The criterion seems quite 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.
However, as I noted in the electrocardiogram section of the myocardial infarction article in the English Wikipedia (I used to edit the Wikipedia quite often, but I probably won’t anymore since I have a blog):
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.
Brady et al. 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? In Cause of ST segment abnormality in ED chest pain patients (Am J Emerg Med 2001 Jan;19(1):25-8) Brady et al. performed a retrospective ECG review of adult chest pain patients in a university hospital emergency department (ED) 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).
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%)
44 patients had AMI as the final diagnosis of whom 31 showed ST segment elevation on presentation to the ED. In 2 of 31 (6%) cases of STEMI, the ST segment waveform was atypical for acute infarction.
“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.”
As a side note, I find it a bit unusual that paced rhythms are not mentioned (unless they fell into the nonspecific BBB category for some reason). It also seems strange that RBBB is listed as a cause of ST segment elevation. In my experience RBBB does not distort the ST segment the way LBBB does. That’s not to say that it’s always easy to identify STEMI in the setting of RBBB, just like it’s not always easy to identify STEMI in the absence of bundle branch block.
*** Update 12/20/08: I recently saw an ECG with sinus tachycardia and RBBB that appeared to show ST segment elevation. The patient was emergently cathed and no culprit artery was found. The absence of a well defined TP segment as a baseline for comparison was a confounding factor. ***
Regardless, the message is clear. It’s not enough to discover ST segment elevation on the 12 lead ECG of a chest pain patient. A monkey could do that. We need to specifically discover the ST elevation of AMI.
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…“
Amazingly, they refer to this as “acceptable.” I guess their standards are low! They’re either satisfied with the care of 1 in 10 patients being compromised by poor data quality, or they think that’s all EMS is capable of.
“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…“
To all the paramedics out there who feel offended that they’re being asked to transmit the 12 lead ECG to the emergency department for physician interpretation, do you know how to identify all of the mimics of acute myocardial infarction? Do you know how to identify acute myocardial infarction in the presence of baseline abnormalities?
We’ve been taught that identifying acute STEMI on the 12-lead ECG is easy! And so it is… to a point. Identifying ST segment elevation that is not STEMI… that’s the trick.
It’s false positives that cause the most problems!
Here’s a final thought from Otto and Aufderheide, Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis fo 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.“
Thanks to ncline7 for reminding me that you can test your ability to identify the mimics of acute STEMI by taking the ACC-D2B ECG Challenge!