ST-Segment Elevation – Beyond False Positives


The criteria to identify acute STEMI patients in the ECC guidelines — those who are eligible for immediate reperfusion therapy — used to seem relatively simple.

“In the absence of contraindications, reperfusion therapy should be administered to patients with symptom onset within the prior 12 hours and ST elevation greater than 0.1 mV (1 mm) in at least 2 contiguous precordial leads or at least 2 adjacent limb leads, or new or presumably new LBBB on the presenting ECG.”

With the 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction it got a bit more complex.

“New ST elevation at the J point in at least 2 contiguous leads of ≥2 mm (0.2 mV) in men or ≥1.5 mm (0.15 mV) in women in leads V2–V3 and/or of ≥1 mm (0.1 mV) in other contiguous chest leads or the limb leads…”

(Note that “new” left bundle branch is no longer considered to be a STEMI Equivalent unless it meets Sgarbossa’s criteria.)

However, as I noted in the electrocardiogram section of the myocardial infarction article in the English Wikipedia:

“This criterion is problematic […] acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients. Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.”

Do you see why this is hard?

For the moment we will ignore the fact that the proposed millimeter criteria in the guidelines are essentially arbitrary because they fail to take into account the rule of proportionality. In other words, they do not take into account the depth of the S-wave. We will address this in a future blog post.

Brady said it best in Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians. Acad Emerg Med 2001; 8(4):349-360:

“ST segment elevation is perhaps the “most demanding” of the electrocardiographic features seen in the chest pain patient; it is “demanding” in that its presence must be explained and, if the etiology involves AMI, urgent therapeutic decisions must be made. Unfortunately, STE is a not uncommon finding on the ECG of the chest pain patient; its cause infrequently involves AMI.”

Think about that. Its cause infrequently involves AMI.

How infrequently?

Brady studied this in Cause of ST segment abnormality in ED chest pain patients. Am J Emerg Med 2001 Jan;19(1):25-8, a retrospective ECG review of adult chest pain patients in a university hospital emergency department over a 3-month period. ST segment elevation was determined if the ST segment was elevated >1 mm in the limb leads or >2 mm in the precordial leads (in at least two anatomically contiguous leads).

A total of 902 patients were enrolled in the study. Of those, 202 patients (22.4%) had ST segment elevation on their initial 12 lead ECG. Of those, only 31 patients (15%) had a discharge diagnosis of STEMI.

In other words, 171 patients (85%) had a non-AMI cause of ST segment elevation on their initial 12 lead ECG.

So what were the other causes of ST segment elevation?

  • Left ventricular hypertrophy (LVH) – 51 cases (25%)
  • Left bundle branch block (LBBB) – 31 cases (15%)
  • Benign early repolarization (BER) – 25 cases (12%)
  • Right bundle branch block (RBBB) – 10 cases (5%)
  • Nonspecific BBB – 10 cases (5%)
  • Ventricular Aneurysm – 5 cases (3%)
  • Pericarditis – 2 cases (1%)
  • Undefined or unknown cause – 35 cases (17%)

A total of 44 patients had acute myocardial infarction as the final diagnosis. Of those 31 had ST-segment elevation on the initial 12-lead ECG. In 2 cases (6%), the ST-segment waveform was “atypical” for acute infarction.

Their conclusion:

“AMI is not the most common cause of ST elevation in ED chest pain patients. LVH is most often responsible for electrocardiographic STE followed by AMI and LBBB which occur at equal frequencies.”

The message is clear. It’s not enough to discover ST-segment elevation on the 12-lead ECG. We need to specifically discover the ST-segment elevation of acute myocardial infarction. 

