When the STEMI disappears before you get to the ED!

So what do you do when your STEMI disappears? 

Spontaneous reperfusion (SR) is well-described in the cardiology literature. One moment you have a classic STEMI on the ECG, and the next you have nada. I wrote about just such a patient in a prior post. In that case, EMS had acquired this ECG in a patient with chest pain:

However, when her symptoms improved they ran a second ECG, and found:

This dramatic improvement suggests 2 questions. First, is this a good sign? Second, did the medics do anything (like oxygen, nitro, or aspirin) that could have caused the improvement?

Is this a good sign?
Yes.
 
In a 2008 study (Spontaneous reperfusion in ST-elevation myocardial infarction: comparison of angiographic and electrocardiographic assessments.), finding ≥ 70% resolution of ST elevation on the ECG was a very good sign, and predicted a far lower rate of bad things - mortality and re-infarct rates were 0% as illustrated in this graph:

SR = Spontaneous reperfusion

Other studies have also shown that  resolution of the ST elevation before PCI is associated with patent vessels before PCI, after PCI, and better outcomes overall. The table below gives you the numbers. (TIMI 3 flow = normal blood flow in the coronary artery, 0 = complete occlusion)

Source

Even if PCI was significantly delayed, the patients with SR in a 2008 study did very well. Only 8% of those patients had primary PCI (as opposed to 100% of the patients with persistent ST elevation. Again, check the graph:

A = PCI or lysis;  B = Primary PCI only

Onto the second question...

 

Do oxygen, aspirin, nitroglycerin, or morphine cause spontaneous reperfusion?

Hard to say. 

Although SR may occur in up to 15% of STEMIs, this isn't well-studied. One of the studies mentioned above (Relation of clinically defined spontaneous reperfusion to outcome in ST-elevation myocardial infarction) checked whether SR occured more often in patients who received aspirin or heparin from EMS or in the ED, and didn't find an association:

Dr Smith describes a STEMI case in which he felt that nitroglycerin had caused SR, and thus contributed to a delay in PCI. In his discussion he cites an abstract (copied below) from an EMS study, possibly the world's only clinical study on this topic. The brief version is that 6% of STEMI patients had partial or total SR in the period after NTG administration. Of course, it was retrospective, uncontrolled, etc. 

On top of that, it's hard to say if 6% is a high rate or not. Some researchers think the overall rate of SR in STEMI is about 15%, so 6% may actually be lower than expected.

Source

As for oxygen, there's no evidence of any sort, good or bad.

The Bottom Line
Although a good number of patients have serial ECGs that show resolution of ST elevations, we don't exactly know why. Although these patients appear to be at lower risk of complication, it is hardly zero risk. When in doubt, get ECGs early and often.



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Mahoney BD, Hildebrandt DA, Allegra P. 
Normalization of Diagnostic For STEMI Prehospital ECG with Nitroglycerin Therapy. 
Prehospital Emergency Care 2008;15:105, Abstract 24.
Hypothesis. The decision to take a patient for emergent reperfusion therapy is largely determined by an ECG diagnostic for ST Elevation Myocardial Infarction (STEMI). Hildebrandt et al have proven that  prehospital 12 Lead ECGs followed by an immediate call for reperfusion team mobilization reduce door to balloon times.We hypothesize that prehospital ECGs will normalize in some STEMI patients after  nitroglycerin (NTG)therapy or due to spontaneous reperfusion.  NTG therapy before an ECG, or the absence of a prehospital ECG capacity in some services may lead to missing the early diagnosis of STEMI thus delaying reperfusion therapy. 

Methods. A prospective analysis of consecutive adult patients  presenting to an urban/suburban two paramedic ambulance service fromJuly 15, 2006, to August 15, 2007, who have diagnostic ECGs for STEMI.  Paramedics managing a possible myocardial infarction patient were instructed to obtain rapidly an ECG prior to treatment with NTG. If the initial ECG was diagnostic for STEMI the paramedic called to mobilize the reperfusion team. A second ECG was done prior to arrival at the ED. The ECGs were later reviewed by emergency physicians and cardiologists who confirmed the presence of a diagnostic prehospital ECG and STEMI.  

Results. During the 13 month interval, 87 patients had an initial ECG that was diagnostic for STEMI. These patients received no NTG from the paramedics prior to obtaining the first ECG. An average of 16 minutes 42 seconds later, 3 patients had an ECG that was no longer diagnostic for STEMI and 3 had a partial normalization in their ECG that made diagnosis of STEMI more difficult. 

Conclusions. Prehospital ECGs diagnostic for STEMI can normalize or become nondiagnostic after NTG administration or due to spontaneous reperfusion or evolution. In the absence of a prehospital ECG, it is possible that 6 of 87 (7%) of STEMI patients in this study would have had reperfusion delayed due to a rapid change in their ECG. Limitations include no control group receiving NTG prior to the first ECG.