Hello Vivek - this is an area I work in extensively and am happy to help - so feel free to ask question either publicly or privately.

A couple of initial comments:

TIMI, GRACE, Goldman were Not developed to rule-out ACS in the ED (ie not "fit for purpose").  Having said that, we ran the first RCT in this field in which we tested TIMI against standard practice  - the so called ADAPT protocol(see link).  It was both safe and enabled ruling out more patients.

We then developed a fit for purpose score, EDACS.  We compared this to TIMI in another RCT (see attached).  Also safe.  We are not ruling out about 1/3rd of patients in the ED.  In the past two years nearly all of Queensland Australia is using ADAPT, and all of New Zealand is using EDACS or ADAPT.  I can provide you with examples of the pathway documentation if you want.

Of the others you mentioned, HEART is also "fit for purpose".  The main difference between HEART and EDACS is that the scoring has a more subjective element (clinician estimate of the likelihood of ACS) and was developed differently.  Having said that, in most studies it seems to perform reasonably well.

With respect to the qualitative troponins.  The ADAPT pathway came out of an investigation using point of care testing (the ASPECT study -see link). An Indian hospital (Medanta—The Medicity, Gurgaon) was part of the ASPECT study.  

Could you give some more details about the analytical characteristics of the troponin kits you are using?  (especially above what concentration does it show "positive"?).  

As I said, happy to help more.

All the best

John

http://archinte.jamanetwork.com/article.aspx?articleid=1748796&resultclick=1

Article Effectiveness of EDACS Versus ADAPT Accelerated Diagnostic P...

Thank you ! John for you inputs. I appreciate your extensive work and interest in this area. I am sure you would be able to guide me in this.

Troponin kits usually diagnose above 100 ng/L.

Problem in our hospitals is false negative results due to use of qualitative kits. Patients may get discharged based upon negative results of troponin kits especially when ECG changes are not significant.

Hello Vivek

100 is quite high, and as you say, difficult to rule-out. Having said that, we are trialling the EDACS pathway with a POC troponin (I think with a minimum threshold of ~30) to see if it can be safely used.  

Do you know your current false negative rates (eg from people being readmitted within, say, 30 days with an MI)?

You could run an observational study with EDACS or another score to find a threshold below which with a negative ECG and negative troponin you have a low false negative rate.  

ps attached is the protocol currently in use in our hospital.

Hello John

Thank you for sharing the Chest pain pathway of your hospital.

Looks like a nice pathway.

We have availability of CK-MB quantitative levels. It is quite cheap almost 10% the cost of qualitative troponins and 5% the cost of Quantitative troponins. What is your experience of CK-MB levels. I have not seen any of the scores using CK-MB now. What cut-off shall we use if we want to have a pathway based upon CK-MB.

Hello Vivek,  

That's a good question.  As I do the biostats for this kind of research, I may be able to find some old data and try and work something out from our data (it may take a while).  However, I am not sure what the clinical consequences of using CKMB instead of a qualitative trop would be - I'll talk with some of my clinical colleagues.  Have a look too at the ASPECT study.  

John

 Hello John,

I found this article that says why CK-MB is not as good as Troponin

http://clinchem.aaccjnls.org/content/49/8/1331.long#T1

Some reasons are the Gender differences in CKMB. Since some CKMB comes from muscles in normal people, it depends upon the total muscle mass in individuals and so 99th percentile for cutoff is twice as high in males as compared to females. This has to bee taken care of by us.This does not happen with Troponins. I think if we take care of this fact and use separate cutoff levels for males and females, we should be able to use CKMB in our setting in place of Troponins.

I am trying to get some more info on CKMB levels in males and females that we can put into the pathways.

I am also not sure whether damage to heart will cause equal rise irrespective of gender, which should be the case.

So, when there is MI, the rise in CKMB levels should be equal in males and females. In my opinion we cannot score based upon the multiples of 99th percentile in case of CKMB in becasuse in males CKMB 99th percentile is already twice as high as in females. We need to have definite levels above which we would give 2 score, 1 score or 0 score separately for males and females.

What do you say?

Hello Vivek, I don't know a lot about CKMB, but will look at our data for you and will consider sex-specific thresholds.  This may take a some time.

I do know that troponin is a better assay - but for rule-out you need to be able to measure reasonably accurately down to at least the 99th percentile (and it sounds to me the qualitative troponin you have has a minimum threshold much greater than that).

Hello John,

I have a question regarding the protocol you are using currently using POC in your hospital.

Are you using single troponin or 0,2 hr trop using POC?

As I see in the protocol shared by you, you are doing only single trop to classify them into low risk, whereas the publication of EDACS-ADP used 0,2 hour trops to classify low risk.

I am a little confused. Please clarify.

HI John,

I want to ask on what basis you have developed disposition pathway for intermediate risk on EDACS 16-21?

low risk < 16 is clear.

but for 16-21 is discharging them okay? What is the evidence for this as in HEART score we admit intermediate risk.

Can you please share the evidence on the basis of which you have developed disposition pathway for intermediate risk?

Regards

Vivek

Hello Vivek - very good question.  Indeed, I have often asked clinical colleagues, particularly cardiologists this qn.  The answer is "it depends".  It seems to depend on the capacity and willingness of the cardiology department (which isn't always in the same hospital) to admit "false positives" for further observation/investigation.

In Christchurch, we chose EDACS 21 (or ECG with evidence of ischaemia or hs-cTnI>99th) to assign to the high-risk stream on the basis that if all were admitted to cardiology it would have about the no more (actually a few less) and similar or better PPV as prior to the implementation of the pathway.  

The intermediate patients

Hi John,

Thankyou for a quick reply.

Do you know what protocol was used for intermediate score in the EDACS ADP 2 hour rule out study?

Regards

Vivek

Yes

Intermediate was Modified TIMI =4 (Low being either EDACS

Thankyou John

Do you think HEART score is still relevant for low risk?

The T component says troponins X 2 and X 3 times and still patient can be low risk.

The 3rd universal definition says any troponin above 99th percentile with chest pain and ECG changes is MI.

So, In absence of ECG changes do we label a patient of atypical chest pain with trops X 3 times and all other risk factors normal with a HEART score of 2 as low risk.

I think the original HEART score with troponins as part of the score is a problem. I think it would be unlikely that many ED physicians would think of someone with a raised troponin as low-risk even if all other components are low.  

Much the same could be said for the ECG component of the HEART score.

However, I've noticed that a modified version of the HEART score without the troponin component is being used.  Eg Simon Mahler used a HEART pathway in which Low risk was HEART score

Addition of 0,3 hours Troponin tells that HEART is problematic. I don't think that you can modify HEART by adding 0,3 hour trops because Trop iis an integral component of HEART score on which this scoring was validated.