ST-segment elevation: Differential diagnosis, caveats

Cleveland Clinic Journal of Medicine. 2015 June;82(6):373-384 | 10.3949/ccjm.82a.14026

June 1, 2015|Cleveland Clinic Journal of Medicine

Elias B. Hanna, MD;David Luke Glancy, MD

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.

KEY POINTS

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.

LEFT VENTRICULAR HYPERTROPHY

In left ventricular hypertrophy, a deep S wave is seen in leads V₁ to V₃, with ST elevation and T waves that are discordant with the QRS complex. Rarely, ST elevation may be straight or convex. The following findings imply MI:

ST elevation or depression that is concordant with the QRS.
Inverted T waves that are concordant with the QRS in more than one lead, or biphasic T waves in more than one lead (eg, V₁ to V₃).
A discordant ST segment or a T wave that is very large may imply ischemia. In left ventricular hypertrophy, ST elevation is usually less than 2.5 mm in leads V₁ to V₃ and is rarely seen in the inferior leads, where it would be less than 1 mm.³⁴ When ST elevation is seen in leads V₁ to V₃ in left ventricular hypertrophy, an ST magnitude of 25% or more of the total QRS voltage has a 91% specificity for STEMI.³⁴

On another note, right ventricular hypertrophy and right bundle branch block may lead to ST-segment depression and T-wave inversion, but not to ST elevation. Thus, ST elevation occurring with right ventricular hypertrophy or right bundle branch block implies STEMI. While only left bundle branch block poses a diagnostic challenge, both types of bundle branch block, if secondary to STEMI, represent equally high-risk categories.³⁸

PREEXCITATION

Figure 10. At first glance, it seems there is ST-segment elevation in the inferior leads II, III, and aVF, with a wide Q wave. Moreover, there is a wide and tall R wave in lead V1 suggesting an associated posterior infarction. All this is consistent with acute inferoposterior STEMI. On further analysis, however, a slur is seen on the upslope of QRS in leads V1 to V6 (arrows), and the P wave is “riding” this slur. In the inferior leads, the P wave is riding the Q wave, which is in fact a negative delta wave. Thus, this electrocardiogram represents preexcitation. The ST deviations are secondary to the preexcitation and have an orientation opposite to the delta wave.

Preexcitation may be associated with negative delta waves that mimic Q waves, and with ST elevation in the leads where the negative delta waves are seen, ie, ST elevation discordant with the delta wave (Figure 10). The QRS morphology and the delta wave allow preexcitation to be distinguished from STEMI.

HYPERKALEMIA

Figure 11. There are ST-segment elevations in leads V1–V4, ST-segment depressions in the inferior leads, and peaked T waves in leads V3–V5. These T waves have a narrow base and seem to “pull” the ST segment, creating ST elevation in the anterior leads and ST depression in the inferior leads (arrows). This shape is consistent with hyperkalemia. In addition, the downsloping ST elevation seen in V1 and V2 is consistent with hyperkalemia (arrowhead). Occasionally, STEMI may have a similar ST-T shape. An rSR’ pattern is seen in V1–V2; this is consistent with STEMI but also with hyperkalemia, in which conduction blocks are common. The serum potassium level was 7.4 mmol/L (normal 3.5–5), and coronary angiography revealed normal coronary arteries.

The most common finding in hyperkalemia is a peaked, narrow-based T wave that is usually, but not necessarily, tall. ST elevation may be evident in leads V₁ to V₃ (Figure 11). In contrast with hyperkalemia, the T wave of STEMI is typically wide.

OTHER CAUSES OF ST-SEGMENT ELEVATION

Takotsubo cardiomyopathy

Takotsubo cardiomyopathy mimics all electrocardiographic features of anteroapical STEMI. ST elevation may extend to the inferior leads but cannot be isolated in the inferior leads.³⁹ As in apical STEMI, reciprocal ST depression is uncommon. Within 24 to 48 hours, ST elevation evolves into deep anterior T-wave inversion and a prolonged QT interval. Transient Q waves may be seen.

Myocarditis

Myocarditis may have one of two electrocardiographic patterns: a pericarditis pattern, or a typical STEMI pattern with Q waves sometimes localized to one area.⁴⁰

Atrial flutter waves

Figure 12. Atrial flutter that simulates ST-segment elevation. An “F” indicates the negative flutter wave; an asterisk indicates the upslope of the flutter wave that is superimposed on the ST segment, mimicking ST elevation.

Atrial flutter waves, particularly of 2:1 atrial flutter, may deform the ST segment so that it mimics an injury pattern on the electrocardiogram. Flutter waves may mimic ST elevation or ST depression (Figure 12).

Large pulmonary embolism

A large pulmonary embolism may be associated with T-wave inversion in the anterior leads or the inferior leads, or both, reflective of cor pulmonale. Less commonly, ST elevation in the anterior or inferior leads is seen. In fact, changes of both anterior and inferior ischemia should always suggest a pulmonary embolism.^41,42

Brugada syndrome

Figure 13. Type 1 Brugada pattern in V1 and V1, with a downsloping ST-segment elevation that creates a pseudo-R’ wave (pseudo-right bundle branch block). The QRS does not have a right bundle branch block morphology in leads V5 and V6.

Brugada syndrome is characterized by ST elevation and a right bundle branch block or pseudo-right bundle branch block pattern in at least two of the leads V₁ to V₃. In pseudo-right bundle branch block, the QRS adopts an rSR morphology in the anterior leads but is normal in the lateral leads. Type 1 Brugada pattern, the pattern that is most specifically associated with sudden death, is characterized by a coved, downsloping ST elevation of 2 mm or more with T-wave inversion (Figure 13).⁴³ The Brugada pattern can be transient, triggered by fever, cocaine, or class I antiarrhythmic drugs.

Hyperkalemia, Brugada syndrome, and sometimes pulmonary embolism are characterized by an ST elevation that slopes downward (Figures 11 and 13), which contrasts with the upsloping, convex ST elevation of STEMI.

References

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