Thursday, July 14, 2011

Should we activate the cath lab if the STEMI is spontaneously reperfused?

Will be on vacation until August.  Last post until then!

I received a question yesterday: "If spontaneous reperfusion (or aspirin/nitro assisted reperfusion) occurs, why is it so important to rush for reperfusion therapy?"  This is a very good question.  To my knowledge, there is no randomized trial of immediate PCI vs. delayed PCI for transient STEMI.  There is a study that randomized patients with NSTEMI to early vs. delayed PCI. It showed that patients at high risk, as measured by a GRACE score of 140 or greater (corresponding to an in-hospital mortality of 3%), had better outcomes if they underwent immediate angiogram and PCI.
[Mehta SR et al.  NEJM May 21, 2009; 360(21):2165.]

I do let the following anecdote affect my practice: 

This was a 52 year-old male I saw a few years back.  He was playing cards with his friends when his left hand became numb.  He had no CP or SOB, no arm or jaw or other pain.  His friends thought he was having a stroke and called 911.  The medics wisely recorded the following ECG prehospital.

He arrived in the ED still without any chest pain, and the medics showed me this ECG:
There is marked ST elevation in anterior precordial leads, and reciprocal ST depression in inferior leads.  This is diagnostic of proximal LAD occlusion.





I activated the cath lab at 2129 in spite of the fact that the patient was asymptomatic.

We then recorded this ECG:
There is some ST depression in V2 and V3 and hyperacute T-waves.  


Hyperacute T-waves can occur "on the way up" or "on the way down" as I like to say; this means they can be present shortly after occlusion before ST elevation, or shortly after reperfusion, after ST segments have resolved.  I considered this to be diagnostic of reperfusion.


So I de-activated the cath lab at 2135.

Then the patient became hypotensive.  We recorded this ECG:
Obvious anterior STEMI
I re-activated the cath lab at 2145.  The total delay, then, was 16 minutes.

Shortly after the LAD angiogram, which showed 100% occlusion, the patient arrested and could not be resuscitated.

If I had let the cath lab be activated in spite of reperfusion, he would be alive.

This was a big mistake of mine.

Any STEMI is very high risk, even if reperfused.  I don't believe you'll ever be criticized for activating the cath lab if you have just one ECG that is diagnostic of STEMI.

3 comments:

  1. Hi Steve,
    Think your book and your blog are fantastic.
    Here in regional NZ we are still lysing STEMIs - which makes reperfusion criteria pretty concrete. May I ask your opinion re wether to give lytics to -
    - the patient with chest pain which resolves, but ST elevations are not? How long do you wait before lysing?
    - the patient with little or better yet no CP, with ECG changes that look fairly acute (STE with reciprocal changes, not q'ed out, not flipped t's - as per your book)and you are pretty sure new?. If you have a high trop with above - would this sway decision?
    Cheers
    Scott Cameron FACEM, FACEP
    Whangarei , NZ

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  2. I think in there is subtotal occlusion transforming to total in turns.Actually in 2nd ekg u are not facing obvious STEMI but still patient is high risk U.A and early invasive strategy could be the best option.

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  3. Scott,

    Great questions. Here is my opinion, based in part on the paper I've pasted below, and on others

    If ST elevation persists, even after 12 hours and even in the absence of chest pain, PCI is indicated. After 12 hours, lytics not indicated unless the ECG shows high "acuteness" (large upright T-waves especially). But absence of chest pain should not dissuade if the ECG is diagnostic. Before 12 hours, lytics would be indicated.

    See this article:

    Mechanical reperfusion in those with > 12 hours of CP, Time window for reperfusion depends more on EKG than on duration of CP

    Schomig A et al. JAMA, Vol. 293 No. 23, June 15, 2005 Is in my documents under medical articles/MI ACS

    Schomig, A., J. Mehilli, et al. (2005). "Mechanical reperfusion in patients with acute myocardial infarction presenting more than 12 hours from symptom
    onset: a randomized controlled trial." Jama 293(23): 2865-72.
    full text: http://jama.ama-assn.org/cgi/reprint/293/23/2865.pdf

    Basically proves that it is the EKG, not the duration of chest pain, that makes a difference.

    CONTEXT: No specifically designed studies have addressed the role of primary percutaneous coronary intervention in patients with acute ST-segment elevation myocardial infarction (STEMI) presenting more than 12 hours after symptom onset. Current guidelines do not recommend reperfusion treatment in these patients. OBJECTIVE: To assess whether an immediate invasive treatment strategy is associated with a reduction of infarct size in patients with acute STEMI, presenting between 12 and 48 hours after symptom onset, vs a conventional conservative strategy.Design, Setting, and
    PATIENTS: International, multicenter, open-label, randomized controlled trial conducted from May 23, 2001, to December 15, 2004, of 365 patients aged 18 to 80 years without persistent symptoms admitted with the diagnosis of acute STEMI between 12 and 48 hours after symptom onset. INTERVENTIONS:
    Random assignment to either an invasive strategy (n=182) based predominantly on coronary stenting with abciximab or a conventional conservative treatment strategy (n=183). MAIN OUTCOME MEASURES: The primary end point was final left ventricular infarct size according to single-photon emission computed tomography study with technetium Tc 99m sestamibi performed between 5 and 10 days after randomization in 347 patients (95.1%). Secondary end points included composite of death, recurrent MI, or stroke at 30 days. RESULTS: The final left ventricular infarct size was significantly smaller in patients assigned to the invasive group (median, 8.0%; interquartile range [IQR], 2.0%-15.8%) vs those assigned to the conservative group (median, 13.0%; IQR, 3.0%-27.0%; P<.001). The mean difference in final left ventricular infarct size between the invasive and conservative groups was -6.8% (95% confidence interval [CI], -10.2% to -3.5%). The secondary end points of death, recurrent MI, or stroke at 30 days occurred in 8 patients in the invasive group (4.4%) and
    12 patients in the conservative group (6.6%) (relative risk, 0.67; 95% CI, 0.27-1.62; P = .37). CONCLUSION: An invasive strategy based on coronary stenting with adjunctive use of abciximab reduces infarct size in patients with acute STEMI without persistent symptoms presenting 12 to 48 hours after symptom onset.

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