasing.
  • The prevalence of CAD is increasing.
  • There is a shift in coronary heart disease burden to the women and elderly.
  • In patients presenting with ACS, each increment of 10 years of age increases the risk of death or MI by a factor of 1.3.
The ACC guidelines for STEMI do have an epidemiology section. I'll try to look some stuff up in the near future.
Ksheka 14:27, 7 December 2006 (UTC)

I would imagine that MI is the most prevalent presentation of IHD (most people who have one end up in a hospital), but it is probably not the most frequently occuring (angina attacks can be self-limiting or can be treated by the patient taking their medication; so they don't present to a doctor). As for total number of patients suffering from MI vs suffering from angina (which is I think what this is getting at), I really don't know, although I would expect a big overlap between the two groups. --John24601 17:00, 7 December 2006 (UTC)

[edit] Immediate care

The following line is under immediate care: "When symptoms of myocardial infarction occur, people wait on average 3 hours, instead of calling for help immediately." This should probably be reworded, since it sounds like we are advocating waiting around for 3 hours before calling for help. Maybe add a line about community teaching to call 9-1-1 immediately, the whole "time is myocardium" thing and progressive permanent myocardial damage prior to being evaluated? Ksheka 17:58, 13 December 2006 (UTC)

[edit] Image in Histopathology section

Am I being dense, or is the caption in Image:Myocardial infarct emmolition phase histopathology.jpg confusing, i.e. "7 days of duration"? Does it mean 7 days post-onset, or an MI that went on for 7 days? :) Fvasconcellos 01:23, 14 December 2006 (UTC)

Changed it to post-infarction. Sounds better. Ksheka 01:28, 14 December 2006 (UTC)
Thanks. Fvasconcellos 01:30, 14 December 2006 (UTC)

[edit] Image:Intracoronary_thrombus.png

Great that we have PCI images, wow! But, as often with footage from interventions, students like myself have difficulties to understand what exactly were looking at; you say they have been removed, so were are they now? What is the blue edge? I have difficulty understanding so maybe the caption needs to explain more.--Steven Fruitsmaak (Reply) 12:25, 14 December 2006 (UTC)

Hmmm.... Well, what I used is known as a transit catheter (particularly, the Export catheter (tm)), which is basically just a really long hollow tube. I put the catheter in the coronary artery down to the level of the thrombus and sucked back the contents of the artery (a combination of blood and thrombus) using a syringe. I then ejected the contents of the syringe onto a wire mesh filter that comes with the Export catheter. This filter is basically a small blue cup with a fine wire mesh for the walls. Feel free to adjust the caption as needed to make it more clear (I'm too subjective to know what "clear" means in this case).
By the way, I'll put in the references for the PCI section when I have time. Things are quite busy for the next couple days at least. I want to keep the wording as PCI, and not angioplasty because (as this picture shows) angioplasty (using a balloon to dilate the artery) is only a small part of the procedure.Ksheka 12:35, 14 December 2006 (UTC)
Maybe it will look better if I include a zoom-out of the cup with thrombus in the upper left corner of the picture? Ksheka 12:46, 14 December 2006 (UTC)
Well, yes that would indeed make it more clear, at least for me.--Steven Fruitsmaak (Reply) 15:33, 14 December 2006 (UTC)
Done. Ksheka 22:05, 16 December 2006 (UTC)

[edit] CPort trial

Just a reminder to myself (or if anyone can take a look), this reference [2] needs to be fixed. It's the CPort trial. I'll try to look it up properly later. Ksheka 14:53, 18 December 2006 (UTC)

Took the liberty of looking it up. Is this it?

Aversano T et al. (2002). "Thrombolytic therapy vs primary percutaneous coronary intervention for myocardial infarction in patients presenting to hospitals without on-site cardiac surgery: a randomized controlled trial". JAMA 287 (15): 1943-51. PMID 11960536. 

Fvasconcellos 16:06, 18 December 2006 (UTC)
That look like it. Thanks. Ksheka 16:17, 18 December 2006 (UTC)

[edit] Epidemiology and Risk Factors

The article says the risk factors for atherosclerosis may be risk factors for coronary artery disease. This is like saying the risk factors for losing all of your money may be the risk factors for bankruptcy. Coronary artery disease is caused by atherosclerosis. MoodyGroove 16:11, 23 December 2006 (UTC)MoodyGroove

[edit] Reperfusion

The citation needed to show that fibrinolytic therapy is contraindicated for Non-ST Segment Elevation MI is _Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Lancet 1994;343:311-22_. Unfortunately, I do not yet possess the skills to insert this in the article. MoodyGroove 16:44, 23 December 2006 (UTC)MoodyGroove

[edit] Thrombolytic Therapy

The citations needed for the first paragraph are _Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour. Lancet 1996; 348:771-75._ Figure 4. on page 773 should be of particular interest, which is essentially a graph of the data from the FTT Collaborative Group (see previous citation under reperfusion) showing mortality against treatment delay. No reason you can't use that citation as well as it was a meta-analysis of all major thrombolytic trials and looked at over 60,000 patients. MoodyGroove 17:39, 23 December 2006 (UTC)MoodyGroove

Added to article. MoodyGroove 15:22, 26 December 2006 (UTC)MoodyGroove

[edit] C Reactive Protein (CRP)

