The Great Masquerade

David Didlake

Firefighter / Paramedic

Acute Care Nurse Practitioner

@DidlakeDW

Peer review by Dr. Stephen Smith

@SmithECGBlog

CASE

My colleagues and I responded to a 49 y/o Male who called 911 after experiencing new onset chest discomfort that forced him to pull over while driving. At the time of initial contact, he expressed symptom alleviation and felt that Fire/EMS services were no longer necessary. He at least agreed to a full examination in the ambulance and stated that during its peak the pain was squeezing in nature, centrally located, 8/10 severity, associated with both diaphoresis and one episode of vomiting.

Rx Medications: None

History: HTN and HLD (both poorly controlled), Smoking

Vitals

• NIBP 134/76

• HR 64

• RR 14 (BBS CTA)

• SpO2 99 (RA)

This is the time-zero ECG during a pain free state at 0853 hours.

Raw findings include Sinus Rhythm, narrow QRS duration, normal frontal plane axis and QRS/T angle, early R wave progression, appreciable q-waves in II/III/aVF with an ST segment that glides just above The PQ junction and terminates with T wave inversion, a subtle “scooped out” appearance of the aVL ST, and a q-wave in V4.

What concerned me the most in that moment, of all the items listed, was the terminal T wave inversion in II/III/aVF, especially its presence in the context of an ACS-compatible circumstance. Said differently, my suspicion was that we had captured ST/T attenuation of a previously occluded RCA, or LCx – now open via spontaneous thrombolysis as manifested by Wellens-type “inferior” reperfusion T waves.

The constellation of findings and concerns (e.g. high pretest probability) were conveyed to the patient and he agreed to be transported to the nearest PCI center. The leading hypothesis was that one of two circumstances would most likely unfold downstream – 1) Patient remains pain free and we bear witness to continued evolution of reperfusion T waves, or 2) Patient will experience a sudden restoration of pain and the predicted ischemic footprint will reemerge as changes consistent with either STEMI or OMI. The best way to remain ahead of the curve in both cases is with serial ECG’s.

ASA 324mg was administered. As my colleague was placing the IV catheter the patient leaned forward with Levine sign and expressed chest discomfort with apparent facial grimmace. We immediately captured the following 12 Lead at 0901 hours.

My gestalt reaction was unequivocal LAD occlusion. There is significant STE V1-V5 with associated Hyperacute T waves (HATW). The HATW’s extend to Leads I/aVL, and there is a down-up T wave in aVF. The inverted TW in III is reciprocal to the HATW in aVL. As an aside, it should be noted that the LifePak 15 does not seem too concerned about these changes. Many EMS providers know that when the machine interprets profound shifts to the ST segment it spontaneously ejects a new tracing with acute injury suspected. This is a testament to the power of provider-directed serial ECG’s. A pre-hospital STEMI alert was then transmitted.

This ECG was so pathognomonic to me that I initially didn’t consider it necessary to apply the 4-variable equation for the differentiation of LAD OMI versus Early Repolarization, but ultimately decided this imperative as I feared the receiving facility would disregard the changes for reasons soon to be disclosed.

• QTc 446 ms

• STE 60 ms after the J-point in V3 2 mm

• R wave height V4 10 mm

• QRS voltage V2 13 mm

• Result: 20.67

During transport the patient verbalized symptom alleviation once more. He leaned back into the stretcher displaying ability to establish a position of comfort. This next ECG was recorded at that time (0911 hours).

It is essentially identical to the original time-zero ECG, and validating that our initial encounter with the patient, during a pain free state, was artery opening due to dynamic thrombolysis.

Upon arrival at the receiving PCI center the patient once again verbalized restoration of pain with facial grimace and Levine sign. This is the ED admission 12 Lead after transfer from EMS cot to the stretcher.

Yet again, a near identical ischemic presentation upon juxtaposition to our prehospital tracing when the pain returned. There is, however, one additional feature here that further supports LAD OMI versus Early Repolarization. Do you see it? There is terminal QRS distortion (TQRSD) in V3!

Despite the dynamic ST/T changes, 4-variable validation, and presence of TQRSD, the receiving ED provider still did not believe the findings warranted emergent PCI -- the rationale being that the most profound ST changes did not show accompanying reciprocal changes and the most dramatic ST segments were concave, rather than convex, and were thus the ebb and flow of Early Repolarization. The STEMI activation was subsequently cancelled.

At the time of this case I was in my first semester of clinical rotations for Nurse Practitioner school and, rather serendipitously, was precepting with the very interventional cardiologist taking STEMI call that day at the respective facility. I snapped pictures of all the ECG’s presented here and texted them directly to the interventionalist pleading with him/her to take the patient for emergent PCI. I was so concerned that this patient would lose the anterior wall of his left ventricle that I considered such cavalier actions necessary.

