Wednesday, May 28, 2025

What does this ECG represent in the setting of "negative" troponins?

This was written by Mark Hellerman, Cardiology Fellow at Stony Brook:


The Case: 

A 60 year old man with no reported medical history presents to the ED for evaluation of chest pain. 


For the past 3 days he has been experiencing substernal, exertional chest pain that resolves with rest. 


At the time of evaluation in the emergency department he is pain free at which time the following ECG is obtained: 


The above tracing and clinical vignette were sent to Dr. Smith who responded with the following: 


“It looks like a reperfused, inferior and lateral OMI. The tall T waves in V1-V3 might represent reperfusion of the posterior wall as well”



Initial high-sensitivity cardiac troponin T (hs-cTnT) value returned at 24 ng/L (2 ng/L above the 99th percentile for men according to the package insert).

3 hours later, repeat hs-cTnT returned at 20 ng/L (2 ng/L below the 99th percentile).


8 hours after presentation hs-cTnT returned at 18 ng/L and the following ECG was obtained: 

 

The patient was admitted to the cardiology service for further workup of his chest pain


12 hours after presentation the patient developed lightheadedness and nausea. Vitals revealed a blood pressure of 81/53.


The following ECG was recorded:  

The cath lab was immediately activated.

A repeat troponin was collected at this time which eventually returned with at 17 ng/L.

Smith: notice also the large ST Elevation and hyperacute T-wave in V1. This is likely a right ventricular MI and one would expect a proximal RCA occlusion.


While awaiting for the cath lab team to arrive the following ECG was obtained: 

Angiography revealed 100% thrombotic occlusion of the proximal RCA: 


 

Pre-PCI

Post-PCI


A repeat ECG was obtained 1 hour after PCI:



Once again we see subtle biphasic terminal T wave inversion in the inferior and lateral territories – this time associated with reperfusion after PCI.  An echocardiogram obtained the next day revealed a normal ejection fraction with no wall motion abnormalities. 


This case reminds us of two important pearls: 

  1. Reperfusion (Wellens) pattern on ECG can be subtle, but when identified, can help us more thoughtfully risk stratify – and thus ultimately manage – patients who present with recent anginal symptoms.

  2. Unstable Angina (UA) still exists, even in the era of high-sensitivity cardiac troponin assays

Reperfusion (Wellens) pattern: 


As reviewed in numerous previous posts, Wellens syndrome is a syndrome of transient occlusion myocardial infarction (OMI), in which the ECG was not recorded at the time of the anginal symptoms, but only after spontaneous resolution of those symptoms, at which time the ECG shows reperfusion T-waves with preservation of R-waves.

When trainees are learning about Wellens syndrome, many are only taught to recognize “Pattern B” (characterized by deep symmetric T-wave inversion), failing to appreciate that the this “Pattern B” morphology often evolves from the more subtle biphasic terminal T-wave inversion characteristic of “Pattern A” (see figure below) 




More examples of subtle “Type A Pattern” reperfusion waves can been viewed inthe following posts: 


More examples of “Type B Pattern” reperfusion waves can be viewed in the following posts: 


Because this ECG pattern is associated with a high rate of coronary reocclusion and subsequent transmural MI, these patients should be monitored closely with prompt administration of antiplatelets and continuous heparin while awaiting angiography.  Threshold for serial ECG should be very low.  


Unstable Angina


The advent of the high-sensitivity troponin assay led many to wonder if it would usher in the end of the era of unstable angina.  While this assay seems to have significantly reduced the incidence of UA, it has not eliminated it completely.


Importantly, one trial of 925 consecutive STEMI-positive occlusion myocardial infarctions found that 26% had presentation troponin values < 99th percentile when then presented less than 2 hours from symptom onset and 14% had values < 99th percentile when they presented with symptoms for greater than 2 hours.  


“Myocardial injury” was technically present on admission in this case (as the first troponin value was 2 ng/L above the 99th percentile sex-specific cutoff), and thus some may argue his presentation should not be classified as “unstable angina.” I would argue, however, that it’s not hard to imagine a scenario where the patient presented to the ED just a bit later when his troponin level would have likely been below the 99th percentile. Moreover, it is well established that age also influences troponin concentration – and at the age of 60 a hs-cTnT level of 24 ng/L is below the 99th percentile upper reference limit:

A study which included a healthy reference population of 2,746 individuals found that men 60 years of age and older had a 99th percentile upper reference limit 33 ng/L (see figure below).  For this reason I think it is reasonable to classify the presenting diagnosis of the patient in this case as “unstable angina” when we take into account sex AND age-specific hs-cTnT concentration thresholds.   



The Case

In this case, it is likely that the patient auto-lysed a culprit lesion prior to presentation to the ED.  The occlusion was likely too brief to injure enough myocardium to produce an impressive troponin leak.  Autolysis and reperfusion the right coronary artery prior to ED presentation was likely responsible for the subtle biphasic terminal T wave inversion seen on his presenting ECG. 12 hours after presentation the right coronary artery likely RE-occluded, manifesting in the clear ST segment elevation myocardial infarction seen at 2:00 AM. 


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