ST segment elevation is a well‐recognized electrocardiographic sign of acute coronary syndrome (ACS), in particular, ST segment elevation myocardial infarction (STEMI). There are, however, many other different clinical situations that are capable of causing ST segment elevation (Figure 25.1 and Table 25.1). The correct management of the patient is dependent on the correct diagnosis.

In certain individuals, ST segment elevation is benign and considered a normal variant; benign early repolarization (BER) is a common cause of non‐pathologic ST segment elevation. In other persons, ST segment elevation indicates some form of cardiac illness, whether it be acute or chronic in nature, including STEMI, Prinzmetal’s angina, left bundle branch block (LBBB), left ventricular hypertrophy, pericarditis/myopericarditis, left ventricular aneurysm, ventricular paced rhythm, Brugada syndrome, hyperkalemia, and major non‐cardiac causes such as intracranial hemorrhage, pulmonary embolism, and aortic dissection.

ST segment elevation myocardial infarction is diagnosed when the patient presents with the appropriate symptoms (e.g. chest pain, dyspnea, etc.) and electrocardiographic ST segment elevation. ST segment elevation seen in STEMI must be at least 1 mm in height above the electrocardiographic baseline and present in at least two anatomically contiguous leads; note that the baseline is defined as the TP segment. The morphology of the ST segment (Figures 25.2 and 25.3) is commonly convex (or “bulging upward”), although it may often be straight (flat) or concave (or “sagging downward”). Other ECG findings associated with STEMI include new T wave inversion, ST segment depression in leads opposite to those with elevations (i.e. reciprocal change or reciprocal ST segment depression), evolving/changing ST segment and T wave morphologies with serial ECGs, and the presence or development of Q waves. Figures 25.4–25.6 present different forms of ST segment elevation associated with STEMI.

Prinzmetal’s angina is a cause of ST segment elevation that may appear identical to STEMI. In this case, the ischemia is generally reversible as it is caused by coronary artery vasospasm as opposed to the acute plaque rupture with thrombus formation and blockage of arterial flow seen in STEMI. Resolution is often spontaneous, although treatment with nitroglycerin or calcium channel blockers can hasten resolution. This entity should be considered in patients with typical symptoms and ECG findings of STEMI that resolve before reperfusion treatment (e.g. fibrinolytic agents or percutaneous coronary intervention). The distinction between the ST segment elevations seen in STEMI and Prinzmetal’s angina is extremely difficult, if not impossible, based on initial assessment and ongoing evaluation and serial ECGs may be required with a low threshold to default to the more serious condition (STEMI) if there are ongoing symptoms, concerns, or doubts as to the diagnosis.

LBBB and ventricular paced rhythms are both common causes of ST segment elevation, both generally discordant to the QRS complex (Figure 25.7). The ST segment elevation of LBBB is generally concave in shape and discordant to the QRS complex (Figure 25.8). “Discordant to the QRS complex” means that the ST segment elevation is directed in the opposite direction (discordant) from the major terminal portion of the QRS complex; thus, a patient with LBBB‐related ST segment elevation will demonstrate a predominantly or entirely negatively oriented QRS complex – such is the case in leads V1–V3. Although some ST segment elevation is normal in LBBB, excessive ST segment elevation (>5 mm) in patients with a convincing clinical presentation for ACS should prompt consideration of acute myocardial infarction (MI). Similar findings are noted in the patient with a ventricular paced rhythm (Figure 25.9; Clinical Presentation Box 25.1).

Left ventricular hypertrophy may also cause concave ST segment elevation, especially in leads V1–V3 (Figure 25.10). Like LBBB, these ST segment elevations are discordant with the major portion of the QRS complex – that is, directed opposite to a negatively oriented QRS complex. These elevations are typically less than 5 mm and do not evolve, or change, with serial ECG evaluation.

Acute pericarditis (or acute myopericarditis) can be present with diffuse concave ST segment elevation (Figure 25.11). In acute pericarditis, ST segment elevation is usually less than 5 mm in height and widely distributed across the ECG, seen in all leads except leads aVR and V1. Other ECG clues to acute pericarditis include the absence of ST segment depression, the presence of PR segment changes (depression in the inferior leads and lead V6) and elevation (lead aVR), and ST segment elevation that does not change with repeated ECG evaluations.

BER is a common cause of diffuse, concave ST segment elevation that is often most remarkable in the precordial leads V1–V4. It is most often encountered in the anterior leads alone. It can also be seen simultaneously in the anterior and inferior leads; “isolated” findings limited to the inferior leads are unusual in BER. BER (Figure 25.12) may be identified by an elevated and irregular or notched J point (point at which QRS complex ends and the ST segment begins); the T waves are tall with a symmetric structure. This is a benign variant of normal ECG appearance and is unchanging over time. It is often very difficult to distinguish from the ST segment elevation seen in acute pericarditis.

Left ventricular aneurysm is a cause of ST segment elevation in patients with past myocardial infarction; in most cases of left ventricular aneurysm, the myocardial infarction has been extensive and has not been interrupted with acute reperfusion therapy. The resulting infarcted segment produces an outpouching, or aneurysm, of the ventricular wall. Most commonly, the left ventricular aneurysm is seen in anterior leads V1–V4 (Figure 25.13). Frequently, significant Q waves are seen, signifying a large, completed myocardial infarction; small, inverted T waves are also found. The magnitude of the ST segment elevation is usually minimal with 1–3 mm encountered in most patients; in the rare patient, ST segment elevation approaching 5 mm is seen. There are often associated non‐specific T wave abnormalities, yet reciprocal changes are uncommon; repeated ECG examinations demonstrate an absence of change in the ST segment. Without prior history or old ECGs, this diagnosis may be difficult and is often confused with STEMI.

Brugada syndrome is a genetic syndrome associated with mutations of cardiac sodium ion channels that predispose patients to sudden death from malignant ventricular rhythms, such as polymorphic ventricular tachycardia and ventricular fibrillation. Characteristically, it is seen as an apparent right bundle branch block (RBBB) (rSr^‘) pattern in leads V1 and/or V2 with associated ST segment elevation. The RBBB can be complete with a QRS complex duration greater than 0.12 seconds in width or incomplete with minimal QRS complex widening. The ST segment elevation can be present in one of three morphologies: Type 1 with coved‐type ST elevation with at least 2 mm J point elevation and a gradually descending ST segment and a negative T wave; Type II with a saddle‐back pattern with at least 2 mm J point elevation and at least 1 mm ST segment elevation with a positive or biphasic T wave; and Type III with a saddle‐back pattern with less than 2 mm J point elevation and less than 1 mm ST segment elevation with an upright T wave. These abnormal findings are typically isolated to leads V1 and/or V2.