In their recently published report, Taglieri et al reported the 1-year prognoses of patients presenting with non–ST-segment elevation acute coronary syndromes with ST-segment depression in ≥1 electrocardiographic (ECG) leads accompanied by ST-segment elevation in lead aVR. The investigators also confirmed the relatively high incidence of left main or triple-vessel disease in such patients, which had previously been reported. In an attempt to remove confounders, they independently analyzed patients with complete left bundle branch block and right bundle branch block (“pattern 5”). Patients with left bundle branch block exhibited abnormally wide QRS-T angles secondary to a slight leftward shift of the QRS axis and a marked rightward shift of the T-wave axis in the frontal plane. Much more common than left bundle branch block in patients, 80% of whom have histories of hypertension as in this study, is the presence of increased left ventricular (LV) mass. Nowhere in the investigators’ report do they appear to address this particular confounder. In most coronary-prone aged subjects, LV hypertrophy shifts the QRS axis slightly leftward in the frontal plane, with secondary ST-T abnormalities directed rightward. Indeed, the classic “LV strain pattern” is most often noted in limb leads 1 and aVL because of an ST-segment vector directed between +60° and +240°. An ST-segment vector directed anywhere between +120° and +240° will also exhibit ST-segment elevation in lead aVR. Indeed, ST-segment vectors oriented between 180° and +240° might be of sufficient magnitude to generate ≥1.0-mm ST-segment elevation in lead aVR, thus mimicking “pattern 4” (ST-segment depression plus ST-segment elevation in lead aVR), reported to have relatively high positive predictive value for left main or triple-vessel disease by the investigators. Although including patients demonstrating LV hypertrophy by voltage criteria in the “ECG confounder” group may have been helpful, it is well known that some patients with increased LV mass may exhibit repolarization abnormalities and yet fail to demonstrate adequate voltage criteria for ECG LV hypertrophy. Moreover, “LV hypertrophy with strain pattern” itself is a risk factor for sudden death, myocardial infarction, heart failure, and total mortality, the latter even in the absence of known coronary artery disease. Indeed, the inclusion of some of these patients in pattern 4 by the investigators may have contributed to the adverse prognoses observed in these patients. This additional insight should not detract from the value of their study but rather should alert the reader to more effectively exclude increased LV mass as a cause of ST-segment elevation in lead aVR accompanied by depression in other electrocardiographic leads.