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We sought to evaluate the prognostic significance of ST-segment elevation (STE) in lead aVR in unselected patients with non-STE acute coronary syndrome (NSTE-ACS). We enrolled 1,042 consecutive patients with NSTE-ACS. Patients were divided into 5 groups according to the following electrocardiographic (ECG) patterns on admission: (1) normal electrocardiogram or no significant ST-T changes, (2) inverted T waves, (3) isolated ST deviation (ST depression [STD] without STE in lead aVR or transient STE), (4) STD plus STE in lead aVR, and (5) ECG confounders (pacing, right or left bundle branch block). The main angiographic end point was left main coronary artery (LM) disease as the culprit artery. Clinical end points were in-hospital and 1-year cardiovascular death defined as the composite of cardiac death, fatal stroke, and fatal bleeding. Prevalence of STD plus STE in lead aVR was 13.4%. Rates of culprit LM disease and in-hospital cardiovascular death were 8.1% and 3.8%, respectively. On multivariable analysis, patients with STD plus STE in lead aVR (group 4) showed an increased risk of culprit LM disease (odds ratio 4.72, 95% confidence interval [CI] 2.31 to 9.64, p

More than a century after it was invented, standard ECG is enjoying a renaissance of sorts. With regard to acute ischemic heart disease, this phenomenon is due mainly to the availability of large databases that in an ordered and predefined manner collect patient ECG patterns along side their clinical and coronary angiography details as well as outcome data. The present review critically analyses the diagnostic role of standard ECG in acute coronary syndromes with or without ST-segment elevation (STEMI and NSTEMI, respectively) and focuses on interpretation pitfalls and patterns that can contribute to therapeutic decision-making. In front of a patient with a clinical presentation suggestive of acute myocardial infarction the ECG can help answer many questions. In case a STEMI is suspected: are we sure we can exclude an infarction? (the problem of false negatives); are we sure it is a real infarction and not a false positive? Which is the obstructed coronary artery and at what level? Has there been reperfusion? In case an NSTEMI is suspected: are we sure it is a real myocardial infarction, rather than a pulmonary embolism or an aortic dissection? Are we sure it is NSTEMI rather than a "masked" dorsal STEMI? Which coronary substrate and what ischemia extension can we hypothesize in this patient? In particular, is the substrate of such high risk suggesting an emergency invasive approach?