troponins, CHF, MI, and cocaine question

[duckie99]

So I have a question that I cannot seem to find a good answer to (and maybe there isn't one...).

Essentially, a 58 yo homeless patient with a very recent positive NM exercise stress test (two new 10% reversible defects in both anterior and lateral myocardium), hx of DM, HTN, DL, CHF stage II/III (previously said to have NICM, EF <20%), poor medical compliance and cocaine abuse comes in with CP and ADCHF. Guy gave a good history for ACS and was found to have elevated toponin-I of 0.13 ng/l initially that rose to 0.15 ng/l (CPK-MB went from 8.5 to 10.5) 4 hours later with what was thought to be some dynamic T-wave changes on ECG. He also is in ADCHF with BNP >2000 and some volume overload on exam and CXR. Finally, he did cocaine 2 days prior and then 1 day later the CP started... Cardiology didn't want to cath him a few weeks earlier because they were afraid to put stents in a guy who would not take his meds; they noted he could have progression of CAD though. A previous cath a few years ago showed luminal irregularities.

And so my thought was that this presentation is most definitely an NSTEMI from whatever the cause be it cocaine, new plaque rupture, etc and needs a cath, ideally. However the medicine team said that the troponin results were "negative" and that this is cocaine-induced CP/ demand ischemia and not an MI. The pt's chronic seeming troponin levels are around 0.08-0.09 or so and they weren't impressed with the increases (they assumed these increases happen in CHF exacerbations). btw I was on the emergency medicine team who admitted the guy.

I'm just confused as to when a MI could be classified in a guy like this? His troponins and CPK-MBs both rose, he is high risk from stress test, old ischemic changes on ECG, his history was good, etc... So when do you blow off troponin increases as just being from "demand ischemia" or from cocaine? How high would troponins go in ADCHF and would they change acutely like in this guy? I'm basically just having trouble following the medicine team's thought process (no cards notes). Would greatly appreciate any insight.

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[ArkansasHogMD]

So I have a question that I cannot seem to find a good answer to (and maybe there isn't one...).

Essentially, a 58 yo homeless patient with a very recent positive NM exercise stress test (two new 10% reversible defects in both anterior and lateral myocardium), hx of DM, HTN, DL, CHF stage II/III (previously said to have NICM, EF <20%), poor medical compliance and cocaine abuse comes in with CP and ADCHF. Guy gave a good history for ACS and was found to have elevated toponin-I of 0.13 ng/l initially that rose to 0.15 ng/l (CPK-MB went from 8.5 to 10.5) 4 hours later with what was thought to be some dynamic T-wave changes on ECG. He also is in ADCHF with BNP >2000 and some volume overload on exam and CXR. Finally, he did cocaine 2 days prior and then 1 day later the CP started... Cardiology didn't want to cath him a few weeks earlier because they were afraid to put stents in a guy who would not take his meds; they noted he could have progression of CAD though. A previous cath a few years ago showed luminal irregularities.

And so my thought was that this presentation is most definitely an NSTEMI from whatever the cause be it cocaine, new plaque rupture, etc and needs a cath, ideally. However the medicine team said that the troponin results were "negative" and that this is cocaine-induced CP/ demand ischemia and not an MI. The pt's chronic seeming troponin levels are around 0.08-0.09 or so and they weren't impressed with the increases (they assumed these increases happen in CHF exacerbations). btw I was on the emergency medicine team who admitted the guy.

I'm just confused as to when a MI could be classified in a guy like this? His troponins and CPK-MBs both rose, he is high risk from stress test, old ischemic changes on ECG, his history was good, etc... So when do you blow off troponin increases as just being from "demand ischemia" or from cocaine? How high would troponins go in ADCHF and would they change acutely like in this guy? I'm basically just having trouble following the medicine team's thought process (no cards notes). Would greatly appreciate any insight.

It sounds like this guy had whats referred to as a Type II myocardial infarction. It is basically demand ischemia as a result of hypotension, anemia, spasm (cocaine), etc. and not a primary event such as a plaque rupture (type I MI). He most likely was experiencing a subendocardial ischemia and not transmural given the lack ot ST changes and the lack of huge troponin bump. See this article.

http://www.ncbi.nlm.nih.gov/pubmed/22745356

 

[duckie99]

It sounds like this guy had whats referred to as a Type II myocardial infarction. It is basically demand ischemia as a result of hypotension, anemia, spasm (cocaine), etc. and not a primary event such as a plaque rupture (type I MI). He most likely was experiencing a subendocardial ischemia and not transmural given the lack ot ST changes and the lack of huge troponin bump. See this article.

http://www.ncbi.nlm.nih.gov/pubmed/22745356

Great article. Thanks for it. I do understand that they are assuming a type II MI in this situation. I just disagree. The reason I do is because they, for some reason, still consider this guy to have a NICM while he had a recent positive stress test which should be diagnostic of CAD.

