Electrocardiographic ST segment elevation: A comparison of AMI and non-AMI ECG syndromes

Chest pain (CP) patients presenting to the ED may manifest electrocardiographic ST segment elevation (STE). AMI (acute myocardial infarction) is a less frequent cause of such abnormality and one of many patterns responsible for ST segment elevation in ED CP patients. We performed a retrospective comparative review of the electrocardiographic features of various STE syndromes, focusing on differences between AMI and non-AMI syndromes. The electrocardiograms (ECGs) of consecutive ED adult CP patients (with 3 serial troponin I determinations) were interpreted by 3 attending emergency physicians. These ECGs with STE represented the study population used for analysis. Various electrocardiographic features such as STE, ST segment depression (STD), STE morphology, anatomic distribution of STE, and the number of leads with STE were recorded; derived values such as total STE, total ST segment deviation, and average STE per lead were calculated. Interobserver reliability concerning STE morphology was determined. AMI was diagnosed by abnormal serum troponin I values (>0.1 mg/dL) followed by a rise and fall of the serum marker; STE diagnoses of non-AMI causes were determined by medical record review. Five hundred ninety-nine CP patients were entered in the study with 212 (35%) individuals showing STE, 55 (26%) with electrocardiographic AMI and 157 (74%) with non-AMI electrocardiographic syndromes. Anatomic location within the AMI group included 32 inferior and inferior variants, 18 anterior and anterior variants, and 5 lateral; non-AMI anatomic locations included 56 inferior and inferior variants, 98 anterior and anterior variants, and 3 lateral; anterior STE occurred significantly more often in non-AMI syndromes. Total STE was 15.3 mm in AMI patients and 7.4 mm in non-AMI patients (P =.0004). The number of leads with STE was not significantly different between the two groups, 3.4 mm in AMI and 4.1 in non-AMI syndromes. ST segment elevation per lead was not significantly different in the 2 groups, 4.4 mm in AMI versus 1.8 mm in non-AMI syndromes. Total ST segment deviation (sum of STE and STD) was significantly greater in AMI syndromes, 17.8 mm in AMI compared with 10.5 mm in non-AMI syndromes (P =.00009). The presence of STD occurred at statistically similar rates in both groups. The morphology of the STE occurred in significantly different rates between AMI and non-AMI patterns, concave more often in non-AMI patterns (P <.00001) and nonconcave more often in AMI (P <.00001). Non-AMI causes of STE account for the majority of electrocardiographic syndromes encountered in ED chest pain patients. These findings alone are not adequate to determine the electrocardiographic cause of the ST segment elevation in chest pain patients. When determining AMI versus non-AMI with the ECG, these various findings should be used in the consideration of the overall clinical picture (history, examination, and electrocardiogram) in chest pain patients with ST segment elevation.