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ST segment

The ST segment is the electrically neutral portion of an electrocardiogram (ECG) waveform that extends from the J point—the junction between the end of the QRS complex and the beginning of the T wave—to the onset of the T wave, representing the period between ventricular depolarization and repolarization.^[1]^[2] Physiologically, the ST segment corresponds to the plateau phase (phase 2) of the ventricular myocardial action potential, during which there are minimal voltage gradients across the cell membrane, resulting in an isoelectric (flat) line on the ECG under normal conditions.^[1]^[2] In a normal ECG, the ST segment is typically isoelectric or nearly so, with the J point serving as the reference for measuring deviations; subtle variations, such as early repolarization patterns, may cause minor J-point elevation up to 3 mm in young males or 1.5 mm in females in precordial leads V2-V3 (assuming standard 10 mm/mV calibration), but these are considered benign and influenced by factors like age, gender, and race.^[1]^[2] Abnormal ST segment changes, such as elevation or depression relative to the baseline (using the PQ junction as reference per ACC/AHA guidelines), are key indicators of cardiac pathology, particularly myocardial ischemia or infarction.^[1] ST elevation of ≥1 mm in two or more contiguous limb leads or ≥2 mm in precordial leads V2-V3 (≥1.5 mm in women) often signals acute ST-elevation myocardial infarction (STEMI) due to transmural injury, while ST depression of ≥0.5 mm (horizontal or downsloping) suggests subendocardial ischemia, as seen in non-STEMI or unstable angina.^[2]^[1] Other causes include pericarditis (diffuse concave-upward elevation), electrolyte imbalances like hypokalemia (depression), or non-ischemic conditions such as left ventricular hypertrophy; clinical correlation and serial ECGs are essential for accurate interpretation, as morphology (e.g., convex vs. concave) and reciprocal changes aid in differentiation.^[1]^[2]

Definition and Physiology

Anatomical Position in ECG

The ST segment is defined as the portion of the electrocardiogram (ECG) tracing that extends from the J point, which marks the end of the S wave in the QRS complex, to the onset of the T wave.^[2] This segment represents the transition from the completion of ventricular depolarization to the start of repolarization, bridging the QRS complex and the T wave in the cardiac cycle.^[1] In relation to the QRS complex, the ST segment immediately follows the downslope of the S wave, signifying the end of the rapid depolarization phase and the entry into the plateau of the action potential where early repolarization begins.^[3] It thus connects the depolarized state of the ventricles, captured by the QRS, to the subsequent repolarization phase depicted by the T wave.^[4] Visually, the ST segment appears as a flat, isoelectric line at the baseline level in most ECG leads under normal conditions, though it may exhibit a slight upward concavity or minimal curvature, particularly in precordial leads (V1-V6) where it can show minor elevations up to 2.5 mm (0.25 mV) in leads like V2-V3, contrasting with the more consistently horizontal profile in limb leads (I, II, III, aVR, aVL, aVF).^[2] This lead-specific variation arises from the angular projections of the heart's electrical activity but maintains an overall isoelectric quality without significant deviation.^[3] The nomenclature and positional description of the ST segment originated in the early 20th century with Willem Einthoven's pioneering work on the string galvanometer, which enabled detailed recording and labeling of ECG waveform components, including the sequence from QRS to T wave.^[5] Einthoven's systematic analysis in the 1900s established the standard framework for identifying the ST segment within the PQRST complex.^[6]