Under risk factors, the article states, "Moreover, some drugs for MI might also reduce CRP levels." This could be more clear, in my opinion. I didn't edit it because I wasn't sure what the previous author was trying to say. "Drugs for MI" is very ambiguous. Are we talking about drugs used to prevent MI? MoodyGroove 21:45, 23 December 2006 (UTC)MoodyGroove

It refers to the pleiotropic effects of statins.--Steven Fruitsmaak (Reply) 17:37, 24 December 2006 (UTC)

[edit] Acute Coronary Syndromes

I think it would simplify matters greatly if we placed acute myocardial infarction in its appropriate context under the umbrella of the acute coronary sydromes (ACS). That way, we could clearly separate atherosclerosis, plaque rupture, coronary ischemia, chronic stable angina, acute myocardial infarction (including non-ST segment elevation MI and ST segment elevation MI), cardiac arrest, cardiac biomakers (myoglobin, CK-MB, the troponins, etc.) and makers of infammation like CRP. We're trying to throw it all under the heading of myocardial infarction or "heart attack" and the article is suffering. I would like some comments on this suggestion. Thanks! MoodyGroove 21:55, 23 December 2006 (UTC)MoodyGroove

Hi. It looks like you know what you are talking about. I take it you are a cardiologist? I had the same thought a couple months ago, but didn't know what to do with it. How about we do this in a 3 pronged approach:
Agreed. MoodyGroove 14:43, 24 December 2006 (UTC)MoodyGroove
The article should focus on physiology of plaque rupture and treatment options for ACS. It will define STEMI/NSTEMI. It should also talk about acute coronary ischemia and cardiac biomarkers.
Agreed, especially since USA and NSTEMI are indistinguishable without a rise and fall of cardiac biomarkers. I also like the idea of a more precise discussion of ischemia. MoodyGroove 14:43, 24 December 2006 (UTC)MoodyGroove
  • 2. Create separate articles for Chronic stable angina and Coronary artery disease. Coronary artery disease will talk about the physiology of progression of atherosclerotic plaque, the role of inflammation (and markers of inflammation) and about primary prevention. Chronic stable angina will likely talk about treatment options for chronic stable angina (This is likely to be a small article). The article should refer to the section on coronary ischemia in the ACS article.
Definitely agree that chronic stable angina should be separate from ACS. MoodyGroove 14:43, 24 December 2006 (UTC)MoodyGroove
  • 3. Create a different article on Post-infarction complications (or something like that. I'm not married to the name :-) ). The article will take about the various mechanical complications post-MI (both short-term and late complications), with links to the various articles on Congestive heart failure, cardiogenic shock, etc. Cardiac arrest may go here as well, but I consider that a grab-bag sort of term (no really good definition).
Congestive heart failure will be quite an undertaking. I reviewed the current ACS article, and I feel like it needs to be scrapped and supplanted with information from the current myocardial infarction article. MoodyGroove 14:44, 24 December 2006 (UTC)MoodyGroove
I understand that CHF would be a huge undertaking. I'm not sure if I know enough to take a stab at it (I know enough about CHF to sound intelligent but be wrong :-) ) Ksheka 15:52, 24 December 2006 (UTC)
How about we call the article Complications of coronary artery disease? And list acute coronary syndrome as one of the complications as well? You are absolutely correct in calling ACS as a manifestation of CAD, and makes the categorization a bit easier as well. Ksheka 16:05, 24 December 2006 (UTC)
What do you think about the proposal? I think I addressed the particular issues you mentioned, but there is more that needs to be ironed out. For instance, should secondary prevention be in the ACS article, the Coronary artery disease article, or somewhere else?
I would put it in the coronary artery disease article. I personally don't even like referring to a heart attack as a disease. In my opinion, coronary artery disease is the disease. ACS (including AMI) is a clinical event that is a manifestation of that disease. MoodyGroove 14:44, 24 December 2006 (UTC)MoodyGroove
It's somewhat ironic that I'm the one suggesting the move, since I was the one a couple years about that asked that the article be moved to _Myocardial infarction_, from _Heart attack_. Ksheka 01:09, 24 December 2006 (UTC)
There's a lot of great material to work with here. I just think the restructuring will help out, and enable each topic to be explored in more depth. Should we think about an article on risk stratification? I'm going to do some looking around right now and see how many of these articles already exist. MoodyGroove 14:43, 24 December 2006 (UTC)MoodyGroove
If you see any stray articles, please insert them in the appropriate place over at Cardiology. I've been using that article as a sort of Table of Contents for all cardiovascular disease topics. Ksheka 17:25, 24 December 2006 (UTC)

I agree that there is much clutter and there is a need to sort this out. I wouldn't move the article anywhere, just move parts of it to where they actually belong, and leave stub paraghaphs with a {{main}} tag, explaining the basics, as is appropriate in an article of this size. But as David Ruben points out here, I think only the symptoms section should move to ACS, since a syndrome is still a group of syndromes. Pathophysiology etc. should go to coronary artery disease. Basically, diagnosis and treatment are the core sections that should remain. Risk factors could be tricky; I think that research that is actually about MI, belongs here. I also believe that we should somehow filter out NSTEMI in this article: but we need something for the readers out there who want to read about "heart attack". Please take enough time to discuss this entire operation.--Steven Fruitsmaak (Reply) 17:46, 24 December 2006 (UTC)