Consider Sejersten et al.: Comparison of the Ability of Paramedics With That of Cardiologists in Diagnosing ST-Segment Elevation Acute Myocardial Infarction in Patients With Acute Chest Pain. Am J Cardiol 2002 Nov 1;90(9):995-8:

“Paramedics diagnosed over half of patients as having ST elevation AMI, when in fact they did not. One reason for this may be that the paramedics were concerned about missing patients with this condition. The number of false-positive diagnoses may also have been increased due to the problem of differentiating ST elevation AMI from other electrocardiographic abnormalities that result in ST-segment elevation…”

“The paramedics’ diagnosis of ST elevation AMI was confirmed in 55 patients (45.5%) by acute angiography. In an additional 4 patients (3.5%) who did not undergo angiography due to high-risk assessment or other causes, the diagnosis was confirmed clinically by typical electrocardiographic changes in evolving ST elevation AMI accompanied by transient elevation of creatine kinase-MB. Thus, the paramedics’ true positive rate was 49% (n = 59). The paramedics’ decision was not confirmed in the 23 patients (19%) with no thrombus at angiography, and in the 38 (31%) who did not undergo coronary angiography because the attending cardiologist judged them not to have an evolving ST-elevation AMI […] The false-positive rate by paramedics was 51% (n = 62)…”

The authors also observe:

“The incidence of poor quality ECGs recorded by the paramedics was calculated to determine the paramedics’ performance in electrocardiographic acquisition. In 13 of 124 patients (10.5%), the ECGs were characterized as poor quality…”

They refer to this as “acceptable.” I suppose that depends on whether or not your loved one was one of the 10.5%! Their conclusion?

“This study concludes that paramedics’ true-positive rate of ST elevation AMI diagnosis is high in patients presenting without confounding factors, but decreases when the ECG has confounding factors. This is in contrast to an experienced cardiologist whose true-positive rate was high and not affected by confounding factors. The results demonstrate that before implementation of electrocardiographic transmission directly to a cardiologist’s handheld device, there is a need to provide education and training to paramedics responsible for acquiring and interpreting prehospital ECGs, with special emphasis on confounders…”

Here’s a final thought from Otto and Aufderheide in Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis of acute myocardial infarction. Ann Emerg Med 1994 Jan;23(1):17-24:

“Fifty-one percent of patients whose prehospital 12-lead ECG met 1 mm or more ST segment elevation criteria had non-myocardial infarction diagnoses. ST-segment elevation alone lacks the positive predictive value necessary for reliable prehospital myocardial infarction diagnosis. Inclusion of reciprocal changes in prehospital ECG myocardial infarction criteria improved the positive predictive value to more than 90% and included a significant majority (62% to 86%) of acute myocardial infarction patients with ST segment elevation who received thrombolytic therapy within five hours after hospital arrival. ST-segment elevation criteria that include reciprocal changes identify patients who stand to benefit most from early interventional strategies.”

Most interventional cardiologists I speak with believe that prehospital activation of the cardiac cath lab should be reserved for clear-cut STEMI. Other patients, they argue, can and should receive further investigation in the Emergency Department.

I agree provided that really sick patients are transported to PCI hospitals.

Some paramedics bristle at the idea of transmitting 12-lead ECGs to the hospital for physician over-read. To be honest it has never bothered me except those occasions when the transmission didn’t work.

In my own system ECG transmission helped build trust between paramedics and emergency physicians. They saw that in most instances when we called “Code STEMI” from the field it really was a STEMI.


When it comes to STEMI care there is no “one size fits all” solution. What works in one system may not work in another.

However, to optimize both sensitivity and specificity, clinicians who read 12-lead ECGs should:

  1. Be well versed in STEMI recognition, with a solid understanding of hyperacute T-waves, ST-segment morphology, and reciprocal changes.
  2. Understand how QRS confounders like left ventricular hypertrophy, bundle branch block, and ventricular paced rhythm cause secondary ST/T-wave abnormalities that can often resemble acute STEMI.
  3. Develop strategies to identify early repolarization and less common mimics like hyperkalemia, pericarditis, and ventricular aneurysm.

Keep in mind there are times when it’s appropriate for patients to receive urgent coronary angiography when the diagnosis is uncertain or when patient is symptomatic and does not respond to medical therapy.

The patient will occasionally be found to have a diagnosis other-than-STEMI like takotsubo cardiomyopathy or myocarditis but that does not necessarily mean the cath was inappropriate.

My friend and colleague Russell Griffin (@CareFliteMedic) has suggested that we look beyond “false positive” cath lab activations and instead think in terms of “activation without intervention” to help emphasizes this point. It could go a long way toward developing a culture of continuous quality improvement.

It sounds like an excellent suggestion to me!


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