ECG tutorial: ST and T wave changes

INTRODUCTION — ST- and T-wave changes may represent cardiac pathology or be a normal variant. Interpretation of the findings, therefore, depends on the clinical context and presence of similar findings on prior electrocardiograms.

NONSPECIFIC ST-T-WAVE CHANGES — Nonspecific ST-T-wave changes are very common and may be seen in any lead of the electrocardiogram. The changes may be seen in all or most of the leads (diffuse changes), or they may be present contiguous leads, such as the inferior, lateral, or anterior leads.

The types of abnormalities are varied and include subtle straightening of the ST segment, actual ST-segment depression or elevation, flattening of the T wave, biphasic T waves, or T-wave inversion (waveform 1). In the absence of a clinical history or symptoms, T-wave abnormalities and flattened and depressed ST-segment changes are nonspecific. Some of the causes of these changes include:

●Functional and physiologic variants (eg, postprandial)

●Myocardial ischemia

●Any cardiomyopathy

●Myocarditis

●Pericarditis

●Post-cardiac surgery

●Pulmonary emboli or intrinsic pulmonary disease

●Drugs such as digoxin

●Fever

●Anemia

●Acidosis or alkalosis

●Electrolyte or other metabolic abnormalities

●Endocrine abnormalities

●Endogenous catecholamines

●Acute abdominal process

●Cerebrovascular accidents

Flat T waves and small ST-segment changes may also be seen in healthy individuals, including well-trained athletes, leading to mistaken diagnosis of heart disease. T-wave inversions, however, are more concerning for cardiomyopathy or other cardiac syndrome, depending on the clinical context.

Right precordial T-wave inversion — Right precordial T-wave inversion in adults may also represent myocardial disease such as ischemia, the Brugada syndrome (especially with coved-type ST elevations), or arrhythmogenic right ventricular cardiomyopathy (see "Brugada syndrome: Epidemiology and pathogenesis", section on 'Brugada pattern versus Brugada syndrome' and "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis", section on '12-lead ECG'). Lead misplacement, especially when the right-mid precordial leads are located above their usual positions, may also account for this pattern.

The prevalence and prognostic significance of right precordial T-wave inversion were evaluated in a study of over 10,000 middle-aged (mean age of 44 years) Finnish citizens followed for an average of 30 years [1]. T-wave inversion in leads V1 to V3 was present in 0.5 percent (more commonly in women) but this pattern did not predict increased mortality compared to individuals without this pattern. In contrast, those with T-wave inversions in leads other than V1 to V3 had an increased mortality compared with no T-wave inversions.

Persistent juvenile T-wave pattern — Another cause of right precordial T-wave inversion is the persistent juvenile T-wave pattern. The T-wave vector may be directed posteriorly in children, resulting in an inverted T wave in the right precordial leads V1 to V3. The vector usually becomes anterior with age, resulting in upright T waves in these leads; however, the T waves may remain inverted in V1 to V3 in a minority of adults, a finding known as a persistent juvenile pattern (waveform 2).

Black/African athlete repolarization variant — In up to 13 percent of Black/African athletes, a pattern of dome-shaped ST elevation with T-wave inversions, sometimes with biphasic T waves, may be seen in leads V1 to V4 [2]. This is considered a normal pattern in the asymptomatic athlete unless there is a positive family history or abnormal physical exam. ST changes or T-wave inversions in other leads are considered abnormal. T-wave inversions in the inferior leads may also be normal in Black/African athletes, but this variant needs further study [3].

ST-T-WAVE CHANGES ASSOCIATED WITH SPECIFIC DISEASE STATES — Specific patterns of ST-T-wave changes may be seen in association with various pathophysiologic states.

Myocardial ischemia, injury, and infarction — The electrocardiographic abnormalities seen with myocardial ischemia, injury, and infarction are presented separately. (See "ECG tutorial: Myocardial ischemia and infarction", section on 'Acute myocardial ischemia and infarction'.)

Pericarditis — ST-T-wave changes that are suggestive of pericarditis are usually seen diffusely in most or all limb and precordial leads, although in some cases, the changes may be isolated to only a few leads. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Electrocardiogram'.)

There is J-point elevation and ST-segment elevation, which has a concave morphology (waveform 3). The ST-segment elevation continues to have a normal concave morphology, regardless of how high the ST segment elevates (table 1). There are no reciprocal changes present, and the T waves maintain a normal morphology. Often, there is associated depression of the PR segment, although this does not have to be present to diagnose pericarditis. The PR and ST segment return to the isoelectric baseline. Some patients may later develop T-wave inversions after the ST segment has normalized, which frequently returns to normal over time (figure 1).