Why the attachment to the title myocardial infarction? It just doesn't lend itself to exactness or completeness. As evidence, you indicate a wish to filter out NSTEMI. But this would be a mistake, since NSTEMI is just as much a heart attack as a STEMI. They are all manifestations of coronary artery disease, and they all tend to cause chest pain. Isn't it quite arbitrary to pick out one type of ACS and proclaim it to be a true heart attack? MoodyGroove 18:55, 24 December 2006 (UTC)MoodyGroove
I totally agree with MoodyGroove, which is why I suggested the move. The pathophysiology is near-identical for STEMI and NSTEMI, and there is little distinction between UA and NSTEMI. As for time, I won't personally do anything about a move for another week at the very least, to allow people to have time to chime in. Ksheka 03:15, 25 December 2006 (UTC)


I think there must be something wrong with the reasoning here (maybe it's cardiologists bias I don't know), but you seriously cannot expect to have an encyclopedia without an article labelled "myocardial infarction"?

Come now, Steven. You can come up with a better argument than accusing us of some kind of bias and then making an arbitrary statement like this. Myocardial infarction can still be an article. But the lion's share of the current content belongs under acute coronary syndromes. It has nothing to do with bias. It has to do with the prevailing research. You know as well as I do that we are in the evidence based medicine era, and that medicine has been advancing in leaps and bounds. Nowhere is this more evident than in emergency cardiac care. There's a reason the umbrella term acute coronary syndrome was created, and there's a reason that myocardial infarction was divided into STEMI and NSTEMI. What makes the term myocardial infarction more acceptable as the main title for this topic from the average reader's perspective? It's a medical term, and we're already redirecting the layman's term "heart attack." As long as the average reader is redirected to the acute coronary syndromes article, what difference does it make? MoodyGroove 15:19, 25 December 2006 (UTC)MoodyGroove

I don't see why we should put the entire article under ACS, since that would add more content to it, i.e. angina pectoris.

That's not true. Chronic stable angina pectoris might be mentioned, but it's unstable angina that's listed with STEMI and NSTEMI as an acute coronary syndrome. MoodyGroove 15:19, 25 December 2006 (UTC)MoodyGroove

As David puts it, ACS is just a "clinical impression from history and examination, that pain may originate from the heart".

I'm sorry, but that's not correct. An acute coronary syndrome is a set of signs and symptoms suggestive of sudden cardiac ischemia, which is almost always a manifestation of coronary artery diease. Because the history and exam are not reliable in this complicated set of patients, there are evidence based guidelines for risk stratification, triage, and management. In other words, you cannot have an article about myocardial infarction and reasonably discuss the diagnosis and treatment without opening up the can of worms that is the acute coronary syndromes. So the question becomes, what is the most reasonable portal to the discussion? I can't put it any more clearly than that. MoodyGroove 15:19, 25 December 2006 (UTC)MoodyGroove

Redirecting to ACS seems like a really bad idea to me. The suggestion to create a separate post-MI article illustrates the need to have an article on AMI itself. I adhere to the title "myocardial infarction" because there's simply some much research under that header. You cannot say that it is a non-entity, a vague concept that does not allow clear discussion.

I do not recall anyone making the claim that AMI is a non-entity. The issue at hand is how to approach the discussion. See above. MoodyGroove 15:19, 25 December 2006 (UTC)MoodyGroove

I've suggested earlier to remove content from this article that is not exclusive to this article: indeed, ischemia doesn't need to be discussed in detail here, and can move to ACS. But we should at least leave a stub explanation of all these concepts in this article, because we want to provide our readers with an overview in a single article, and the possibility to read more if they want to. I think David's idea will really help readers to navigate trough the maze here.

I think what you are suggesting is drastic, and unlikely a definitive solution.

What makes it drastic? I think the strongest argument in favor of moving it under acute coronary syndromes is the fact that it will definitively solve a lot of these problems by making it the main table of contents for a complicated issue. MoodyGroove 15:19, 25 December 2006 (UTC)MoodyGroove

I think we can solve the problems of "throwing it all under MI" by following the simple rule that anything that is specific for MI should be discussed here, and anything that belongs in a more general concept, should be discussed there.--Steven Fruitsmaak (Reply) 13:57, 25 December 2006 (UTC)