He was found to have a 100% proximal LAD occlusion (imaging below with red dash indicating the abrupt contrast dye termination at the occlusion). One stent deployed. The initial ED Troponin I was undetectable, but later peaked at 0.40 ng/mL. The next day Echo showed slight apical WMA with 45% EF. He was discharged home on DAPT and Carvedilol.

DISCUSSION

Early publications from Wasserburger and Kambara defined features of Early Repolarization as end-QRS notching / slurring, ST segment elevation (sometimes dramatic), and tall, symmetrical T waves. A subsequent consensus report from the JACC echoed said criteria as it pertains to the ECG while simultaneously presenting new data to suggest that this entity is not entirely “benign” – as is traditionally common vernacular – but is linked to a small increase in the long term risk of idiopathic VF arrest. [1] As an aside, we have previously seen that categorizing HATW’s as “tall” or “symmetrical” is often unhelpful (in the absence of proportionality) and equally confusing because these same descriptors are applied to non-ischemic conditions, such as Early Repolarization.

Smith comment: The irony is that, in general, anterior early repolarization (normal variant STE) has asymmetric T-waves (slower upstroke than downstroke) whereas HATW are more symmetric. This of course is not universally true. In fact, we (Smith et al.) showed that the T waves in subtle anterior OMI versus normal variant are the same height; it is the ratio of their height to the R wave which is greater because the R wave in OMI is smaller.

Smith, S. W., et al. (2012). Electrocardiographic differentiation of early repolarization from subtle anterior ST-segment elevation in myocardial infarction. Annals of Emergency Medicine. Vol 60, No 1.

Two confounding features in today’s case compelled the receiving ED physician to label the ECG’s as Early Repolarization versus LAD occlusion: 1) the lack of conventional reciprocal changes, and 2) the concave morphology when the ST elevation was present.

We must face the difficult reality that 30-60% LAD occlusion often does not present with clear reciprocal changes, often due to the varying arrangement of the 1st Diagonal and Septal Perforator branches in the general population, and the lesion’s respective proximity therein. [2, 3] However, I feel that subtle reciprocal changes were present in the pre-hospital ECG recorded during maximal pain. Here it is presented again. Notice the down-up T wave in Lead aVF. Although small and easily overlooked this finding is an ischemic signature that is reciprocal to the primary injury vector in the anterior wall.

It should also be mentioned that upwardly concave ST segments are frequently encountered in LAD occlusion. [4] Furthermore, in the original 3-variable formula (cited above) it was found that half of 355 LAD occlusions were upwardly concave in all of V2-V6!

When faced with such a vexing circumstance – that is, an ECG that might be LAD occlusion while masquerading as Early Repolarization – one can deploy the improved 4-variable linear regression formula to help better establish the likelihood of an ischemic event. [5] This tactic worked in the pre-hospital phase of this case, however was not applicable for use during ED admission. The reason for this is that the ED ECG showed TQRSD. Lead V3 is absent of both S and J waves, and this feature was found to have 100% specificity for LAD occlusion as TQRSD was never observed in Early Repolarization. [6]

When the pretest probability is high consider it irresponsible to entertain the masquerader. Although the ST/T changes in this case were, by all accounts, glaring, it is nonetheless a testament to the fact that reliance on conventional STEMI criteria undermines the clinician’s ability to fully appreciate true emergent ischemic changes.

[1] Macfarlane, P. W., et al. (2015). The early repolarization pattern: A consensus paper. Journal of the American College of Cardiology. Vol 66, No 4.

[2] Birnbaum, Y. & Drew, B. J. (2003). The electrocardiogram in ST elevation acute myocardial infarction: Correlation with coronary anatomy and prognosis. Postgraduate Medical Journal; 79. 490-504.

[3] Bayes de Luna, A. et al. (2004). Evolving myocardial infarction with ST elevations: Ups and downs of ST in different leads identifies the culprit artery and location of the occlusion. Annals of Noninvasive Electrocardiology. Vol 9, No 2.

[4] Smith, S. W. (2006). Upwardly concave ST segment morphology is common in acute left anterior descending coronary occlusion. The Journal of Emergency Medicine. Vol 31, No 1. 69-77.

[5] Smith, S. W., et al. (2017). A new 4-variable formula to differentiate normal variant ST segment elevation in V2-V4 (early repolarization) from subtle left anterior descending coronary occlusion – adding QRS amplitude of V2 improves the model. Journal of Electrocardiology; 50. 561-569.

[6] Lee, D. H. & Smith, S. W. (2016). Terminal QRS distortion is present in anterior myocardial infarction

but absent in early repolarization. American Journal of Emergency Medicine. 34(11). 2182-2185.