2 middle aged males presented with chest pain.
Which had the more severe chest pain at the time of the ECG?
Here is the ECG of patient 1, recorded about 2 hours after pain onset:
A Massive Anterolateral STEMI/OMI
Peak troponin I over 60,000 ng/L
Here is the ECG of patient 2, recorded about 2 hours after pain onset:
This is OMI, but it is not STEMI
Peak troponin I 440 ng/L
Patient 1 at the top with the massive ST Elevation complained of 5/10 chest pain at the time the ECG was recorded.
Patient 2 at the bottom with a very subtle OMI complained of 10/10 chest pain at the time the ECG was recorded.
The point is this: The severity of a patient's pain has little correlation with ST Elevation, the size of the infarct, or the severity of the pathology (see reference 1 below). However, pain severity is associated with rapid intervention because patients with severe pain seek attention earlier and providers pay more attention to them (see reference 2 below).
See these 2 articles
Author links open overlay panel
Methods and Results
Patients with confirmed ST elevation myocardial infarction (STEMI) treated by emergency medical services were included in this retrospective cohort analysis of the AVOID study. The primary endpoint was the association of pre-hospital initial chest pain severity, cardiac biomarkers and infarct size based on cardiac magnetic resonance imaging. Groups were categorized based on moderate to severe chest pain (numerical rating scale pain ≥ 5/10) or less than moderate severity to compare procedural and clinical outcomes. 414 patients were included in the analysis. There was a weak correlation between initial pre-hospital chest pain severity and peak creatine kinase (r = 0.16, p = 0.001) and peak cardiac troponin I (r = 0.14, p = 0.005). Both were no longer significant after adjusting for known confounders. There was no association between moderate to severe chest pain on arrival and major adverse cardiac events at 6 months (20% vs. 14%, p=0.12). There was a weak correlation between history of ischemic heart disease (r = 0.16, p = 0.001), percutaneous coronary intervention (r = 0.16, p = 0.001), left anterior descending artery (r = 0.12, p = 0.012) as the culprit vessel and a weak negative correlation between age (r = -0.14, p = 0.039) and chest pain.
Conclusion
Only a weak association between pre-hospital chest pain severity and markers of myocardial injury was identified, supporting more judicious use of opioid analgesia with a focus on patient comfort.
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This article shows that pain intensity is associated with shorter door to balloon times and thus smaller infarcts.
Having severe pain drives people to the ED for faster treatment! It is good to have terrible pain!
And as we have shown before, morphine leads to slower times to treatment and worse outcomes.
Abstract
Current ST-segment elevation myocardial infarction (STEMI) guidelines require persistent electrocardiogram ST-segment elevation, cardiac enzyme changes, and symptoms of myocardial ischemia. Chest pain is the determinant symptom, often measured using an 11-point scale (0-10). Greater severity of chest pain is presumed to be associated with a stronger likelihood of a true positive STEMI diagnosis. This retrospective observational cohort study considered consecutive STEMI patients from May 02, 2009 to December 31, 2018. Analysis of standard STEMI metrics included positive electrocardiogram-to-device and first medical contact-to-device times, presence of comorbidities, false-positive diagnosis, 30-day and 1-year mortality, and 30-day readmission. Chest pain severity was assessed upon admission to the primary percutaneous coronary intervention hospital. We analyzed 1409 STEMI activations (69% male, 66.3 years old ± 13.7 years). Of these, 251 (17.8%) had no obstructive lesion, consistent with false-positive STEMI. Four hundred sixty-six (33.1%) reported chest pain rating of 0 on admission, 378 (26.8%) reported mild pain (1-3), 300 (21.3%) moderate (4-6), and 265 (18.8%) severe (7-10). Patients presenting without chest pain had a significantly higher rate of false-positive STEMI diagnosis. Increasing chest pain severity was associated with decreased time from first medical contact to device, and decreased in-hospital, 30-day and 1-year mortality. Severity of chest pain on admission did not correlate to the likelihood of a true-positive STEMI diagnosis, although it was associated with improved patient prognosis, in the form of improved outcomes, and shorter times to reperfusion.
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MY Comment, by KEN GRAUER, MD (9/26/2023):
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Today's post by Dr. Smith emphasizes the very important clinical point: "The severity of a patient's CP has little correlation with the amount of ST elevation, the size of the infarct, or the severity of the pathology."
- That said, having more severe CP often conveys an unanticipated advantage — namely, that emergency providers tend to pay more attention to patients with severe CP — which (as per Dr. Smith) — has resulted in faster cardiac cath, therefore more salvaged myocardium with outlook for a better longterm prognosis.
The 2nd patient in today's case (who presented with ECG #2) — had severe (10/10) CP at the time his initial ECG was recorded. But, even if this patient's history was of much less severe CP — any history of new CP in association with an initial ECG like this patient had — should promptly result in cath lab activation (or at the least — in prompt repeat within minutes of this initial ECG — plus search for a prior tracing for comparison — with strong suspicion that prompt cath will very soon be needed).
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Take another LOOK at the initial ECG that was recorded in today's case on Patient 2 (that for clarity — I have reproduced in Figure-1).
- WHY should this initial ECG justify prompt cath (or at the least, very close scrutiny with suspicion that prompt cath will very soon be needed) — even if CP is not severe?
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| Figure-1: I've reproduced and labeled the initial ECG from Patient 2. |
MY Thoughts on the Initial ECG from Patient 2:
There is marked baseline artifact in ECG #2. Given the importance of accurate ECG assessment in any patient with new symptoms — I would have immediately repeated this initial tracing. That said:
- Our "eye" should promptly be captured by the QRST appearance in lead III — in which there is a disproportionately large Q wave (virtually as deep as the R wave in this lead is tall) — in addition to subtle-but-real ST segment straightening + elevation + terminal T wave inversion.
- Less prominent but-still-present — is a subtle hyperacute appearance of the ST-T wave in neighboring lead aVF.
- In a patient with any new CP (even if relatively mild) — The ST segment straightening with slight depression in lead aVL is consistent with a reciprocal change that supports suspicion of recent or acute inferior OMI.
- Normally — there should be slight upward-sloping ST elevation in anterior leads V2,V3. But this is not what we see in the chest leads with BLUE arrows that instead suggest slight-but-real ST depression that may well indicate associated posterior OMI.
- To EMPHASIZE: The above ECG findings are extremely subtle. But given the "Takeaway Point" highlighted by Dr. Smith above ( = severity of symptoms does not necessarily correlate with the severity of pathology) — and, the presence of even mild CP in a patient with the findings seen in ECG #2 — very close scrutiny is needed (ie, follow-up with serial tracings and troponins + search for a prior ECG on the patient) — with the thought that we need to prove that prompt cath is not indicated (rather than the other way around).
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