How do you discuss the diagnosis and treatment of AMI without opening up a discussion of the acute coronary syndromes? I don't think that's possible. MoodyGroove 15:19, 25 December 2006 (UTC)MoodyGroove
I didn't mean to accuse you guys of anything or to offend you, and if I did I'd like to apologise. ACS is a relative newcomer. I will hapilly move out the lion's share of this article to that page, provided that we still have an article with sufficient basics here. As for the redirect from heart attack, I think that should be replaced with a discussion to explain what the relation is to MI, ACS etc.--Steven Fruitsmaak (Reply) 15:31, 25 December 2006 (UTC)
No offense taken! I apologize if I've given that impression. MoodyGroove 16:33, 25 December 2006 (UTC)MoodyGroove
It would be easier to follow the discussion it was set-up as Oppose/Support. I OPPOSE merging into myocardial infarction into ACS -- based on the definition. ACS is:
Pronunciation: ( a-kyut kor¢ŏ-nar-e sin¢drom) A general term for clinical syndromes due to reduction of blood flow in coronary arteries (unstable angina, acute myocardial infarction). syn: acute myocardial infarction syn: unstable angina syn: preinfarction angina [3]
I think it is definitely worthwhile to disambig and I think renal dialysis should be a guide to how it is done. Beyond that... one can create a flowchart/family tree (as in dysphagia) that shows the relationship and/or a template. Nephron  T|C 07:13, 31 December 2006 (UTC)
I'm not sure I understand why your definition of ACS precludes you from enthusiastically supporting the merge (if it's even a merge we're talking about). My position is that the majority of the current article belongs under Acute Coronary Syndromes, and that "heart attack" should redirect to Acute Coronary Syndromes. Consider the following:
"It has been recognized that acute coronary syndromes are a diagnostic and pathophysiologic continuum ranging from unstable angina to Q-wave myocardial infarction. At the interface between unstable angina and myocardial infarction, these entities become nearly indistinct as most features are shared."[3]
Also consider:
"Traditionally, ischemic heart disease has been divided into several separate syndromes: stable coronary artery disease, unstable angina, non-Q-wave myocardial infarction (MI), and Q-wave MI. However, recent understanding of the conversion of a stable atherosclerotic lesion to a plaque rupture with thrombosis has provided a unifying hypothesis for the etiology of acute coronary syndromes. The concept of myocardial ischemia as a spectrum provides a framework for understanding the pathogenesis, clinical features, treatment, and outcome of patients."[4]
In other words, it's impossible to intelligently discuss acute myocardial infarction without placing it in its proper context within the acute coronary syndromes. Why the attachment to the phrase Myocardial Infarction as the portal to this discussion? MoodyGroove 16:57, 31 December 2006 (UTC)MoodyGroove
The argument you bring above could be made about autism and Asperger's syndrome--they are both on a spectrum yet have separate articles. I think it makes sense to make some distinction as, clinically, MI and unstable angina have different outcomes.
Clinically speaking, how do UA and NSTEMI have different outcomes? MoodyGroove 23:28, 1 January 2007 (UTC)MoodyGroove
I don't find the argument about etiology particularly convincing 'cause atherosclerosis in the coronaries, carotids, and abdominal aorta isn't much different -- yet their symptoms (classically)--chest pain, unilateral weakness, claudication are quite different--as is the associated morbidity and mortality. I think it makes sense to explain that it is a spectrum... but that doesn't have to be done with a merge and can be done in the ACS article.
That's fine. I'm not advocating a merge as such, and major improvements have been made to the article since this discussion started. MoodyGroove 23:28, 1 January 2007 (UTC)MoodyGroove

Also, if "the majority of the article" belongs under ACS-- that doesn't precluding rearranging and moving things between articles. Nephron  T|C 19:10, 1 January 2007 (UTC)

I agree with that. MoodyGroove 23:28, 1 January 2007 (UTC)MoodyGroove

[edit] Proposal

The above discussion was kinda difficult because it was poorly structured and not clearly defined what was exactly proposed. I propose the following, please indicate support or oppose.