The article you posted says:
In the context of an acute HF syndrome, the coronary artery anatomy may often be well known; such knowledge may be leveraged to interpret abnormal troponin results; if normal coronaries are present, either a Type II event or a non-coronary mechanism for troponin release may be invoked. On the other hand, when the coronary anatomy is not established, the recognition of myocardial necrosis reflected in a troponin value about the 99th percentile alone is not sufficient to make a diagnosis of acute MI due to coronary artery disease, nor is it able to identify the mechanism for the abnormal troponin value (i.e. Type I vs. Type II vs. non-coronary); in this context, clinicians are thus advised to consider troponin values above the 99th percentile in a patient with an acute HF syndrome indicative of myocardial necrosis, but a troponin value above the 99th percentile is not necessarily diagnostic of MI, without supportive evidence as above.7,11 In this setting, further information (such as myocardial perfusion studies or coronary angiography as well as haemodynamic assessment) is often required to better understand whether a Type I MI, Type II MI, or non-coronary cause for abnormal troponin values is present. In many cases, it may be difficult to establish the reason for troponin abnormalities, even after such investigations.

So in this case I would say that his troponin increase was likely a type I MI that lead to his ADCHF (other supporting factors include: positive stress test, rising troponins and MBs, dynamic T-wave changes in ECG, pmhx, high risk patient, and his story fit so dang well). I say it isn't a type II because he the stress test is diagnostic of CAD. Also, he did not appear that volume overloaded on exam. It wasn't like he was a young guy with few other risk factors I guess is my point. Sure it could be type II but you wouldn't know without a cath and this guy I feel warrants one.

However the treatment is the same for this guy whether it is type I or II since he would not be a candidate for a stent so really there's no point in doing a cath to prove either way. But yeah a good article I will hold on to.

I will also add that a cardiologist told me once that you could ask 5 different cardiologists and get 5 different opinions. So because this particular patient is such a muddled mess it's a tough call I guess. I think if he was medically compliant he would be taken to the cath lab for sure. But his social situation precludes it unfortunately.

 

[glorfindel]

What did the emergency medicine team think?

What did the medicine team do with him?

How come no cardiology notes?

I'm not too impressed by the troponins either, but the whole clinical picture as you paint it is strongly suggestive of acute MI -- at least you don't report anyone suggesting that he be sent home from the ER.

You say he gave a good story for ACS, so I'm assuming chest pain for this guy wasn't a daily thing. Pain onset a day after doing cocaine makes it unlikely that this pain is due to acute cocaine use. His troponins aren't up much, but they're up in the setting of (presumably new) chest pain and clear chf on exam (as you note and are worried about). He probably had a small MI independent of acute cocaine (unless he's lying which would not shock me), which led to his chf exacerbation.

Bottom line for me: I would not blow off his troponins; I think he did have an acute ischemic event; I would consult interventional cardiology re: cath lab. Let them decide.

 

[glorfindel]

btw, I've never in my experience had cardiology refuse to cath a 50s male because he was homeless or had been noncompliant.

Refuse to transplant his liver, sure, but never refuse to cath.

 

[ArkansasHogMD]

Great article. Thanks for it. I do understand that they are assuming a type II MI in this situation. I just disagree. The reason I do is because they, for some reason, still consider this guy to have a NICM while he had a recent positive stress test which should be diagnostic of CAD.

The article you posted says:
In the context of an acute HF syndrome, the coronary artery anatomy may often be well known; such knowledge may be leveraged to interpret abnormal troponin results; if normal coronaries are present, either a Type II event or a non-coronary mechanism for troponin release may be invoked. On the other hand, when the coronary anatomy is not established, the recognition of myocardial necrosis reflected in a troponin value about the 99th percentile alone is not sufficient to make a diagnosis of acute MI due to coronary artery disease, nor is it able to identify the mechanism for the abnormal troponin value (i.e. Type I vs. Type II vs. non-coronary); in this context, clinicians are thus advised to consider troponin values above the 99th percentile in a patient with an acute HF syndrome indicative of myocardial necrosis, but a troponin value above the 99th percentile is not necessarily diagnostic of MI, without supportive evidence as above.7,11 In this setting, further information (such as myocardial perfusion studies or coronary angiography as well as haemodynamic assessment) is often required to better understand whether a Type I MI, Type II MI, or non-coronary cause for abnormal troponin values is present. In many cases, it may be difficult to establish the reason for troponin abnormalities, even after such investigations.