Normal Morphology and Duration

The ST segment in a normal electrocardiogram (ECG) represents the interval from the end of the QRS complex, specifically the J point, to the onset of the T wave, spanning the early phase of ventricular repolarization. Under healthy conditions, its duration typically measures 80 to 120 milliseconds, corresponding to less than 2 to 3 small squares (each 40 ms) on standard ECG paper.^[7] This duration reflects the time during which ventricular myocytes maintain a relatively stable membrane potential following depolarization. The segment is measured precisely from the J point, the junction where the QRS complex transitions to the ST segment, to the point where the T wave begins its upslope, ensuring accurate assessment of repolarization dynamics.^[7] In terms of morphology, the normal ST segment appears isoelectric, lying at the same baseline level as the PR segment in most leads, with a slight upward concavity that contributes to its smooth transition to the T wave. This flat or minimally sloped configuration arises from balanced voltage gradients across the ventricular myocardium during the plateau phase. Amplitude deviations from the baseline are minimal, typically less than 2.5 mm (0.25 mV) in precordial leads, though lower in limb leads; slight elevations up to 0.25 mV in precordial leads like V2-V3 can occur without pathology, particularly in younger individuals. Physiological variations influence this morphology; for instance, faster heart rates may shorten the segment slightly due to compressed repolarization timing, while age and sex affect elevation thresholds—males under 40 years often show up to 0.25 mV elevation in V2-V3, compared to 0.15 mV in females, with thresholds decreasing with advancing age.^[1]^[1]^[8] The physiological basis of the ST segment lies in phase 2 of the ventricular action potential, the plateau phase, where inward calcium currents balance outward potassium currents, maintaining a near-zero net voltage change across the myocardium. This equilibrium results in the isoelectric appearance, as subepicardial and subendocardial regions repolarize synchronously without significant injury currents. Ethnic variations can introduce benign deviations; for example, individuals of African descent may exhibit higher normal ST elevations (e.g., ST segment 60 ms after the J point up to 0.35 mV in V2 for Black males versus 0.30 mV for White males), reflecting genetic differences in ion channel expression. Additionally, early repolarization patterns, characterized by J-point elevation and a rapidly upsloping ST segment, are common in athletes with prevalence ranging from 10% to over 50% in young athletes due to enhanced vagal tone and physiological hypertrophy, and considered a normal variant rather than a risk factor in this population.^[1]^[1]^[9]

Measurement Techniques

Manual Measurement Methods

Manual measurement of the ST segment in electrocardiography (ECG) involves direct visual inspection and physical assessment of paper-based or printed ECG tracings by clinicians, a practice essential for accurate diagnosis in settings without digital tools. This technique relies on identifying key anatomical landmarks and quantifying deviations from the baseline using standardized calibration. The process ensures precise evaluation of potential ischemic changes, with measurements typically expressed in millimeters (mm), where 1 mm corresponds to 0.1 mV under standard ECG amplification of 10 mm/mV.^[1] The step-by-step process begins with identifying the J point, defined as the junction where the QRS complex ends and the ST segment begins, marking the offset of ventricular depolarization. Next, establish the reference baseline using the PQ junction (the end of the PR segment) as recommended by the American College of Cardiology/American Heart Association (ACC/AHA) guidelines, since the TP segment may be obscured in conditions like tachycardia. For ST elevation, measure the vertical deviation from this baseline to the J point in each lead. For ST depression, particularly in cases of sloping segments, measure the deviation 60-80 ms after the J point (ST60 or ST80), adjusting to 60 ms if the heart rate exceeds 120 beats per minute to account for shorter cycle lengths. If the ST segment is upsloping or downsloping, some protocols involve drawing a tangent line from the PQ junction parallel to the initial ST slope to determine the deviation point, ensuring consistency across leads.^[1]^[10]^[11] Tools for manual measurement include ECG calipers—a pair of adjustable metal points used to bridge distances on the ECG paper—or a straight ruler for linear assessments. Calipers are placed from the baseline to the measurement point (J point or ST60/ST80), with the distance read against the grid lines for quantification. Lead-specific criteria apply: in precordial leads V2-V3, measurements account for age and sex variations (e.g., higher thresholds for younger males), while limb and other precordial leads use uniform standards of ≥1 mm (0.1 mV) for significant deviation. All ECGs must be standardized to 10 mm/mV gain to avoid measurement errors from variable amplification.^[1]^[10]^[2] Common pitfalls in manual measurement include baseline wander caused by patient movement or electrode issues, which distorts the isoelectric line and requires selecting a stable segment for reference. Artifacts from muscle tremor or loose leads can mimic ST changes, necessitating verification of tracing quality before measurement. Difficulty identifying the J point in morphologies like left ventricular hypertrophy or early repolarization may lead to over- or underestimation, so clinicians should cross-check multiple leads and cycles for reproducibility. The normal ST segment duration typically spans 80-120 ms, but manual methods focus on deviation rather than length.^[1]^[2] Historically, manual measurement with calipers has been a cornerstone of ECG interpretation since the 1920s, following Willem Einthoven's development of the string galvanometer in 1903, which produced paper-based tracings requiring physical tools for analysis. By the 1920s, clinicians routinely used calipers to assess ST deviations in diagnosing myocardial infarction, predating digital systems and establishing the foundation for modern standardization efforts. This hands-on approach persisted in clinical settings through the mid-20th century, emphasizing clinician training in precise, reproducible techniques.^[6]^[12]

