A 41-year-old male with no reported past medical history presents to the emergency department (ED) with one week of cough, dyspnea on exertion, palpitations, and exertional chest pain. Initial vital signs are all within normal limits. An index ECG is obtained and brought immediately to the emergency physician for review (Figure 1).
Interpretation:
Rate: 67 bpm; Rhythm: normal sinus rhythm; Axis: right axis deviation (I: neg., II: pos., aVF: pos.) Intervals: PR: 120, normal; QRS: 154, wide; QT: 412, normal; P-Waves: present, sinus orientation; QRS Complex: wide with a delta wave; ST Segment/T-waves: 1mm ST depression in II, III, aVF, V3-V6, T-wave inversions V2-3
What findings are concerning on this ECG? Would it make sense to activate the cath lab in the setting of this patient’s ST depressions and T wave inversions?
Discussion:
The patient was ultimately admitted for telemetry observation due to his persistent chest pain with recurrent sensation of palpitations and given a new diagnosis of Wolff-Parkinson-White (WPW) syndrome. Electrophysiology was consulted. A stress ECG was performed, showing pre-excitation with a likely left anterolateral accessory pathway.
ST depressions are often found in non-ischemic events (1). At first glance, it is easy to focus on the obvious ST depressions in this ECG (Figure 1) and, in the setting of active chest pain, be concerned for an ischemic event. However, delta waves - the slurred upstroke of the QRS complex - are also highly characteristic of WPW. While the presence of delta waves does not necessarily exclude an occlusive myocardial infarction (OMI) as the cause of the ST depression, they do suggest a possible alternative cause. When analyzing an ECG with ST depressions, one should keep a broad differential, which can be aided by the mnemonic ST DEPRESSED:
Secondary: abnormal conduction
Delayed conduction (RBBB, LBBB/paced)
Enlarged ventricle (LVH, RVH)
Pre-excitation (WPW)
Primary: acute coronary occlusion
Reciprocal to ST elevation
Early occlusion (deWinter T wave)
Primary: supply/demand mismatch
SVT (rate related)
Subendocardial ischemia (including non-occlusive MI, massive GI bleed, PE, sepsis)
Primary: metabolic/medication
Electrolyte (hypokalemia)
Digitalis (2).
Baseline ST depressions in WPW are caused by repolarization changes secondary to the abnormal depolarization of the myocardium via the accessory pathway (2). As seen with ECG stress testing, worsening of these depressions is caused by demand ischemia at rapid heart rates (4). ST changes that do not resolve with rest, are disproportionate in a particular vascular distribution (e.g. Sgarbossa criteria for LBBB), or are still present when accessory conduction is absent are all highly concerning for OMI.
Take Away Points:
Use the ST DEPRESSED mnemonic to help form your differential for ST depressions on ECG.
WPW commonly causes ST depressions related to depolarization/repolarization abnormalities through the accessory pathway and from secondary demand ischemia when tachycardia is present.
Not all ST depressions are related to ischemic events. However, presence of a secondary cause for ST depressions does NOT rule out a primary ischemic cause.
Authored by Taylor Wahrenbrock, MD; Michael Hohl, MD; and Ari Edelheit, MD.
References:
1. Pollehn T, Brady WJ, Perron AD, Morris F. The electrocardiographic differential diagnosis of ST segment depression. Emerg Med J. 2002;19(2):129-135. doi:10.1136/emj.19.2.129
McLaren J. ECG Cases 18 – ST Depressed Mnemonic and Occlusion MI. Emergency Medicine Cases. February 9, 2021. Accessed March 4, 2025. https://emergencymedicinecases.com/ecg-cases-st-depressed-mnemonic-occlusion-mi/.
Shah PP, Nair M, Dhall A, et al. False-positive exercise stress electrocardiogram due to accessory pathway in the absence of manifest preexcitation. Pacing Clin Electrophysiol. 2000;23(6):1051-1053. doi:10.1111/j.1540-8159.2000.tb00897.x
Larson NP, Rosenthal JB, Bridwell RE, Tannenbaum L, Cibrario A. Hide and Seek: Intermittent Preexcitation Wolff-Parkinson-White Syndrome Case Report and Management Overview. Cureus. 2020;12(7):e8971. Published 2020 Jul 2. doi:10.7759/cureus.8971