ST interval

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Schematic representation of normal ECG segments

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

The ST interval represents the initial, slow phase of ventricular repolarization.[1] The ST segment commonly refers to the morphology of the segment between the end of the S wave (the terminal deflection of the QRS) and the beginning of the T wave.

The Normal ST segment

The ST segment represents the ventricular repolarisation. Repolarisation follows upon contraction and depolarisation. During repolarisation the cardiomyocytes elongate and prepare for the next heartbeat. This process takes much more time than the depolarisation. Repolarisation is not passive elongation by stretch, it is an active process during which energy is consumed. On the ECG, the repolarisation phase starts at the junction, or j point, and continues until the T wave. The normal ST segment should not be flat. It should have an upward concavity sometimes referred to as a “take-off”.

The T wave is usually concordant with the QRS complex. Thus if the QRS complex is positive in a certain lead (the area under the curve above the baseline is greater than the area under the curve below the baseline) than the T wave usually is positive too in that lead. Accordingly the T wave is normally upright or positive in leads I, II, AVL, AVF and V3-V6. The T wave is negative in V1 and AVR. The T wave flips around V2, but there is some genetical influence in this as in Blacks the T wave usually flips around V3.

The T wave angle is the result of small differences in the duration of the repolarisation between the endocardial and epicardial layers of the left ventricle. The endocardial myocytes need a little more time to repolarise (about 22 msec). This difference causes an electrical current from the endocardium to the epicardium, which reads as a positive signal on the ECG. [2]

ST Segment Changes

EKG manifestations of acute myocardial injury or ischemia

EKG manifestations of acute myocardial injury or ischemia in absence of left ventricular hypertrophy and LBBB as follow[3] [4]

In general, ST segment elevation reflects myocardial injury, which may be irreversible (unlike ischemia which may be reversible) and which is associated with a risk of necrosis. ST elevation is defined as new ST segment elevation at the J point in two contiguous leads with the cut off points ≥0.2 mV in men or ≥0.15 mV in women in V2-V3 and ≥0.1 mV in other leads.

In general, ST depresstion represents reversible ischemia (less likely to result in irreversible necorsis). One exception is the presence of ST depression in the anterior precordial leads that can reflect posterior injury rather than anterior ischemia. Ischemia is defined as new horizontal or downsloping ST segment changes as ≥0.05 mV in two contiguous leads and/or T wave inversion ≥0.1 mV in two contiguous leads with prominent R wave or in situations which R wave amplitude / S wave amplitude ratio is >1.

Althought it is not observed in women, the J point elevation in men decreases with increasing age.[5]

The term of contiguous lead represents lead groups such as anterior leads (V1-V6), inferior leads (II, III, and aVF), or lateral/apical leads (I and aVL).

Measurements

In this diagram ST elevation is measured 60ms or 80ms after the J point.

The optimal time after the J point to measure ST elevation is debated. This example shows the technique of measuring the magnitude of ST elevation 60 milliseconds or 1.5 small boxes after the J point.[6]

Causes of ST Segment Depression

  • Ischemia particularly if the ST segment is downsloping
  • "Reciprocal changes" which are associated with a pattern of injury (ST segment elevation) in other leads. It is unclear if the ST depression is truly simply a reciprocal change which is a mirror image electrically of the injury in the other leads or if the ST depression is due to active ischemia in the other territory. Reciprocal changes are associated with a poorer prognosis. Reciprocal changes in the anterior precordial leads in association with an inferior MI are associated with slower flow in the LAD
  1. Dig effect (concave up;"reverse-checkmark")
  2. LV "strain"-associated with LVH (asymmetric ST depression, concave up, with slow downstroke and rapid upstroke, most often in I, aVL, V4-6)
  3. RV "strain"-associated with RVH (asymmetric ST depression, concave up, with slow downstroke and rapid upstroke, most often in V1-2)
  4. Hypokalemia (usually slight ST depression)
  5. Hypercalcemia

Causes of ST Segment Elevation

Myocardial Injury

  • The ST elevation is usually localized to an anatomic distribution that follows the coronary arteries (e.g. leads II,III, aVF).
  • In the setting of myocardial injury, "reciprocal changes" representing ischemia in other leads or a mirror like effect of the ST elevation presenting as ST depression in other leads, may be present. For example, ST elevation in the anterior leads in acute MI may be accompanied by ST depression in the inferior leads.
  • Prinzmetal's angina can cause transient ST elevation during chest pain.
  • Contact of the needle can cause a "current of injury" and ST segment elevation during pericardiocentesis.

Pericarditis

Hyperkalemia

Hyperkalemia may not affect all leads.

Ventricular Aneurysm

  • Ventricular aneurysm should be suspected if the ST segment elevation persists > 6 weeks after acute MI and if there is a wall motion abnormality on echocardiography.

Early Repolarization

  • "J point" elevation aka "early repolarization" is a concave-upward ST segment deflection.
  • It is a normal variant
  • Vaulting ST segment or J point elevation is a normal variant in leads V1-V3

Examples of Early Repolarization and Other Normal Variants of ST Elevation

Shown below is a example of an ECG demonstrating early repolarization ST changes.


Shown below is an example of an ECG showing variants of ST elevation.


References

  1. Hammill S. C. Electrocardiographic diagnoses: Criteria and definitions of abnormalities, Chapter 18, MAYO Clinic, Concise Textbook of Cardiology, 3rd edition, 2007 ISBN 0-8493-9057-5
  2. Braunwald, Eugene; Zipes, Douglas P. (2005). Braunwald's heart disease: a textbook of cardiovascular medicine. St. Louis, Mo: Elsevier Saunders. ISBN 0-8089-2305-6.
  3. Wong C-K, French JK, Aylward PEG, Stewart RAH, Gao W, Armstrong PW, Van De Werf FJJ, Simes RJ, Raffel OC, Granger CB, Califf RM, White HD. Patients with prolonged ischemic chest pain and presumed-new left bundle branch block have heterogenous outcomes depending on the presence of ST-segment changes. J Am Coll Cardiol. 2005;46:29–38. PMID 15992631
  4. Sgarbossa EB, Pinsky SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, Califf RM, Wagner GS. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle branch block. N Engl J Med. 1996;334:481–87. PMID 8559200
  5. Mcfarlane PW. Age, sex, and the ST amplitude in health and disease. J Electrocardiol. 2001; 34: 235–241. PMID 11781962
  6. Gibbons RJ, Balady GJ, Bricker JT, Chaitman BR, Fletcher GF, Froelicher VF; et al. (2002). "ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines)". Circulation. 106 (14): 1883–92. PMID 12356646.

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