Automated and Digital Analysis

Automated and digital analysis of the ST segment in electrocardiography (ECG) employs computer algorithms to detect and quantify deviations, enabling objective evaluation beyond manual methods. These systems process ECG signals through stages including preprocessing for noise reduction, fiducial point identification, feature extraction such as slope and amplitude measurements, and classification for clinical interpretation.^[13] Core algorithms begin with fiducial point detection, particularly the J point, which marks the junction between the QRS complex and ST segment. This point is typically identified within a 100 ms window starting 20 ms after the R-wave peak, using criteria like a slope threshold of ≤2.5 μV/ms to ensure accuracy amid variability in heart rate or noise.^[13] Slope analysis follows, measuring the ST segment's incline from the J point to points like J80 (80 ms post-J) or J60 during tachycardia (heart rate >120 bpm), to identify ischemic patterns through quantitative gradients.^[13] Deviation scoring quantifies ST displacement relative to the isoelectric baseline (TP segment), often flagging elevations or depressions ≥0.1 mV sustained for ≥30 seconds as potential indicators of acute events.^[13] Signal processing techniques, such as Short-Time Fourier Transform (STFT) or wavelet transforms, preprocess signals by applying band-pass filters (e.g., 0.2–100 Hz) to mitigate baseline wander, muscle artifacts, and power-line interference, enhancing reliability.^[13] These algorithms integrate into clinical devices like 12-lead ECG machines and Holter monitors for continuous or snapshot analysis, supporting real-time ST segment tracking in ambulatory or inpatient settings.^[14] The American Heart Association (AHA), American College of Cardiology (ACC), and Heart Rhythm Society (HRS) recommend standardization in automated ECG processing, including high-fidelity sampling (≥500 Hz) and validation against manual measurements to achieve diagnostic accuracy comparable to experts, with specific guidelines for ST interpretation in complex rhythms like left bundle branch block.^[14] Advantages include real-time monitoring for dynamic changes and quantitative indices like the ST integral, which computes the area under the ST segment curve from J point to T-wave onset, providing a sensitive metric for ischemia severity over amplitude alone.^[15] However, limitations arise in arrhythmia detection, where irregular rhythms can distort fiducial points and lead to false positives or missed deviations, necessitating hybrid approaches with manual oversight.^[13] Post-2010 advancements leverage artificial intelligence (AI), particularly deep learning networks, to enhance ST segment detection by analyzing raw waveforms for subtle patterns overlooked by rule-based methods. Convolutional neural networks (CNNs) trained on large datasets like PhysioNet have achieved sensitivities >90% for ST-elevation myocardial infarction (STEMI), surpassing traditional algorithms in noisy or atypical cases.^[16] These AI models integrate multimodal data, such as demographics, to refine predictions, with ongoing validation emphasizing explainability and generalizability across populations.^[17]