  • Moving part of the content that would be better discussed under the general header of acute coronary syndrome or ischemic heart disease to those article, but leaving enough material to still discuss myocardial infarction itself as an entity, using tags like Further information: acute coronary syndrome.. This will off-load the article and reduce the confusion caused by trying to explain everything related to ischemic heart disease and ACS under this header.
  • Support as nom.--Steven Fruitsmaak (Reply) 17:15, 31 December 2006 (UTC)
  • Support. Sounds good to me. I'm all for offloading + making less confusing... remember WP is for the masses. Nephron  T|C 19:36, 1 January 2007 (UTC)
  • Support.Ksheka 00:28, 2 January 2007 (UTC)
  • Changing the redirect from [[heart attack]] to myocardial infarction into a short page explaining what can be meant by heart attack: it's actually an acute coronary syndrome, but it could by myocardial infarction or unstable angina. Reader entering heart attack might equally be looking for myocardial infarction as for a general article on chest pain originating from the heart.
  • Support as nom.--Steven Fruitsmaak (Reply) 17:15, 31 December 2006 (UTC)
  • Support. It is essential to disambig this. Comment - I think myocardial infarction is the most commonly understood meaning of heart attack.[4][5] If someone says... "I've had a heart attack", in my experience, it refers to a MI not a past episode of unstable angina. Nephron  T|C 19:36, 1 January 2007 (UTC)
Just like a "stroke" refers to a CVA and not a TIA? And yet, laypersons call TIAs "mini-strokes" or "pin strokes." And many people who experience TIA have microinfarcts on their CT scan. The line between UA and NSTEMI is not as clear as you make it out to be. I treat patients all the time who say they've had "small heart attacks." There's no way to know what they mean without looking at their medical chart. I understand the bias toward STEMI. It's sexier than UA/STEMI. But there's a good reason the ACS paradigm was invented. Any line you attempt to draw will be, in the last analysis, arbitrary. MoodyGroove 23:28, 1 January 2007 (UTC)MoodyGroove
Deciding whether a given patient has a MI or not isn't so arbitrary-- troponins are either considered positive or negative, an EKG either has ST elevation or it doesn't... the WHO criteria are either satisfied or they aren't.
That's not true. The WHO criteria is not that straight forward in clinical practice. What if only 2 of the 3 criteria are met? What if the chief complaint is new exertional dyspnea or acute pulmonary edema, there are T wave changes on serially obtained 12 lead ECGs, and the troponins are negative, or there's a small bump with a negative CK-MB? Forget about ST segment elevation. Most chest pain patients who present with ST segment elevation are not experiencing AMI (so that criteria is also not straight forward in clinical practice). Regardless, the issue at hand is the commonality between UA and NSTEMI. Actually, there is no issue at hand, since I support the current proposal. MoodyGroove 15:01, 3 January 2007 (UTC)MoodyGroove
On the topic of continuum vs. discrete... you're not going to convince me. A person with a fasting blood glucose of 6.6 mmol/L... isn't normal but they don't have DM. A person with a sodium of 134 mmol/L is hyponatremia... 135 isn't. The concept of threshold is all over medicine. As for what people call what... I think majority rules is the way to go--WP should NOT redefine terms. The lay terms are perfectly fine as long as one explains things along the way. Doctors don't talk to their patients in medical-speak. Nephron  T|C 06:38, 3 January 2007 (UTC)
Well, it doesn't seem arbitrary until you deal with these people on a daily basis. I have patients that tell me that they had a MI 10 years ago. I do an echo & a nuclear stress test and they are both absolutely normal. Records from the hospital state that his biomarkers (at the time, CPK/CPK-MB) were elevated during an episode of sepsis and ARF. Did he have an MI? Did he have an acute coronary syndrome? I told him I wasn't sure if he had a problem with his arteries at the time, but there is no evidence of infarction/dead heart muscle. I had a lady last month who developed a fairly large MI (EF went from 40-50 to 20-25) due to tachycardia causing ischemia without any acute coronary rupture. I told her she had an infarction/death of some heart muscle without any unstable plaque in the artery. (She had humongous collaterals from the apical LAD supplying a chronically occluded proximal RCA.) While I am sorry I can't convince you, that doesn't mean that you are correct. We are running into a language issue here because either are terms are not precise or we don't understand them sufficiently. Ksheka 13:04, 3 January 2007 (UTC)
It is well known that renal failure can cause a bump in the enzymes without there actually being any damage to the heart muscle. Thresholds have a place in medicine and they help guide treatment. Any case, I didn't say "...ignore the patient and treat the numbers" as you seem to suggest. A lab value doesn't necessarily drive treatment... but an abnormal value needs some explanation/rationalization why it is so. Nephron  T|C 01:24, 30 January 2007 (UTC)
  • Support. We are running into 2 problems. One is that the general belief for decades (even among cardiologists) is that coronary artery is a progressive disease; that coronary artery plaques gradually increase in size, with the lumen area (eventually) slowly becoming stenotic. Based on this belief, people could slowly (insidiously) develop exertional symptoms that slowly worsen with time as a "stable" angina. This is wrong. Coronary artery plaques rupture and heal all the time (without clinical sequelae), and the stenotic lesion is a lesion that has (possibly) ruptured and healed a number of times prior to causing symptoms. Under this model, the first symptoms are due to a plaque rupture event.
The second problem is the definition of unstable angina. I don't recall the exact numbers, but everyone with stable angina has had an episode of unstable angina. This is because the definition of unstable angina includes angina of recent onset. Given the plaque rupture model that I just described, it is obvious (but sometimes difficult to believe) that everyone with stable angina has had an acute coronary syndrome. Ksheka 00:28, 2 January 2007 (UTC)

[edit] Navigation Box

Would creating a navigation box help direct readers through the maze of related terms for pathology, symproms, diagnoses? As a outline (yes description need be summarised right down):
Atherosclortic cardiac disorder outline
(Conditions may have more than one cause) 
Pathology in arteries
 Atheroma - lump of inflammatory cells, lipids and connective tissue within artery walls
 Atherosclerosis - atheroma, underlying cholesterol crystals and calcification
 * Coronary heart disease (aka coronary artery disease) - disease (atherosclorisis or other) occuring in the heart
 * Ischaemic heart disease - reduced blood supply to the heart muscle.
Symptoms
 Angina pectoris - chest pain due to ischemia
 Acute coronary syndrome - clinical impression from history and examination, that pain may originate from the heart.
Clinical events
 Myocardial infarction (aka heart attack) - interruption to blood supply to part of heart.
 Cardiac Arrest -  abrupt stop of normal circulation due to failure of the heart

David Ruben Talk 03:27, 24 December 2006 (UTC)

[edit] MI = disease?

The intro says it's a disease, but is it not a clinical event? I admit it's kinda weird to call it a disease, but the term disease, although not clearly defined, is in my view a pathophysiological state with a known cause. There is no way of proving that it is or is not a disease, since the term "disease" is ill defined. But it's a convenient way to keep the intro simple.--Steven Fruitsmaak (Reply) 13:57, 25 December 2006 (UTC)

[edit] Some reverts

For the lead section, I'd like to refer to WP:LEAD:

  • Is MI a "clinical event" or a "disease"? Well, I think we should write for the average, 65-year-old reader who just suffered a MI and comes here to read the article: we need clarity, and writing for the average reader (cf. WP:MEDMOS). So, let's keep it simple. Similarly, I don't think we need to mention diaphoresis.
  • Someone should try to find a decent definition for "heart attack", a reference explaining what it encompasses besides MI.
  • I've re-added "a shorter education and lower income (particularly in women)" for clarity; that's what the referenced study showed.
  • For the average reader, I would explain "myocardial infarction" in the intro of the pathophysiology section.
  • In the intro, the details of therapy and diagnosis don't mather that much, imho: so no IV medication, 12 lead ECG, the addition of anticoagulants... Also I prefered the "break down of blood clots" for the average reader.

