Thursday, August 19, 2021

A 60 year old man with chest pain -- many fascinating aspects to this ECG

Written and submitted by Lucas Goss MD, peer reviewed by Smith, Meyers, Bracey

A 60-year old man with history of CAD and prior stents to the LAD and ramus presented with acute chest tightness and shortness of breath. He arrives to the ED at about 1 hour and 15 minutes after onset of pain, and his triage ECG is shown below:

ECG#1 (no baseline available for comparison):

What do you think?

Sinus rhythm with PVC

No evidence of hyperkalemia

QT within normal limits

Negative P-wave in V2, so at least V1 and V2 are placed too high

STE in V2-V5, as well as lead II, III, aVF

Terminal QRS distortion (TQRSD) in V3 and perhaps almost also V4 

---TQRSD means absence of BOTH S-wave and J-wave in EITHER of leads V2 or V3 -- this is never seen in normal ST Elevation -- see this article: Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization

Evidence of OMI in the PVC!

--------For this PVC, there is inappropriate isoelectric ST segment in V3 (since the PVC is of RBBB morphology there should be discordant STD from the R' wave, usually with TWI, but here we have an isoelectric ST segment and upright T wave). Moreover, V2 is nearly isoelectric, and the ST segment is upsloping and convex ("coved" ST segment), which is highly suggestive of LAD OMI. In addition, the T-wave is biphasic, down-up. A normal ST-T following the R'-wave in RBBB would be negative and downsloping with a fully negative T wave. 

Q waves which are too wide to be normal (in this context, considered pathologic until proven otherwise) in II, III, aVF, V4-6

Likely hyperacute T waves in V2-V4 and inferior leads, if compared to prior

Dr. Goss sent this ECG to me (Meyers) without any information, and I responded that I was worried about possible anterior and inferior OMI findings, worrisome for LAD OMI, but I was not quite ready to call it diagnostic. I recommended looking for a prior, getting the history, and serial ECGs. I later sent it to Dr. Smith with no information, and he instantly responded, "Terminal QRS distortion in V3, looks like LAD occlusion." Dr. Smith needed no extra information in this case.

At this point, no definite signs of OMI were appreciated by the treating physician, but the story was concerning enough to trigger serial ECGs.

ECG#2 (15 minutes later):

Obviously there is progression of hyperacute T wave and STE, but also there is a change in the QRS pattern in the anterior leads which makes me think there was probably a change in the electrode positions between the first and second ECGs. In fact, the P-wave in lead V2 is no longer fully negative, so it is placed lower on the chest. In this ECG, there is no lead with terminal QRS distortion, because V1-V6 all have an S wave. Subtle reciprocal depression is now present in aVL.

In this ECG you can now see clear and obvious hyperacute T waves in the anterior leads with approximately 1mm of STE that does not meet STEMI criteria in 2 consecutive leads. This ECG was interpreted as "subtle ST elevation in V4-V6 without reciprocal changes."

Initial high sensitivity cardiac troponin I was 129 ng/L (99% URL for men for this assays is 20 ng/L).  

Smith note: In the only U.S. study to look at it, the positive predictive value of an initial troponin at 129 ng/L was about 55% for any MI and about 45% for type 1 MI. Many such elevated troponins are due to type II MI or non-AMI myocardial injury. This is why the clinical presentation and ECG are so important. 

Sandoval Y, Smith SW, Schulz K, Sexter A, Apple FS. Rapid identification of patients at high risk for acute myocardial infarction using a single high-sensitivity cardiac troponin I measurement. Cin Chem 2020; 66:620-2.

A third repeat ECG was obtained 30 minutes later, ECG#3:

A code STEMI was called after this ECG. 

At this point, the ECG shows obvious STEMI(+) OMI. The patient was emergently transferred to a hospital with PCI capabilities. Cardiac catheterization was performed approximately 3.5 hours after initial symptoms. 

Catheterization Lab Findings:

LAD: 100% mid-thrombotic occlusion - stented

D1: Ostial 99% - stented

Ramus intermedius: 100% thromotic occlusion - stented

ECG after reperfusion: 

Significant loss of R waves with persistent STE, but also with some reperfusion as evidenced by the significant terminal T wave inversion in the LAD distribution. This likely indicates incomplete microvascular reperfusion ("no reflow phenomenon"). The presence of QS-waves portends complete transmural MI. If LVA develops (and this is quite likely), then T-waves may be inverted (or upright), but will not remain so deep. 

This patient went to the lab at only about 2 hours after onset of symptoms, with hyperacute T waves on the first few ED ECGs. There was not much delay, and it was electrocardiographically hyperacute before intervention. Hopefully this portends that this patient has a decent chance of recovery of the anterior wall and apex (stunning vs. infarction), but based on the ECG, troponins, and explanation below, it seems unlikely.

Echo one day after catheterization: "EF 31%. Akinesis of the apical LV segments and mid-septum (LAD distribution)."

Multiple repeat troponins were greater than 25,000 ng/L (our lab's upper limit of reporting).  

Smith: These very high troponins further support a very large MI and portend a poor prognosis in spite of rapid therapy.  It is consistent with the persistently high ST segments after reperfusion.  Both these findings together suggest some element of "No Reflow" due to microvascular obstruction with platelet-fibrin aggregates.  ST resolution is the best indicator of microvascular reperfusion, and can also be measured by TIMI myocardial perfusion grading on the angiogram.

See this post: 

Poor Microvascular Reperfusion ("No Reflow"): Best Diagnosed by ECG

ECG progression (lead 4):

This is a very nice demonstration of the main concepts of the OMI progression. Hyperacute T waves inflate with area under the curve as the R wave diminishes, with rising ST segments, development of small Q waves which grow bigger as the R wave diminishes, then total QS waves with persistent STE.

Learning Points

Frequent repeat ECGs are extremely important for the detection of OMI, especially with a concerning story. Within 15 minutes this patient's ECG demonstrated clear and obvious evidence of evolving OMI. This was particularly important in this case, as early detection was essential to ensure prompt transfer to PCI.

Terminal QRS distortion occurs when the enlarging T wave and rising ST segment obliterates the end of the QRS complex, characterized by lack of BOTH 1) an S-wave and 2) a J-wave. When this finding is in V2-3 of a normal QRS complex, it has been shown to have high specificity for OMI.

Do not rely on the ECG becoming such an obvious STEMI(+) OMI as it did in this case. Many patients with OMI will not manifest STEMI criteria, and even when they do, experts can recognize the life-saving need for reperfusion much earlier than STEMI criteria. In this case, Dr. Smith recognized OMI about 30 minutes earlier than STEMI criteria. It is conceivable that reducing the time of identification of OMI to reperfusion in cath lab will improve morbidity or mortality in a common, deadly condition. 

PVCs should be inspected for signs of ischemia and can provide additional evidence of OMI in borderline cases (such as this one).

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