Clinical Significance in Adults

ST Elevation Patterns

ST segment elevation refers to an upward displacement of the ST segment above the baseline on the electrocardiogram (ECG), typically assessed at the J point (the junction between the QRS complex and ST segment) and confirmed 60 ms later to distinguish from transient changes. The standard diagnostic criterion for pathological ST elevation, particularly in the context of ST-elevation myocardial infarction (STEMI), requires new elevation of ≥2.5 mm (0.25 mV) in men under 40 years, ≥2 mm (0.2 mV) in men 40 years and older, or ≥1.5 mm (0.15 mV) in women in leads V2–V3, and/or ≥1 mm (0.1 mV) in other contiguous chest or limb leads.^[18] This elevation must occur in at least two contiguous leads to indicate a regional process, with variations based on age, sex, and lead location to improve specificity.^[18] The morphology of ST elevation provides key diagnostic clues, categorized as convex (upward bulging, often "tombstone"-like), concave (scooped upward), or oblique (straight or linearly ascending). Convex or oblique morphologies are highly suggestive of acute transmural injury in STEMI, as they reflect myocardial cell depolarization abnormalities during ischemia, whereas concave patterns are more commonly associated with non-ischemic or benign etiologies.^[19] These shapes influence interpretation: for instance, a convex pattern blending into the T wave increases suspicion for infarction, while a pronounced concave form with preserved J point notching favors non-pathologic variants. Primary causes of ST elevation include acute myocardial infarction (STEMI), pericarditis, and benign early repolarization. In STEMI, resulting from coronary artery occlusion, the elevation signifies transmural ischemia and is often localized to leads overlying the affected territory, such as anterior (V1–V4) or inferior (II, III, aVF) walls.^[18] Pericarditis typically produces diffuse concave ST elevation across multiple leads (except aVR and V1), reflecting subepicardial inflammation, frequently accompanied by PR segment depression.^[20] Benign early repolarization, prevalent in young males, features J-point elevation ≥0.1 mV with concave ST segments and notching or slurring, representing a normal variant without clinical sequelae in most cases.^[21] Diagnostic evaluation emphasizes specific features like reciprocal ST depression in leads opposite the elevation, which strongly supports STEMI—particularly in inferior infarctions where depression appears in anterior leads (aVL, I).^[14] Such changes enhance specificity, as isolated elevation without reciprocity is less indicative of occlusion. Time-sensitive protocols are critical; American Heart Association guidelines recommend door-to-balloon reperfusion within 90 minutes of first medical contact for STEMI to minimize myocardial damage.^[22] ST elevation appears in 5–10% of ECGs obtained in emergency departments, often prompting urgent evaluation, though many cases represent mimics rather than infarction.^[23] In evolving STEMI, the pattern typically progresses from hyperacute T waves—tall, symmetric, and broad-based, indicating early ischemia—to full ST elevation, followed by Q-wave formation if untreated.^[24] This temporal evolution underscores the need for serial ECGs in suspected cases to capture dynamic changes.

ST Depression and Ischemia

ST segment depression serves as an electrocardiographic marker of myocardial ischemia, particularly in adults, where it reflects subendocardial involvement due to an imbalance between myocardial oxygen supply and demand. The diagnostic criteria for ischemic ST depression typically include horizontal or downsloping depression of ≥0.5 mm measured at the J point plus 80 ms in at least two contiguous leads, as this pattern is more specific for ischemia compared to upsloping depression, which is less reliable.^[25]^[26] This measurement is often assessed during exercise or at rest in symptomatic patients to identify reversible ischemia linked to coronary artery disease.^[27] Pathophysiologically, ST depression arises from subendocardial ischemia, where the innermost layer of the ventricular myocardium experiences oxygen deprivation, leading to altered repolarization currents that oppose the normal epicardial vector and manifest as depression on the surface ECG.^[28] This supply-demand mismatch is commonly associated with coronary artery disease, where atherosclerotic narrowing limits blood flow, exacerbating ischemia during increased demand such as physical exertion.^[1] In contrast to ST elevation, which signals acute transmural injury, ST depression indicates more localized, subendocardial changes that are often reversible with treatment.^[14] Clinically, ST depression is prominent in stable angina, where it appears during episodes of chest pain due to exertional ischemia, and in exercise stress testing, such as >1 mm horizontal or downsloping depression during stage III of the Bruce protocol, aiding in the detection of coronary stenoses.^[29] It plays a key role in risk stratification through integration into the Duke Treadmill Score, which combines ST deviation (in mm), exercise duration, and angina index to categorize patients into low-, intermediate-, or high-risk groups for cardiac events, with scores ≤-11 indicating high risk.^[30] This score has been validated in symptomatic patients to predict prognosis and guide further invasive evaluation.^[31] Notably, ST depression can be transient in vasospastic angina (Prinzmetal angina), where coronary artery spasm induces reversible ischemia, often resolving spontaneously or with vasodilators, and may present as ST depression in cases of milder or distal spasm.^[32] In exercise ECG testing among patients with suspected coronary disease, ischemic ST depression occurs in approximately 20-30% of cases, correlating with multivessel disease and influencing decisions for angiography.^[27]