--Steven Fruitsmaak (Reply) 17:36, 24 December 2006 (UTC)

Like Einstein said, we should attempt to make things as simple as possible, but not more so. In my opinion, ACS (MI) is a clinical event that is a manifestation of CAD, which is a disease. Why must we underestimate the intelligence of the average 65 year old reader? 204.116.176.131 17:49, 24 December 2006 (UTC)MoodyGroove
I agree. Let's not underestimate the reader. If the reader has a problem with a word or phrase, it should be wikified to a new article. If we need a "simpler" version of the article for people that have trouble with the main text (Remember, ACS is a complex topic), we can direct them to the Simple English translation (which we should try to update at some point). Taken from the Simple English page, [...]if someone has trouble understanding a concept in complex English they can "fall back" to the Simple. I'm only half-joking here. We should make this article the best it can be. It's going to be technical. It's going to be long. It's going to be complex. (But hopefully only as complex as it has to be.) It's going to take a whlie to get correct. But we're doing great so far, and moving to ACS is just another step to making this article perfect.
Dumbing down the article is going to cause more problems than it solves. Just like you couldn't do the article and have it be called Heart attack, you are going to have to let the technical terms seep in. We should just make sure the first time they are introduced they have a short explaination (couple words) in the main article and (if possible) a link to another article with deeper explaination. Ksheka 19:37, 24 December 2006 (UTC)

I have to say that I completely disagree . Simple-wikipedia is a disgrace because it shows that wikipedia isn't fulfilling the need for an understandable encyclopedia. Don't make the most frequent mistake made by editors of medical articles: trying to write a medical textbook instead of writing for the Average Reader. And that's not synonymous with dumb, it just takes a great editor to explain a difficult concept to an average reader. Have you seen statistics of how much the Average Patient has understood of what the doctor tried to tell them???--Steven Fruitsmaak (Reply) 14:10, 25 December 2006 (UTC)

What does that prove, except that most doctors are not good communicators? MoodyGroove 15:19, 25 December 2006 (UTC)MoodyGroove
I've just made some changes in the intro, which per WP:LEAD is ment only to "ease the reader into the subject instead of being dropped into it". Jargon and technicalities should be tried to make accessable, that's all I'm saying.--Steven Fruitsmaak (Reply) 15:33, 25 December 2006 (UTC)
Just check out the article for DNA. A common word (A word that your grandparent probably has heard about) that has a fairly complex article. (69K long with 95 references) I like how the DNA article uses breakout sections of the form "Further information: xxx". We should use that eventually. Our challenge is that people are more likely to look for useful information under heart attack than under DNA. :-( Ksheka 16:14, 25 December 2006 (UTC)

[edit] Classification image

I've drawn a sketch to illustrate this paragraph... On Commons there is another version in German, probably better, which I've asked the author to translate. Please comment here so I can make improvements on this preliminary version, or remove if it contains big mistakes...--Steven Fruitsmaak (Reply) 15:23, 25 December 2006 (UTC)

I think it looks great! MoodyGroove 16:36, 25 December 2006 (UTC)MoodyGroove
Excellent! Ksheka 20:27, 25 December 2006 (UTC)
The alternative from the German version.--Steven Fruitsmaak (Reply) 12:43, 26 December 2006 (UTC)
I think the one you have posted to the main article is great. It's simple and accurate. It also shows that STEMI does not always develop Q waves. Conversely, it shows that NSTEMI sometimes does develop Q waves. The alternate example is confusing. It also seems to suggest that typical angina is a prerequisite for ACS. I like the original! MoodyGroove 14:46, 26 December 2006 (UTC)MoodyGroove

[edit] Sgarbossa's Criteria

Here is the reference: Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle branch block. N Engl J Med 1996;334:481-7. MoodyGroove 15:28, 25 December 2006 (UTC)MoodyGroove

Added to article. MoodyGroove 15:22, 26 December 2006 (UTC)MoodyGroove

[edit] Pathophysiology, Causes, Classification

I've noticed a lot of overlap between these sections. I'm wondering if they shouldn't be combined into one section that addresses all three topics. If we're going to keep the format the way it is, then it seems to me that we should make a conscious effort to separate the content a little more strictly. I'd like to hear comments, please. MoodyGroove 16:11, 27 December 2006 (UTC)MoodyGroove

