ST-segment elevation: Differential diagnosis, caveats

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ABSTRACTThe differential diagnosis of ST-segment elevation includes four major processes: ST-segment elevation myocardial infarction (STEMI); early repolarization; pericarditis; and ST elevation secondary to an abnormality of the QRS complex (left bundle branch block, left ventricular hypertrophy, or preexcitation). Other processes that may be associated with ST elevation include hyperkalemia, pulmonary embolism, and Brugada syndrome. The clinical setting and specific electrocardiographic criteria often allow identification of the cause. This article reviews ST-T and QRS configurations specific to each diagnosis.


  • Features of STEMI: (1) ST elevation that is straight or convex upward and blends with T to form a dome; (2) wide upright T or inverted T waves; (3) Q waves; (4) ST elevation or T waves that may approximate or exceed QRS height; and (5) reciprocal ST depression.
  • Features of early repolarization include a notched J point and ST elevation not exceeding 3 mm.
  • Features of pericarditis include PR depression greater than 1 mm and ST elevation less than 5 mm.
  • Features of left bundle branch block, left ventricular hypertrophy, and preexcitation: both ST and T are discordant to QRS; ST elevation is less than 25% of QRS height (and less than 2.5 mm in left ventricular hypertrophy); and delta waves, short PR, and pseudo-Q waves are seen in preexcitation.
  • Features of hyperkalemia include narrow-based, peaked T waves “pulling” the ST segment.



When the ST segment is elevated on the electrocardiogram, our first concern is whether the patient is having an ST-segment elevation myocardial infarction (STEMI). However, a number of other conditions can cause ST elevation, and to complicate matters, some of these can coexist with STEMI.

Nevertheless, careful attention to the ST-T and QRS-complex configurations often allows diagnosis of the cause of ST elevation (Figure 1, Table 1). This paper discusses the differential diagnosis of ST elevation.

Figure 1.


ST-segment deviation is usually measured at its junction with the end of the QRS complex, ie, the J point, and is referenced against the TP or PR segment.1 Some authors prefer measuring the magnitude of the ST deviation 40 to 80 msec after the J point, when all myocardial fibers are expected to have reached the same level of membrane potential and to form an isoelectric ST segment.2,3


A diagnosis of STEMI that mandates emergency reperfusion requires ST elevation equaling or exceeding the following cut-points, in at least two contiguous leads (using the standardization of 1.0 mV = 10 mm)4,5:

  • 1 mm in all standard leads other than V2 and V3
  • 2.5 mm in leads V2 and V3 in men younger than age 40, 2 mm in leads V2 and V3 in men age 40 and older, and 1.5 mm in these leads in women
  • 0.5 mm in the posterior chest leads V7 to V9; ST elevation is attenuated in the posterior leads because of their greater distance from the heart, explaining the lower cut-point.6

While ST elevation that falls below these cut-points may be a normal variant, any ST elevation or depression (≥ 0.5 mm) may be abnormal and may necessitate further evaluation for ischemia, particularly when the clinical setting or the ST morphology suggests ischemia or when other signs of ischemia such as T-wave abnormalities, Q waves, or reciprocal ST-segment changes are also present on the electrocardiogram.

Conversely, ST elevation that exceeds these cut-points may not represent STEMI. In an analysis of patients with chest pain manifesting ST elevation, only 15% were eventually diagnosed with STEMI.7 In addition to size, careful attention to the morphology of the ST segment and the associated features is critical (Figure 1).

Other features of STEMI

In STEMI, the ST elevation is typically a convex or a straight oblique line, blending with a wide T wave to form a dome.8 But ST elevation may be concave in up to 40% of anterior STEMIs, especially in the early stage.3,9,10 The nonconcave morphology is highly specific but not sensitive for the diagnosis of anterior STEMI.3,8,9

Four other features characteristic of STEMI may be present (Figures 2 and 3):

  • Concomitant T-wave abnormalities (wide, ample, or inverted T waves)
  • Q waves
  • ST depression in the reciprocal leads. Reciprocal ST depression is seen in all inferior STEMIs and in 70% of anterior STEMIs.11,12 Diffuse ST elevation mimicking pericarditis may be seen with midvessel occlusion of a left anterior descending artery that wraps around the apex and supplies part of the inferior wall.
  • ST or T-wave amplitude may approximate or exceed the QRS amplitude in at least one lead.3,13,14 This finding is characteristic of STEMI, in which the QRS “shrinks” as the infarcted area becomes electrically neutral, whereas the ST-T segments become ample.3,13 In fact, early STEMI may be characterized by a small R wave that seems to be “pulled up” by the elevated ST segment. A small or absent R wave along with an ample, convex ST segment that fuses with the T wave and exceeds the height of the remaining R wave is called “tombstoning” (Figure 3). Tombstoning is most commonly seen with anterior infarction and implies more extensive myocardial damage and a worse prognosis than STEMI without tombstoning.15

Note that ST elevation may not be acute STEMI but an old STEMI with a chronically dysfunctional myocardium (dyskinetic or aneurysmal myocardium). In fact, an old STEMI may manifest as a chronic, persistent ST elevation along with Q waves, and T waves may be inverted or upright, but not ample.14 A history of an old MI, old electrocardiograms, if available, and quick bedside echocardiography may allow the diagnosis. In the case of an old dyskinetic infarct, echocardiography shows a thin, bright (scarred), and possibly aneurysmal myocardium, whereas in acute STEMI, the myocardium is neither thin nor scarred yet. If the patient does not report a history of MI, if the T wave is ample (> 75% the size of QRS), or if the patient presents with atypical ongoing angina, presume it is acute STEMI.

Figure 2. Diffuse ST-segment elevation with ST-segment depression in lead aVR. This initially suggests pericarditis. PR depression in leads II, aVF, V5, and V6 further suggests pericarditis. But the presence of features of pericarditis does not necessarily rule out STEMI. The five STEMI features must be ruled out. In this case, the ST-segment morphology and the abnormally wide T wave are features of STEMI. The ST elevation has an upwardly convex shape with a wide and high T wave fused with the ST segment, typical of STEMI (leads V2–V4, arrows). Also, the size of the ST elevation (ie, > 5 mm in V2–V4 and larger than the QRS complex in V4, a feature called “tombstoning”) is more consistent with STEMI than with pericarditis. In this patient, the left anterior descending artery was found to be occluded on coronary arteriography.
Figure 3. In a patient with lung cancer, sinus tachycardia is seen with diffuse ST-segment elevation, along with ST-segment depression in aVR. The QRS voltage is low, particularly when compared with the electrocardio-gram recorded a few days earlier (left lower panel). PR depression is seen in lead II. The combination of these findings may suggest pericarditis with a pericardial effusion. However, the ST-T morphology in lead V2, where the ST and T are blended to form one dome, is characteristic of STEMI (top arrow). Moreover, the ST elevation and T wave in leads V2–V4 are larger than the QRS, the QRS voltage is “shrinking” (arrowhead), and the R wave is pulled up by the ST segment (star); this is called “tombstoning.” All these features are characteristic of STEMI, wherein the R wave and the QRS complex shrink before forming a deep Q wave. In fact, an electrocardiogram recorded 1 hour later (right lower panel) shows a fully developed Q wave in lead V2 (bottom arrow).

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When does pericarditis merit a workup for autoimmune or inflammatory disease?

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