Applications in Monitoring

Fetal Heart Rate Monitoring

In intrapartum fetal heart rate monitoring, the ST segment of the fetal electrocardiogram (ECG) is analyzed to detect signs of fetal hypoxia and acidosis, serving as an adjunct to conventional cardiotocography (CTG). This technique involves placing a spiral scalp electrode on the fetal presenting part during labor to acquire a direct fetal ECG signal, which is then processed by specialized systems like the STAN (ST Analysis) monitor developed by Neoventa Medical in Sweden.^[33]^[34] The STAN system, introduced for clinical use in 2000 following initial development in the 1990s, automates the detection of ST waveform changes by comparing them to baseline values, integrating this data with CTG tracings for real-time interpretation.^[35] ST segment alterations, such as prolongation, elevation, or biphasic patterns, reflect myocardial metabolic responses to oxygen deprivation, indicating potential fetal distress when occurring alongside abnormal CTG patterns like decelerations.^[36] These changes arise from anaerobic metabolism during hypoxia, with ST elevation (positive ST events) signaling increased risk of acidosis, particularly in the presence of repetitive decelerations, and ST depression (negative ST events) often appearing as an early compensatory response.^[33] When combined with CTG, ST analysis enhances diagnostic specificity, reducing false positives for fetal compromise and thereby decreasing unnecessary interventions; randomized trials, including early Swedish studies from the 1990s, demonstrated up to a 50% reduction in operative deliveries for suspected fetal distress in high-risk cases. While early trials suggested reductions, recent meta-analyses show no overall decrease in operative vaginal and cesarean deliveries but confirm lower rates of metabolic acidosis at birth.^[37]^[38] The STAN approach received conditional FDA approval in 2005 as an adjunct to CTG for term pregnancies with intact membranes and normal fetal heart rate at baseline, based on evidence from pivotal trials showing improved perinatal outcomes.^[34] However, its application is limited in preterm gestations (typically below 36 weeks) due to immature fetal ECG patterns and higher baseline variability, as well as in cases of poor electrode contact, maternal infection risk from scalp placement, or non-cephalic presentations like breech. However, as of 2025, the American College of Obstetricians and Gynecologists (ACOG) recommends against routine use of STAN due to limited evidence of improved perinatal outcomes.^[39]^[40] These constraints underscore the need for strict adherence to guidelines, with ongoing research addressing implementation challenges to optimize its role in intrapartum surveillance. Parallels to adult ECG monitoring exist, where ST changes similarly indicate myocardial ischemia, but fetal applications focus uniquely on intrapartum hypoxia detection.^[36]

Exercise Stress Testing

Exercise stress testing integrates continuous electrocardiographic monitoring of the ST segment to identify inducible myocardial ischemia in adults suspected of coronary artery disease (CAD). Patients undergo graded exercise on a treadmill or cycle ergometer, typically following the Bruce protocol with progressive increases in workload every 3 minutes, until they reach at least 85% of their maximum predicted heart rate (calculated as 220 minus age) or develop symptoms limiting continuation.^[41] ST segment changes are assessed in leads V5 and V6 for maximal sensitivity, with measurements taken at peak exercise and throughout a 6- to 8-minute recovery phase.^[41] A key diagnostic criterion is horizontal or downsloping ST segment depression of 1 mm or greater, measured 60 to 80 milliseconds after the J point, which indicates significant CAD with a sensitivity of 68% and specificity of 77% based on meta-analysis of 147 studies.^[41] Upsloping ST depression is generally non-specific and less indicative of ischemia, occurring in 10% to 20% of healthy individuals, whereas downsloping patterns signal higher-risk multivessel disease.^[41] Prolonged ST depression persisting more than 6 minutes into recovery correlates with adverse prognosis, including increased mortality risk over 5 to 7 years.^[42] Influencing factors can alter ST segment responses; for instance, beta-blockers attenuate heart rate acceleration and may mask ischemic changes, thereby reducing test sensitivity.^[41] To mitigate false-positive results, particularly in patients with baseline abnormalities or low pretest probability, adjunct imaging such as stress echocardiography or myocardial perfusion scintigraphy is often employed to enhance specificity.^[43] These interpretations draw from foundational evidence in the Coronary Artery Surgery Study (CASS) registry of the 1970s and 1980s, which demonstrated that exercise-induced ST depression of at least 1 mm predicts survival benefits from revascularization in patients with preserved left ventricular function, and are reflected in the American Heart Association's 2013 guidelines on exercise standards.^[44]^[41]

References

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