I think we should make the effort because the three seem to be separate to me: the causes are atherosclerosis and some rare others which aren't mentioned yet, the pathophysiology is ischemia, remoddeling, wave front of necrosis, subendocardial and transmural... and the classification explains the whole Q-wave troponin ST-bussiness. Of course you need one to understand the other, but merging would lead to a very lenghty paragraph IMHO.--Steven Fruitsmaak (Reply) 20:22, 27 December 2006 (UTC)
Pathophysiology also includes disruption of atherosclerotic plaque (which is currently mentioned under Classificaiton -- perhaps it should be relocated to Pathophysiology). The other possible mechanism is spastic coronary vasospasm (which can also complicate thrombogenic AMI). Is there a need for a section called Causes? Classification is similar to Risk Stratification, and is difficult to separate from the ECG section. I think you're correct that Pathophysiology and Classification can remain separate. MoodyGroove 20:40, 27 December 2006 (UTC)MoodyGroove
Plaque rupture should indeed be under pathophysiology. A section on etiology (causes for the Average Reader) could contain rare causes of MI, such as spasms, systemic conditions such as Kawasaki's disease, syfilitic aortitis, mechanical trauma, aortic dissection, transplantationcoronaropathy... The idea of the classification section is to set out the different terms for the reader such as STEMI etc, basically explain the figure in that section; other content can be purged. That's why I also believe it should be moved higher up, as the first paragraph to create more context for the rest of the article.--Steven Fruitsmaak (Reply) 23:16, 27 December 2006 (UTC)
Take a look at my last edit and let me know what you think. I moved the first paragraph about ACS from Classification to Pathophysiology and wrote a new introduction to the Classification section with a discussion of risk stratification. I also eliminated some redundant text, and removed a request for references because I wanted to see how the formatting looked. I don't think there's going to be an issue with references between you, me, and Ksheka. MoodyGroove 00:29, 28 December 2006 (UTC)MoodyGroove
Looks good so far. I apologize for not being too active lately. Family issues around the Holidays. :-) Should be better in the next week or two. If you don't have it yet and have access to a Pfizer drug rep, I suggest you ask them for a copy of _Cardiovascular Trials Review_, an excellent book (small format, ~1400 pages) that just summarizes all cardiac trials and broken up into topics. I have to find my rep to get a newer copy. Mine is a few years old. :-) Ksheka 12:51, 28 December 2006 (UTC)
The bit about risk stratification was already mentioned in the prognosis section, so I'd like for it to be removed. The rest looks ok. I'll re-add the reference tags: I know they're annoying but it's a reminder, and I think this is top priority (as mentioned in the to do-box).--Steven Fruitsmaak (Reply) 17:56, 28 December 2006 (UTC)
I thought we were going to explain the pathophysiology more in the ACS article, so I've re-added {{main|Acute coronary syndrome}}. Of course a brief synopsis should be provided here, so I've readded a bit on atherosclerosis under pathophysiology. The explanation of STEMI - NSTEMI should, imho, be in the classification section, next to the scheme. It should be explained more there. Correct me if I misinterpreted something here.--Steven Fruitsmaak (Reply) 18:11, 28 December 2006 (UTC)

I must say, I'm not entirely pleased with the revert. I don't believe that risk stratification belongs at the bottom of the article under Prognosis. I'm also not sure the content has already been covered. Let's compare the two paragraphs in question:

Risk stratification has become the centerpiece of initial evaluation of patients with suspected acute myocardial infarction. Because urgent therapeutic decisions need to be made, the initial assessment must occur rapidly. Currently guidelines recommend that the intial 12 lead ECG be read within 10 minutes of the patient's arrival in the emergency department. A number of factors are considered, including the nature of the chief complaint, the presence or absence of ST segment elevation, ST segment depression or T wave inversion, the patient's age, a history of diabetes, prior revascularization, the presence or absence of congestive heart failure, and serial blood tests to determine if the cardiac biomarkers are elevated, particularly Troponin I or Troponin T.

Now let's look at the Prognosis section at the bottom of the article:

The prognosis for patients with myocardial infarction varies greatly, depending on the patient, the condition itself and the given treatment. Using simple variables which are immediately available in the emergency room, patients with a higher risk of adverse outcome can be identified. For example, one study found that 0.4% of patients with a low risk profile had died after 90 days, whereas the mortality rate in high risk patients was 21.1%.[118] Although studies differ in the identified variables, some of the more reproduced risk stratifiers include age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine concentration, peripheral vascular disease and elevation of cardiac markers.[118][119][120] Assesment of left ventricular ejection fraction may increase the predictive power of some risk stratification models.[121] The prognostic importance of Q-waves is debated.[122] Prognosis is significantly worsened if a mechanical complication (papillary muscle rupture, myocardial free wall rupture, and so on) were to occur.[citation needed]

The risk statification I'm referring to happens immediately on the patient's arrival, and guides therapy. It may be possible to predict mortality rates based on this information, but the most important aspect is to determine whether or not the patient is a candidate for immediate reperfusion therapy. Perhaps risk statification needs its own heading above Classification, but if not, in my opinion it belongs more to Classificaiton than Prognosis. MoodyGroove 15:14, 29 December 2006 (UTC)MoodyGroove

