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Source: Brady WJ, et al. Cause of ST segment abnormality in ED chest pain patients. Am J Emerg Med 2001;19:25-28.
Patients with acute chest pain and ST elevation (STE) on ECG generate intense clinical apprehension and decision pressure in any emergency department (ED). In the presence of acute myocardial infarction (AMI), rapid reperfusion is critical and requires speed and competence on the part of the ED physician. However, earlier studies have acknowledged that STE may arise from a number of causes unrelated to life-threatening coronary syndromes, in which immediate reperfusion attempts are inappropriate and potentially hazardous.
To assess the relative frequencies of AMI vs. non-AMI events associated with STE, Brady and colleagues at the University of Virginia studied 902 patients presenting to an ED-based chest pain center over a three-month span in 1996. Of these, 202 (22%) had atraumatic chest pain and STE as defined by: 1) elevation in two anatomically contiguous leads, and 2) greater than 1 mm elevation in limb leads or greater than 2 mm in precordial leads. Average age was 62 years, with a range from 26 to 101 years. Fifty-four percent were female. ECGs initially were interpreted by the treating ED physician and later were reviewed by a cardiologist who was blind to final clinical diagnoses.
In this cohort, 31 of 202 patients (15%) were proven to have AMIs that were responsible for STE, whereas STE in 171 patients (85%) was attributed to non-AMI etiologies. The nine non-AMI conditions and frequencies included: left ventricular hypertrophy, 25%; left bundle-branch block, 15%; early repolarization, 12%; right bundle branch block, 5%; intraventricular conduction delay, 5%; ventricular aneurysm, 3%; pericarditis, 1%; paced rhythm, 1%; and undefined cause, 17%. Agreement in ECG interpretation between initial ED physician interpretation and subsequent cardiologist review was 94% for AMI and 90-100% for six of nine non-AMI diagnoses.
Commentary by Michael Felz, MD
The authors conclude that non-AMI etiologies of STE are far more common than AMI in patients with acute chest pain. Left ventricular hypertrophy was a more likely explanation by nearly two-fold (25% vs 15%), and a finding of left bundle-branch block was equal in frequency to AMI (15% for each in this series). Seven other entities, all relatively benign, accounted for an aggregate of 44% of STE diagnoses. Although the finding of STE on ECG in a patient with acute chest discomfort is justifiably worrisome, this study predicts a final diagnosis of a reassuring, non-life threatening condition by a ratio of nearly 6:1 compared to AMI. These data are meaningful not only to ED physicians, but also to primary care practitioners who work in busy offices where patients present with chest pain of possible cardiac origin. Three statements by the authors are authoritative and worth repeating: 1) "the presence of STE is demanding and must be explained;" 2) "precise interpretation of ECGs is a mandatory skill for ED physicians;" and 3) "STE is a primary criterion for thrombolysis or angioplasty but also is an insensitive marker of AMI." I believe this study illuminates, in rank-order fashion, the differential diagnosis of STE in ED (or office) patients with chest pain, and could be profitable reading for clinicians interpreting ECGs in urgent care settings. Although we cannot afford to miss the AMI that is evident on ECG, we must not overreact to STE. One might aptly surmise that there is more to the differential diagnosis of STE than meets the eye (for AMI).