Left ventricular hypertrophy — The ST-T-wave abnormalities secondary to left ventricular hypertrophy (formerly termed "strain") are most often seen in the anterolateral leads (eg, I, aVL, V4 to V6); changes may also be seen in other leads when the hypertrophy is very severe (waveform 4A-B) (see "Left ventricular hypertrophy: Clinical findings and ECG diagnosis"). Typical abnormalities include a horizontal or downsloping ST segment and T-wave inversions. In some cases, there is concavity to the ST segment, which has a final downward turn that blends into an inverted T wave. Although most often there will be voltage criteria for left ventricular hypertrophy and often left atrial enlargement or left axis deviation, in some cases, only the ST-T-wave changes are observed.

The ST-T changes associated with left ventricular hypertrophy are termed "strain" but are thought to be either subendocardial ischemia or primary repolarization abnormalities. Subendocardial ischemia results from a relative lack of blood and oxygen supply to the hypertrophied muscle, as demand is greater than supply. Alternatively, the ST-T changes may be due to primary repolarization abnormalities of the hypertrophied cardiac muscle.

Right ventricular hypertrophy — Similar to the situation with left ventricular hypertrophy, ST-T-wave changes may be seen with right ventricular hypertrophy, likely representing subendocardial ischemia or primary repolarization abnormalities of the thickened right ventricle. These changes are seen in the right precordial leads V1 to V3.

Intraventricular conduction delays — ST-T-wave abnormalities secondary to intraventricular conduction disturbances, primarily left or right bundle branch block, are commonly seen and look similar to those that occur during ischemia (waveform 5). (See "Basic approach to delayed intraventricular conduction".)

The ST segments may be depressed or elevated. When there is an ST segment shift present, it is most often in a direction opposite to the polarity of the QRS complex. Similarly, the T wave also has a polarity opposite to the direction of the QRS complex. Thus, there are typically ST-segment depressions and T-wave inversions in leads V1 to V3 with a right bundle branch block, reflecting repolarization abnormalities of the right ventricular myocardium. In contrast, repolarization changes in the left ventricular myocardium due to a left bundle branch block result in downsloping ST depression and T-wave inversion in leads I, aVL, and V5 to V6, while the ST segment is elevated and the T wave is upright in leads V1 to V4.

Persistent ST elevation compatible with an aneurysm — Persistent ST-segment elevation compatible with an aneurysm may be seen in any leads showing changes of a previous myocardial infarction. There is usually coexistent evidence of a chronic myocardial infarction, such as a Q wave, an inverted T wave, and even reciprocal ST depressions (waveform 6). Elevation of the J point and ST-segment elevation, which is convex upward, is typically present, similar to what is seen with an evolving acute myocardial infarction pattern. The suspicion of an aneurysm is based upon the duration of this pattern, greater than three weeks after the acute infarction. The aneurysm is in the anterior wall when these persistent abnormalities are seen in the precordial leads V1 to V6, in the lateral wall when seen in leads I and aVL, and in the inferior wall when they are in the inferior leads II, III, and aVF. As the ST segment elevation is similar to what is seen with an acute myocardial infarction, the clinical history and time course of the acute infarction is important to establish the cause. Patients may have an aneurysm without ST elevation. It is thought that in some patients, persistent ST elevation may be more consistent with a dyskinetic wall rather than true aneurysm, due to abnormal stretch on the ventricular wall.

Prolonged QT interval — The QT interval is primarily a measure of membrane repolarization. The QT interval is measured from the beginning of the QRS complex (either a Q or R wave) to where a tangent line drawn on the downslope of the T wave intersects with the baseline. This is usually easiest to evaluate in leads II or V5. Any U wave, following the T wave, is not considered as part of the QT interval.

The time for ventricular repolarization and therefore the QT interval is dependent upon the heart rate; it is shorter at faster heart rates and longer when the rate is slower. Thus, a QT interval that is corrected for heart rate (QTc) is often calculated based on Bazett’s formula as follows:

Although this approach is simple, it is inaccurate at heart rate extremes and results in overcorrecting at high rates and undercorrecting at low ones.

A prolonged QT interval is present when the corrected QT interval is >0.450 seconds in men and >0.460 seconds in women (waveform 7) [4], although there is debate about whether this cutoff is too low. QT prolongation may be associated with either a prolonged ST segment or broad duration T wave. This may be due to genetic causes (congenital long QT syndrome) or acquired, due to drugs (class 1A or 3 antiarrhythmic agents, phenothiazines, tricyclic antidepressants), hypothermia, cerebrovascular diseases, or ischemic heart disease. A long QT (either acquired or congenital) is associated with a form of polymorphic ventricular tachycardia known as torsades de pointes. A corrected QT interval ≥0.500 seconds on repeated ECGs without a secondary cause is consistent with congenital long QT syndrome. (See "Congenital long QT syndrome: Epidemiology and clinical manifestations" and "Congenital long QT syndrome: Treatment" and "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)

Since the QRS widens in the setting of a bundle branch block, the QT interval will lengthen. This increase in QT interval does not reflect an abnormality of ventricular repolarization, since the increase is due to an abnormality of depolarization. There have not been many descriptions on how to measure QT interval in the setting of QRS widening. In the setting of left bundle branch block, in one study, the QT interval prolonged by about half the QRS duration [5]. Therefore, a modified QT interval using the "Bogossian formula" can be calculated as QT – 48.5 percent (QRS duration). This value must still be corrected for heart rate using Bazett’s or another formula. Another option to correct for left bundle branch block (LBBB) is to measure the JT interval, corrected for rate: QTc – QRS = JTc. The QTc pre-LBBB = JTc plus 95 ms for males or 88 ms for females [6]. (See "ECG tutorial: Basic principles of ECG analysis", section on 'QT interval'.)