In my opinion, classification is ment to "Describe the varieties of the condition, and explain how they are differentiated." In a way, stratification could be interpreted like that, but my natural feeling is that it's more about prognosis: the prognosis guides the therapy. The sections are clearly not identical but there was considerable overlap. I suggest moving the prognosis section higher up, before treatment, and then explaining the prognosis of each treatment under their heading. The main difference between your version and mine seems to be the emphasis on the fact that it guides therapy: this could be added to the current paragraph, and it would be very logical to put it before treatment, no?--Steven Fruitsmaak (Reply) 17:26, 29 December 2006 (UTC)
There's no doubt that risk stratification directly influences the prognosis. Hence the emphasis on evidence based guidelines, so that optimal care is delivered to the correct subsets of patients. If mistakes are made during risk stratification, and there is a delay in therapy, or the wrong therapy is delivered, then the prognosis becomes worse. In other words, I don't necessarily agree that the prognosis guides the therapy. Rather, the therapy (or lack of therapy) alters the prognosis, for better or for worse.
I think of it like this: Chief complaint suggestive of ACS > Risk stratification > Therapy > Prognosis. MoodyGroove 18:06, 29 December 2006 (UTC)MoodyGroove

[edit] Prognosis section rewrite

I've added somewhat to this section, but I mostly found info on risk stratification... Could anyone provide prognostic information after specific therapeutic interventions, e.g. after reperfusion, CABG, ... ?--Steven Fruitsmaak (Reply) 23:18, 27 December 2006 (UTC)

[edit] Ventricular Tachycardia

I recognized this scanned image from another website. It came from here: http://www.emedu.org/ecg/images/wide_3a.jpg. Do we know for a fact that the image isn't copyrighted? MoodyGroove 13:09, 28 December 2006 (UTC)MoodyGroove

I've certainly got good EKGs of VT. I'll scan one in in the next couple of days. I should probably replace (overwrite) the image that is already in wikipedia, right? Ksheka 13:14, 28 December 2006 (UTC)
Seems that way to me, Ksheka! But then I haven't been around very long! :) MoodyGroove 14:58, 28 December 2006 (UTC)MoodyGroove
I don't think it's actually really necessary to have a VT image in this article...--Steven Fruitsmaak (Reply) 17:57, 28 December 2006 (UTC)
Not sure myself if it is necessary. The more pictures, the better however. ;-) Anyway, I uploaded a new image so we are okay for now. When I find one in color I will overwrite the black-and-white one. (My teaching EKGs are all photocopies.) Ksheka 02:53, 29 December 2006 (UTC)
Too much of a good thing can be bad too, however.--Steven Fruitsmaak (Reply) 17:26, 29 December 2006 (UTC)

[edit] Emergency Services

I totally rewrote this section. I may need some help formatting the references. I'm guessing that some of you may not appreciate the hyperlink to the ACC's D2B Initiative (only because I don't see any other hyperlinks throughout the article) but it's the cutting edge of what's happening, and I think it deserves an explanation. Can anyone provide some guidance on this? Steven? Ksheka? MoodyGroove 03:18, 6 January 2007 (UTC)MoodyGroove

I solved the issue by creating a new article for door to balloon and placing the external link to the ACC's D2B page there. MoodyGroove 15:03, 6 January 2007 (UTC)MoodyGroove

[edit] Beta blockers?

What about beta-blockers? I don't see them listed under "First-line treatment", or mentioned until "Secondary prevention" - but at least the last time I was in the ER or CCU, beta-blockers were usually given shortly after arrival (in fact, the mnemonic was amended to B-MOAN), and there is mortality data supporting it. I'm assuming this is still the case - should we add beta-blocker administration to the first-line remedies? MastCell 17:33, 7 March 2007 (UTC)

I think it's one of the first drugs to start, but not in the emergency situation... would need to look it up.--Steven Fruitsmaak (Reply) 16:34, 8 March 2007(UTC)
I added beta blockers and heparin and (possibly) plavix under first line and made it somewhat clear that they are usually not administered by first responders.Ksheka 12:12, 13 March 2007 (UTC)


[edit] Prognostic indicators

"Loss of consciousness and even sudden death can occur in myocardial infarctions and are poor prognostic indicators."

I had a double take reading that line. Yes, loss of consciousness is probably a bad prognostic indicators, but saying that death is a poor prognostic indicator seems a little silly. "Oh, you've died. That doesn't mean you're having a heart..." -72.77.65.81 08:29, 17 March 2007 (UTC)

Hmmm... Not sure about that. (Someone please correct me if I am wrong, I may be a little out of my field on this one) The problem is, sudden cardiac death is a medical term that includes an arrhythmic cause for the heart to stop pumping (generally ventricular fibrillation). There are a number of sudden cardiac death survivers that make it to the hospital. If they develop anoxic brain damage, they likely won't make it out alive. The ones that were resuscitated right away and don't have any brain damage will generally do better so long as a defibrillator is implanted prior to discharge from the hospital. Ksheka 11:17, 18 March 2007 (UTC)

[edit] References

  1. ^ Hayward RA, Hofer TP, Vijan S. "Narrative review: lack of evidence for recommended low-density lipoprotein treatment targets: a solvable problem." Ann Intern Med 2006;145(7):520-30. PMID 17015870
  2. ^ Ray KK, Cannon CP. "The potential relevance of the multiple lipid-independent (pleiotropic) effects of statins in the management of acute coronary syndromes." J Am Coll Cardiol 2005;46(8):1425-33. PMID 16226165
  3. ^ Topol EJ at al. Acute Coronary Syndromes. p. 135. New York: Marcel Dekker, 2001. ISBN 0-8247-0416-9.
  4. ^ Cannon CP at al. Management of Acute Coronary Syndromes. p. 3. New Jersey: Humana Press, 1999. ISBN 0-89603-552-2.
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