So in this case I would say that his troponin increase was likely a type I MI that lead to his ADCHF (other supporting factors include: positive stress test, rising troponins and MBs, dynamic T-wave changes in ECG, pmhx, high risk patient, and his story fit so dang well). I say it isn't a type II because he the stress test is diagnostic of CAD. Also, he did not appear that volume overloaded on exam. It wasn't like he was a young guy with few other risk factors I guess is my point. Sure it could be type II but you wouldn't know without a cath and this guy I feel warrants one.

However the treatment is the same for this guy whether it is type I or II since he would not be a candidate for a stent so really there's no point in doing a cath to prove either way. But yeah a good article I will hold on to.

I will also add that a cardiologist told me once that you could ask 5 different cardiologists and get 5 different opinions. So because this particular patient is such a muddled mess it's a tough call I guess. I think if he was medically compliant he would be taken to the cath lab for sure. But his social situation precludes it unfortunately.

I agree he probably does need a cath but what happens if he gets a stent and doesn't take his plavix. He's at high risk for non compliance. His stress test is diagnostic for CAD but that isn't necessarily the cause of his troponin bump. There could be two separate pathological processes here. He probably has NICM has a result of Etoh abuse, cocaine, thyroid dysfunction, idiopathic, etc, CAD which is complicated by his cocaine use. Since he already has stenosis inducing coronary spasm on top of that probably led to subendocardial ischemia (hence no STEMI) and the small troponin increase. It seems like the inciting event was the spasm not an unstable plaque (NSTEMI) so I still think this is type II. But you are right different cardiologists will have different opinions. If he were to get a stent I think BM would be the way to go since plavix is only necessary for one month.

 

[duckie99]

What did the emergency medicine team think?

They agreed with me that is as an acute ischemic event. We started a heparin drip but the medicine team stopped it. What actually bugs me the most is that they blew off his troponins and stopped the drip without even talking to the patient (they just did it off what we told them).

What did the medicine team do with him?

He was admitted, restarted back on maximal medical therapy, informed to remain compliant, and told to stop using cocaine (all the proper drug services consulted and such I hope). I am not sure where exactly he is right now but I assume they are continuing diuresis until he is stable to leave.

How come no cardiology notes?

I do not think they were consulted or perhaps just gave an opinion to the medicine team over the phone because the last time I checked there were no cards notes (a couple days after we admitted him). The EM resident told me that the medicine team would deal with who to consult beyond the ED because we admitted him within a matter of hours after he was seen. He was pretty stable in the ED.

Previous cardiology notes from his prior admission sounded equivocal on his current condition of whether this guy developed CAD (this was only a couple weeks prior to his new admission and before his stress test).

I'm not too impressed by the troponins either, but the whole clinical picture as you paint it is strongly suggestive of acute MI -- at least you don't report anyone suggesting that he be sent home from the ER. [lol I'd hope not]

You say he gave a good story for ACS, so I'm assuming chest pain for this guy wasn't a daily thing. [correct, CP is not a daily thing for him] Pain onset a day after doing cocaine makes it unlikely that this pain is due to acute cocaine use. [good to know. I always thought the onset of CP after cocaine was a lot sooner after use as well (unless he lied, but imo he did admit to using it before so I don't see why he would have lied...] His troponins aren't up much, but they're up in the setting of (presumably new) chest pain and clear chf on exam (as you note and are worried about). He probably had a small MI independent of acute cocaine (unless he's lying which would not shock me), which led to his chf exacerbation.

Bottom line for me: I would not blow off his troponins; I think he did have an acute ischemic event; I would consult interventional cardiology re: cath lab. Let them decide.

yeah, I wanted to consult cardiology in the ED but as I noted above the EM resident said he'd leave it up to medicine because that is just how they typically do things there (I do not necessarily agree but, hey, I have no power as a student).

btw, I've never in my experience had cardiology refuse to cath a 50s male because he was homeless or had been noncompliant.

From my understanding, I think their reasoning was that potentially stenting a patient who would be noncompliant with anti-platelet/coag therapy would be put him at high risk for thrombosis/future large area MIs. And so I wouldn't say that cardiology was "refusing" but just weren't too keen on doing one. I'm not sure of guidelines and research regarding these types of situations. I'm just trying to report prior admission notes.

thanks for the reply btw

 

[Mobitz3]

If he has a couple 10% areas of reversible ischemia on a nuclear test, thats probably not going to account for his EF<20%.