Short QT interval — A short QT interval, indicative of acceleration of ventricular repolarization, is present when the QTc is <0.36 s (waveform 8). A short QT interval is seen with hypercalcemia, hyperkalemia, or digitalis use. A hereditary short QT syndrome has also been described as associated with increased risk of sudden cardiac arrest due to ventricular tachyarrhythmias [7]. (See "Short QT syndrome".)

Tall T waves — Tall T waves may be seen in a variety of settings. Classical peaked or "tented" narrow-based T waves are usually the result of hyperkalemia, which may be systemic or localized (waveform 9). While no frequently-used criteria have been validated, they may be generally >10 mm in height as measured in the precordial leads, and >5 mm in height in the limb leads, or only relatively tall compared with baseline. This appearance is in contrast to the normal T wave, which is asymmetric (the initial upstroke is slow while the end or downstroke is rapid) regardless of its amplitude. Tall T waves may be seen with left ventricular hypertrophy or even in normal subjects who have tall QRS complex amplitude.

In addition to hyperkalemia, prominent (so-called "hyperacute") T waves may be seen in the early phases of an acute myocardial infarction or with myocardial ischemia (possibly related in part to localized extracellular hyperkalemia) (see "Electrocardiogram in the diagnosis of myocardial ischemia and infarction"). Tall T waves may also be seen in the presence of left ventricular hypertrophy or left bundle branch block, in which the amplitude of the QRS complex is increased, or may even be a normal variant; in these cases, the T waves are not peaked and still have an asymmetric morphology, often as part of the benign early repolarization variant.

Prominent U waves — U waves are positive deflections that are generally seen in leads V2 to V4. They are usually low voltage (<0.2 mV) and have the same polarity as the T wave. U waves may be seen in normal individuals, primarily in the right precordial leads. Their origin is not certain, but they may represent late repolarization of the His Purkinje system or of the mid-myocardial M cells. Abnormalities of the U wave may be seen in the following circumstances:

●A prominent U wave may be indicative of hypokalemia (figure 2). Other conditions that may increase the amplitude of the U wave include bradycardia, class 1A and 3 antiarrhythmic drugs (as well as multiple others), intracranial hemorrhage, and certain forms of the congenital long QT syndrome. In this situation, the U wave is not after the T wave, but is superimposed on the T wave, interrupting it. (See "Congenital long QT syndrome: Epidemiology and clinical manifestations".)

●The polarity of the U wave may reverse (eg, become negative in mid-lateral precordial leads) in the presence of myocardial ischemia or left ventricular overload. Negative U waves during exercise testing have been reported to correlate with significant stenosis of the left main or left anterior descending coronary artery.

SUMMARY

●Nonspecific ST-T-wave changes – Nonspecific ST-T-wave abnormalities are very common and may be seen in any limb or precordial leads of the electrocardiogram (waveform 1). (See 'Nonspecific ST-T-wave changes' above.)

●Disorders with specific ST- and T-wave patterns – More specific patterns of ST-T-wave changes, which may be seen in association with various disease states, include: (See 'ST-T-wave changes associated with specific disease states' above.)

•Acute ischemia – Typically, there are ST-segment changes (eg, depression or elevation) associated with T-wave flattening or inversion. Inverted T waves are often symmetric. (See 'Myocardial ischemia, injury, and infarction' above.)

•Myocardial injury – ST-segment elevation (above baseline, ie, T-P segment) and T-wave abnormalities that are indicative of transmural myocardial ischemia or injury or a myocardial infarction. They are usually localized to those leads that reflect the involved regions of the myocardium. Reciprocal changes (ST depression in other leads) and hyperacute T waves (tall, peaked, and symmetric) are usually present. (See 'Myocardial ischemia, injury, and infarction' above.)

•Pericarditis – ST-T-wave changes that are suggestive of pericarditis are usually diffusely seen in most or all limb and precordial leads, although in some cases, the changes may be isolated to only a few leads (table 1 and figure 1 and waveform 3). Reciprocal changes and hyperacute T waves are not seen. (See 'Pericarditis' above.)

•Intraventricular conduction delays – ST-T-wave abnormalities secondary to intraventricular conduction disturbances (eg, left or right bundle branch block) are commonly seen and look similar to those that occur during ischemia (waveform 5). (See 'Intraventricular conduction delays' above.)