Electrocardiography: Disorders of the ST Segment

I. Problem/Condition.

The ST segment of the standard 12 lead electrocardiogram is defined as the area subscribed from the end of the QRS complex to the beginning of the T wave and corresponds electrically to the time period after ventricular depolarization, represented by the QRS complex, but before ventricular repolarization, represented by the T wave.

The normal ST segment is isoelectric to the prior TP segment (defined as the area between the end of the prior T wave and the beginning of the next P wave). The abnormalities of the ST segment can be broadly categorized into conditions that cause ST segment elevation and conditions that cause ST segment depression.

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Electrocardiograms are performed for a wide array of indications ranging from pre-operative screening in an asymptomatic patient to evaluation of the patient with acute chest pain. The differential diagnosis of an ST segment abnormality in a given patient, therefore, will be greatly informed by the clinical scenario, history, physical examination, and selected laboratory tests.

II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

ST segment elevation:

Transmural ischemia:

Transmural myocardial ischemia, or ST elevation myocardial infarction, is a common and feared cause of ST segment elevation. After acute occlusion of a coronary artery, the ST segment begins to elevate within minutes. The morphology of the ST segment is generally concave downwards, sometimes giving rise to the so-called “tombstone” appearance of the QRS complex-ST segment. Q waves are often associated with the ST segment elevation as are inverted T waves as the infarct evolves.

Benign early repolarization:

Early repolarization is a common finding in young patients and trained athletes. ST segment elevation is present, typically in leads V1-V3 but may be present in other leads. The morphology of the ST segment is concave upwards. A terminal notching of the QRS complex, called a J wave, is often present, and the magnitude of ST segment elevation is usually 1-3 millivolts.

Left ventricular hypertrophy (LVH):

LVH may present with ST segment elevation in leads V1 to V4 (anterior) along with prominent T waves. Leads I, aVL, V5, and V6 (lateral) will typically demonstrate large, prominent, positively oriented QRS complexes with marked ST segment depression and T-wave inversion. Additionally, the presence of left axis deviation and poor R-wave progression are suggestive of LVH as the cause of ST elevation.

Myocarditis and Pericarditis:

Presents with diffuse ST segment elevation, usually in patients who are clinically stable, with associated PR depression. Additionally, there may be a pericardial effusion that would manifest as electrical alternans and/or diminished electrical forces of the QRS complex on EKG. The EKG changes, although dynamic, tend to occur over a much longer period of time than a STEMI.

Ventricular aneurysm:

The EKG in this scenario can present very similarly to a STEMI, and therefore history is vital in determining the diagnosis. A comparison to prior EKG at the time of infarction is helpful. Note that ST depression in reciprocal leads is associated with an acute injury rather than aneurysm. Repeat EKGs with dynamic changes is suggestive of acute STEMI rather than aneurysm.

Brugada syndrome:

The Brugada ECG pattern causes ST segment elevation in leads V1-V3. This pattern on the cardiogram can be associated with malignant ventricular dysrhythmias and sudden cardiac death. An incomplete right-bundle branch block is present with an elevated ST segment of downward coved morphology leading directly into an inverted T wave. Some variants of the Brugada pattern produce an ST segment that is elevated with a biphasic or saddleback morphology.

ST segment depression:

Subendocardial ischemia:

Myocardial ischemia can also cause ST segment depressions. Unlike ST segment elevation, ST segment depression in a specific ECG territory does not correspond to the anatomic area of myocardial ischemia. If there are diffuse ST segment depressions, however, that may suggest a large amount of the left ventricular (LV) mass is ischemic hinting at 3 vessel or left main coronary disease as the underlying lesion. Horizontal or downsloping ST segment depression is more typical of ischemia than upsloping ST segment depression. Finally, ST segment depression can occur in leads opposite those in which ST segment elevation infarction is occurring, so-called “reciprocal changes.” Left ventricular aneurysm can manifest as persistent ST elevations with associated Q waves and an upright T wave long after an acute infarction.

Structural heart disease:

Left ventricular hypertrophy and profound right ventricular hypertrophy can cause ST segment depression due to abnormalities of repolarization. The ST segment vector is transmitted opposite the major deflection of the QRS complex such that the leads with tallest R waves will have the deepest ST segment depression (conversely, the leads with deep S waves can manifest ST segment elevation).

Repolarization and electrical abnormalities:

Abnormalities of conduction can give rise to ST segment depression. Right bundle branch block can cause ST segment depression, usually in leads V1-V3. Left bundle branch block causes expected ST segment depression in leads with dominant R waves including lead I, V5,and V6. As is the case with ventricular hypertrophy, the expected ST segment vector is opposite that of the QRS complex such that the leads with dominant R waves will manifest the deepest ST segment depression.

Metabolic syndromes and miscellaneous causes:

Medications including digoxin and multiple other anti-arrhythmic drugs that affect myocyte repolarization also can cause ST segment depression.

