What is ST Depression?
ST depression is a downward displacement of the ST segment on the electrocardiogram, measured relative to the end of the PR segment (the P-Q junction), representing electrical gradients generated by ischemic vectors across the endocardium and epicardium. 1
Physiological Mechanism
ST depression occurs when demand ischemia during exercise or stress is limited primarily to the endocardium, with reductions in phase 2 plateau amplitude and less negative phase 4 resting membrane potentials contributing to the ST depression visible on the surface ECG. 1 The ST segment is measured at 60 to 80 milliseconds after the J point (the junction between the QRS complex and ST segment) because the T(U)-P segment during exercise becomes difficult or impossible to measure when heart rates are elevated. 1
Types of ST Depression
There are three distinct morphological patterns, each with different clinical significance: 1
Horizontal ST depression: The ST segment remains flat (horizontal) at ≥1.0 mm below baseline at 60-80 ms after the J point—this is considered a positive standard ECG response indicating myocardial ischemia 1
Downsloping ST depression: The ST segment slopes downward at ≥1.0 mm below baseline at 60-80 ms after the J point—this is also considered a positive standard ECG response and is more specific for ischemia than horizontal patterns 1, 2
Upsloping ST depression: The ST segment slopes upward but remains depressed—this is generally considered an "equivocal" test response because it is comparably prevalent in patients with coronary artery disease and in normal subjects, making it not usefully predictive for myocardial ischemia in general populations 1, 3
Diagnostic Criteria
The standard criteria for test positivity include horizontal or downsloping ST depression ≥1 mm (0.1 mV) at 60 to 80 ms after the J point. 1 Three or more consecutive beats in the same lead with a stable baseline should be identified and the average magnitude measured, either manually or by computer-averaged complexes, though visual verification of automated measurements is essential. 1
When modest resting ST depression is present on the upright control ECG before exercise, only additional ST depression during exercise is measured for analysis. 1
Clinical Significance and Severity Markers
The anatomic and functional severity of coronary artery disease relates directly to several characteristics of ST depression: 1
Timing of onset: The lower the workload and rate-pressure product at which ST depression occurs, the worse the prognosis and the more likely the presence of multivessel disease 1
Magnitude: Greater degrees of ST depression indicate more extensive coronary artery disease and worse prognosis 2
Duration in recovery: Prolonged ST depression during the recovery phase correlates with more severe coronary artery disease 1, 2
Number of leads involved: ST depression in multiple leads correlates with more extensive coronary artery disease 2
Reciprocal Changes vs. True Ischemia
A critical pitfall in interpretation is distinguishing true ischemic ST depression from reciprocal changes: 1
ST depression can represent either primary ischemia or the reciprocal of ST elevation occurring in the opposite anatomic region. For example, ST depression in leads V1-V3 may indicate posterior wall ischemia (especially when the terminal T wave is positive), representing the reciprocal of what would be ST elevation if posterior leads were recorded. 1, 2
In patients with prior Q-wave myocardial infarction, ST depression in high lateral leads (I, aVL) often represents reciprocal changes from ST elevation in inferior leads rather than indicating new ischemia—there is a significant inverse linear correlation (r = -0.8) between ST segment shift in inferior and high lateral leads. 4
Common Non-Ischemic Causes
ST depression must be distinguished from non-ischemic causes: 1, 2
Left ventricular hypertrophy: The most common cause of ST depression in hypertensive patients, resulting from structural modifications that alter normal repolarization patterns 5
Bundle branch blocks: Left bundle branch block and right bundle branch block commonly produce ST-T abnormalities 1
Electrolyte abnormalities: Lowered serum potassium can cause ST depression 1
Medications: Cardioactive drugs and thiazide diuretics (causing hypokalemia/hypomagnesemia) may produce ST-segment changes 1, 5
Other conditions: Pericarditis, cardiomyopathies, hypothermia, and intracranial processes 1
Measurement Technique
At ventricular rates >130 beats/min, 60 ms after the J junction is optimal to determine the extent of ST segment displacement. 3 The ST level is measured relative to the end of the PR segment because this remains identifiable even at high heart rates. 1 In the presence of resting ST-segment elevation at 60 to 80 ms after the J point due to early repolarization, only ST-segment changes below the P-Q baseline should be used for analysis. 1