Background: We report on 5 patients who presented to the emergency department (ED) with chest pain, had negative serum troponin levels, and were discharged with a presumed noncardiac diagnosis. Thereafter, retrospective analysis of Holter monitoring data recorded for a clinical trial revealed ST events indicative of transient myocardial ischemia that was unrecognized clinically.
Study aim: The purpose of this analysis was to determine whether initial body surface potential maps estimated from optimal ischemia electrode sites estimated body surface potential map (EBSPM) showed signs of ischemia in the missed ischemia group that could have prevented misdiagnosis.
Methods: This is a secondary analysis of data from a prospective clinical trial in which patients were attached to 2 Holter monitor devices for simultaneous recordings. One Holter device recorded a standard Mason-Likar 12-lead electrocardiogram (ECG) and the other recorded a 10-electrode lead set considered optimal for ischemia detection. A body surface potential map was then estimated from the optimal lead set.
Results: At 1 year, 2 of the 5 patients with missed ischemia died and a third had an acute myocardial infarction (MI) (40% mortality, 60% death/nonfatal MI). In comparison, 1-year mortality was 5.7% in 159 similar patients treated for unstable angina at the same institution over the same period (P = .037). The initial standard ECG showed no abnormalities in 3 patients and showed left ventricular hypertrophy in 1. The fifth patient with a history of recent MI had slight ST elevation in leads III and aVF and Q waves that were considered indicative of recent (not acute) MI. EBSPM data recorded at the time of ED presentation matched the standard ECG (normal in 3, left ventricular hypertrophy or inconclusive in 2). During transient ischemia, all 5 EBSPMs showed areas of ischemia overlapping with standard electrode sites.
Conclusion: Patients evaluated in the ED for chest pain are at high risk for death or nonfatal MI if they have ischemic events with continuous ST-segment monitoring that are unrecognized clinically. In this small cohort with unrecognized ischemia, the initial body surface potential maps estimated from optimal ischemia electrode sites did not improve on 12-lead ST-segment monitoring to identify this high-risk group.