B. Describe a diagnostic approach/method to the patient with this problem.

The diagnostic approach to abnormalities of the ST segment should be influenced strongly by the indication for obtaining the ECG in the first place. For example, characteristic changes of early repolarization in a young patient with atypical chest pain may require no further intervention; in contrast, regional ST segment depressions in a patient presenting with crushing sub-sternal chest pain would require a much different diagnostic approach.

1. Historical information important in the diagnosis of this problem.

A patient’s presenting symptoms should be clearly elucidated when considering the cause of newly discovered ST segment abnormalities. Symptoms such as chest pain, abdominal pain, and dyspnea should be sought and characterized in all domains including tempo, severity, and provoking and alleviating factors. More subtle symptoms such as fatigue and weakness can also be manifestations of cardiac disease, particularly in the elderly and diabetic populations.

A viral prodrome can suggest pericarditis while a history of ischemic heart disease may influence both the pretest probability of ischemia as well as hint at the presence of left ventricular aneurysm. A history of hypertension or obstructive valvular disease would be consistent with ventricular hypertrophy. A full medication history is paramount, and a family history of ECG abnormalities or unexpected demise could support a diagnosis of the Brugada syndrome.

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

General inspection of the patient including demeanor and level of distress can give clues to the acuity of illness. Levine’s sign of a clenched fist in front of the precordium is classically associated with myocardial ischemia. Elevation of the jugular venous pressure, characteristic murmurs, gallop rhythms, or a pericardial friction rub can be helpful in ruling in items on the differential diagnosis of ST segment abnormalities. A dyskinetic apical impulse can suggest LV aneurysm. Finally, significant cardiac disease including ST elevation myocardial infarction can be present despite a normal physical examination.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

If there is a suspicion for myocardial ischemia, serum markers of myocardial injury including creatine kinase and troponin can be helpful, although these markers can also be present in the setting of pericarditis with concurrent myocarditis.

An echocardiogram can be useful in the diagnosis of ventricular hypertrophy and left ventricular aneurysm; if significant ischemia is present, the echocardiogram will often demonstrate regional wall motion abnormalities. If one is unsure if an abnormality of the ST segment represents ischemia or not, serial electrocardiograms may be helpful in that ischemic changes evolve over time while those changes secondary to other conditions such as ventricular hypertrophy do not.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Making the correct clinical diagnosis of a disorder underlying an ST segment abnormality depends on integration of clinical, laboratory, and electrocardiographic data. Specific diagnostic criteria for ST segment elevation myocardial infarction, non-ST segment elevation myocardial infarction, bundle branch blocks, pericarditis, left ventricular hypertrophy, and the Brugada syndrome are discussed in the respective modules.

III. Management while the Diagnostic Process is Proceeding.

A. Management of Clinical Problem Disorders of the ST Segment.

If ST segment abnormalities are noted that are concerning for ischemia, management should be urgently undertaken. If there is ST segment myocardial infarction, urgent reperfusion via either thrombolytic therapy or primary percutaneous coronary intervention should be arranged. Adjunct pharmacotherapy includes nitrates and beta blockade if no contraindications are present, aspirin and clopidogrel, morphine, and oxygen. If ST segment abnormalities are identified that are not concerning for ischemia, management is less time-sensitive and depends on the underlying diagnosis.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.

A common pitfall in diagnosis of ST segment abnormalities is inappropriate assessment of the ST segment itself. Secondly, the availability of a prior tracing for comparison can be invaluable in diagnosis. Finally, integration of concurrent ECG findings as well as clinical findings from history, physical examination and selected laboratory tests in the clinical context in which the ECG was obtained will lead to the correct interpretation of abnormalities of the ST segment.

IV. What’s the evidence?

Morris, F, Brady, WJ. “ABC of clinical electrocardiography: Acute myocardial infarction – Part I”. BMJ. vol. 324. 2002. pp. 831-34.

Channer, K, Morris, S. “ABC of clinical electrocardiography: Myocardial ischemia”. BMJ. vol. 324. 2002. pp. 1023-26.

Edhouse, J, Brady, WJ, Morris, F. “ABC of clinical electrocardiography: Acute myocardial infarction – Part I”. BMJ. vol. 324. 2002. pp. 963-66.

Wang, K, Asinger, RW, Marriott, HJ. “ST-Segment Elevation in Conditions Other Than Acute Myocardial Infarction”. N Engl J Med. vol. 349. 2003. pp. 2128-2135.

Pollak, P, Brady, W. “Electrocardiographic Patterns Mimicking ST Segment Elevation Myocardial Infarction”. Cardiol Clin. vol. 30. pp. 601-615.

Bayés de Luna, A, Fiol-Sala, M, Antman, EM. “The 12-Lead ECG in ST Elevation Myocardial Infarction: A Practical Approach for Clinicians”.