Troponins are too low to be an acute plaque rupture. Likely just due to heart failure exacerbation.

First do no harm. I agree with cards management.

 

[Instatewaiter]

btw, I've never in my experience had cardiology refuse to cath a 50s male because he was homeless or had been noncompliant.

Refuse to transplant his liver, sure, but never refuse to cath.

If you have a wholly non-compliant patient you are going to do more harm putting in a stent. He'll surely have a STEMI when he stops his aspirin and plavix.

You have a guy with a positive stress test (2 if you consider he has a postiive troponin from some heart failure) and a guy who's not going to take his plavix, how is a cath going to change your management and why would you put him through the risk of a cath if you're not going to do anything with the information. If you just want the diagnosis of CAD, why not do a CT angio?

My take on the case without ever seeing him is that he has an essentially flat trop bump from heart failure (demand). It is incredibly common. The increased wall tension causes more demand and the increased wall tension can decrease the diastolic flow through the coronaries (less supply).

Seems to me the medicine mgmt was appropriate.

 

[badasshairday]

My take on the case without ever seeing him is that he has an essentially flat trop bump from heart failure (demand). It is incredibly common. The increased wall tension causes more demand and the increased wall tension can decrease the diastolic flow through the coronaries (less supply).

Seems to me the medicine mgmt was appropriate.

I agree. The troponin is not impressive at all. I see a lion's share of cocaine chest pain (as well as cocaine induced cardiomyopathy) at my hospital. Those trops are common in heart failure as well as severe HTN episodes.. and cocaine vasospasm.

Likely the patient is lying about his last use. I have had patients admit to using cocaine weeks ago, but later have a positive cocaine screen. Or they initially lie then come clean. Sure he can have CAD, he is high risk for it, but the story is more consistant with demand from heart failure and additionally cocaine induced vasospasm. As it also sounds like he has cardiomyopathy from cocaine.

Now it is entirely possible he can have acute plaque rupture from the cocaine induced vasospasm. But the story as well as lab values seem more related to cocaine and acute heart failure exacerbation from it.

You said he had a cath in the past, how long ago was it? Also when was the nuclear stress?

If you want to learn more about cocaine chest pain, this is a really nice article in Circulation.

http://circ.ahajournals.org/content/117/14/1897.long

 

[duckie99]

If you have a wholly non-compliant patient you are going to do more harm putting in a stent. He'll surely have a STEMI when he stops his aspirin and plavix.

You have a guy with a positive stress test (2 if you consider he has a postiive troponin from some heart failure) and a guy who's not going to take his plavix, how is a cath going to change your management and why would you put him through the risk of a cath if you're not going to do anything with the information. If you just want the diagnosis of CAD, why not do a CT angio?

My take on the case without ever seeing him is that he has an essentially flat trop bump from heart failure (demand). It is incredibly common. The increased wall tension causes more demand and the increased wall tension can decrease the diastolic flow through the coronaries (less supply).

Seems to me the medicine mgmt was appropriate.

I agree. The troponin is not impressive at all. I see a lion's share of cocaine chest pain (as well as cocaine induced cardiomyopathy) at my hospital. Those trops are common in heart failure as well as severe HTN episodes.. and cocaine vasospasm.

Likely the patient is lying about his last use. I have had patients admit to using cocaine weeks ago, but later have a positive cocaine screen. Or they initially lie then come clean. Sure he can have CAD, he is high risk for it, but the story is more consistant with demand from heart failure and additionally cocaine induced vasospasm. As it also sounds like he has cardiomyopathy from cocaine.

Now it is entirely possible he can have acute plaque rupture from the cocaine induced vasospasm. But the story as well as lab values seem more related to cocaine and acute heart failure exacerbation from it.

You said he had a cath in the past, how long ago was it? Also when was the nuclear stress?

If you want to learn more about cocaine chest pain, this is a really nice article in Circulation.

http://circ.ahajournals.org/content/117/14/1897.long

So to update the patient was discharged after a couple days. He was not really diuresed as there apparently wasn't that much volume overload (neither by cxr or exam - I know I had said he was here for ADCHF but he didn't really look it; the only thing was his BNP level). I understand it's difficult to present this guy to you all here since I wasn't even apart of the team caring for on the floor but I do appreciate all the responses!

