Pain in the Jaw
Firefighter / Paramedic
Acute Care Nurse Practitioner
The below ECG is an example of a patently obvious pre-hospital Cath activation. It is undeniable. There is simply no room for ambiguity. And this is where conventional STEMI criteria offers some diagnostic utility -- its specificity. That is, when certain criteria is present, odds are that it can be no other than the pathology in question. Marriott would classify this ECG as Grade II Sclarovsky-Birnbaum with Lead III STE greater than the ST is discretely depressed in V3, suggesting a culprit RCA.
Would you believe that this next ECG is a 99% 1st Diag OMI? But it doesn't meet any STEMI criteria, you might think. Exactly! Although reasonably specific, the universal definition of STEMI is horrendously insensitive.
Today I present a case in which a "STEMI" was, by definition, accurately excluded, but an OMI was missed. When conducting QA/QI chart reviews at the fire department I generally commence by reviewing the ECG first, if applicable. This ensures gestalt reaction while simultaneously being blinded to the clinical circumstances. -And I happened upon this:
My immediate Dx: Inferior-Posterior OMI. Activate the Cath Lab! There is an upwardly convex ST segment in leads II, III, and aVF with corresponding T wave inversion (TWI). As and side, the fact that TWI exists here suggests that the conundrum is subacute. Said differently, there is an ongoing, active ischemic event, the duration of which has been long enough to facilitate simultaneous reperfusion (of some magnitude) -- whether via collateral circulation from adjacent coronary tributaries, or a dynamic process of lysis/reocclusion at the level of the lesion that intermittently permits antegrade blood flow through the infarct related artery. There is "scooped out" ST curvature in aVL -- the first reciprocal change. The most sensitive finding on this ECG (at least to me) is the discrete ST depression in V1, but most of all V2, with "inappropriate" baseline ST in V3. It is terribly subtle, but real. Why is this important? There should be a relatively normal / expected amount of STE in V1-V3, even V4, consistent with this patient's sex and age. Rather, there is ST depression (V1 and V2) and baseline ST (V3). The poor R wave progression is most likely incidental here, a natural consequence of the the leftward axis. Finally, the QTc is ~420ms, whereas normal variant ST change is usually in the range of 390ms.
That said, I immediately accessed the patient report. A 45 y/o Male called 911 after he awoke from sleep with jaw pain. EMS found him uncomfortable and endorsing a 10/10 pain scale. Vitals otherwise stable. Approximate duration of symptoms: 2 hours, and worsening. History included poorly controlled Type 2 DM with associated Metabolic Syndrome constellation, and episodic mixed NYHA Class II/III DOE over the past two months, approximately. Below is the ED admission ECG at 0207.
Not much change upon juxtaposition with the EMS tracing. Either way, lingering Inferior-Posterior OMI. The patient was worked up for a potential inflammatory maxillofacial process. CXR resulted negative. CT Maxillofacial with Contrast resulted negative. Blood glucose was 431 and HgbA1C resulted 12.6. CBC, CMP, and BNP were otherwise unremarkable. Initial Troponin I at 0210 hours resulted <0.015 ng/mL. At 0413 hours the second Troponin I returned 0.033 ng/mL with lingering jaw pain. The next ECG was recorded at 0508 hours.
The findings in II, III, aVF (with reciprocal aVL), and V1 / V2 are slightly more dramatic. The ED physician was now worried for ACS and ordered a lipid profile with cardiology consult. Lipid Profile: TC 267, Tg 1112, HDL 29, and LDL 106. The ED physician dictated that on-call cardiology acknowledged the ECG's, reviewed all pertinent data (history, labs, etc), and advised hospital admission with Lovenox anticoagulation. The ECG's, however, did not warrant emergent Cath intervention. The patient was admitted. This is the first ECG on the inpatient floor (0715 hours) after Lovenox administration.
Pay close attention to the fact that the inferior ST changes have returned to baseline (vestigial remnants of STE in Lead II lingering) with Pattern B Wellens Reperfusion T waves. Additional close inspection will reveal this same T wave inversion (of reperfusion) in Lead V6, although more subtle. V1 ST appears to be moving back to an expected baseline. There is now slight ST elevation in V2, a more robust r-wave, and a much larger T wave: Posterior Reperfusion T wave. (We're seeing a mirror image of Pattern B Wellens of the posterior wall.) This was the last ECG recorded during the inpatient stay, so the full picture of ischemic change (e.g. transmural; profound Qr in Lead III) is simply not available.
The third Troponin I resulted 0945 hours at 1.820 ng/mL. This caught the attention of cardiology, and a Cath was scheduled at the first available opportunity. The fourth Troponin I resulted 4.180 ng/mL at 1306 hours, and the patient was taken immediately to Cath with arterial access at 1351 hours.
There was diffuse non-obstructive triple vessel disease, however an acutely thrombosed culprit lesion was identified in the distal RCA with 100% stenosis. The angiographer documented that "multiple" thrombectomy attempts were made before the lesion was successfully removed. Then, "multiple balloon inflations" were deployed to restore optimal TIMI flow. Finally, a single drug-eluting stent was placed at 1425 hours. Below are the angiographic images showing 100% RCA occlusion with subsequent restoration of flow after intervention.
Subsequent 2D Echo showed global hypokinesis, mitral regurgitation, and LVEF 40%. He was placed on DAPT, Spironolactone, Entresto, Metoprolol and Atorvastatin. Discharge Dx: NSTEMI, HFrEF.