The rise in troponin was just attributed to cocaine. His UDS was positive meaning (from the article) he did cocaine within 48-72 hours which was consistent with what he told me. I just disagree this troponin bump was from vasospasm...

reasons: 1. his troponins when he came in almost doubled from the "baseline" we had available - note that his baseline is 0.08 which on the assay this hospital uses is the cutoff for being "elevated"; 2. his troponins were rising in the first few hours; 3. His stress test, which was 1 week prior to admission, showed two new reversible defects of 10% (which is the cutoff for cardiologists I worked with once for cathing a patient); 4. his bnp was elevated but he was not volume overloaded; 5. his last cath was in 2010 which didn't show an significant blockages; 6. he had dynamic T wave changes on ecg (I understand this is nonspecific but they were present regardless); 7. He was a high risk patient who wasn't that young and had a lot of medical comorbidities confounding the picture including DM, which should lower your threshold for cathing a patient since they can present differently

my treatment plan would have been the same... I say that because, as instatewaiter pointed out, he isn't really a candidate for a stent due to his noncompliance. I just think if that wasn't the case THEN he should be cathed or at least deserves one as I would not blow off the troponins. The very least I would have called cardiology. So for this guy as is I don't disagree with the treatment but with the final diagnosis is all. It could be demand ischemia from his cocaine... or it could have been a small plaque rupture, I think it's kinda hard to tell. In any case his troponins show his heart was damaged.

Anyway thanks for the good articles. I am going to keep them and study them up as this type of stuff seems to be pretty common unfortunately, and since I matched internal med I'm going to be dealing with it lol. I guess the point from the articles I gather is the cocaine-associated chest can be ACS but not necessarily... and it seems to be hard dx but cardiac biomarkers are the best choice.

 

[Trifling Jester]

So I have a question that I cannot seem to find a good answer to (and maybe there isn't one...).

Essentially, a 58 yo homeless patient with a very recent positive NM exercise stress test (two new 10% reversible defects in both anterior and lateral myocardium), hx of DM, HTN, DL, CHF stage II/III (previously said to have NICM, EF <20%), poor medical compliance and cocaine abuse comes in with CP and ADCHF. Guy gave a good history for ACS and was found to have elevated toponin-I of 0.13 ng/l initially that rose to 0.15 ng/l (CPK-MB went from 8.5 to 10.5) 4 hours later with what was thought to be some dynamic T-wave changes on ECG. He also is in ADCHF with BNP >2000 and some volume overload on exam and CXR. Finally, he did cocaine 2 days prior and then 1 day later the CP started... Cardiology didn't want to cath him a few weeks earlier because they were afraid to put stents in a guy who would not take his meds; they noted he could have progression of CAD though. A previous cath a few years ago showed luminal irregularities.

And so my thought was that this presentation is most definitely an NSTEMI from whatever the cause be it cocaine, new plaque rupture, etc and needs a cath, ideally. However the medicine team said that the troponin results were "negative" and that this is cocaine-induced CP/ demand ischemia and not an MI. The pt's chronic seeming troponin levels are around 0.08-0.09 or so and they weren't impressed with the increases (they assumed these increases happen in CHF exacerbations). btw I was on the emergency medicine team who admitted the guy.

I'm just confused as to when a MI could be classified in a guy like this? His troponins and CPK-MBs both rose, he is high risk from stress test, old ischemic changes on ECG, his history was good, etc... So when do you blow off troponin increases as just being from "demand ischemia" or from cocaine? How high would troponins go in ADCHF and would they change acutely like in this guy? I'm basically just having trouble following the medicine team's thought process (no cards notes). Would greatly appreciate any insight.

A few thoughts...

I don't know if I'd classify a 10% reversible defect as a high risk stress test, or even necessarily positive - that actually seems like kind of a strange thing to put on a report. Nucs are tricky, and from what I've seen very interpreter dependent. In my experience radiology calls almost everything positive. A cardiology read is more likely to be read as negative, or have its defects attributed to diaphragmattic/breast attenuation etc. (This may be region specific though) It would be useful to know how far he walked too.

If I was seeing the patient I might blow off the troponins given his heart failure exacerbation, depending on how I felt after I saw the patient.

If he's volume overloaded from his heart failure I don't think he should go to the lab prior to diuresis, unless he's having real chest pain, or is hemodynamically or electrically unstable.

If he's known to be medically noncompliant you really aren't doing him any favors by rushing him off to the lab (given his known history... it'd be different for a different patient, I don't want you to think that medically noncompliant patients never get stents, it depends on the clinical picture). But for this guy he's at high risk to close off his stent when he doesn't take his plavix, and I don't see a big benefit for him in going to the lab. There's nothing wrong with medical management, monitoring for any arrhythmias, and diuresing him.

Just my two cents.