ST Morphology

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Author(s) J.S.S.G. de Jong, MD
Moderator J.S.S.G. de Jong, MD
Supervisor
some notes about authorship


ST changes occur when the endocardial and epicardial action potentials cease to counterbalance each other

The ST segment represents ventricular repolarization. Repolarization follows upon contraction and depolarization. During repolarization the cardiomyocytes elongate and prepare for the next heartbeat. This process takes much more time than the depolarization. The elongation that takes place during repolarization is not passive; it is an active process during which energy is consumed. On the ECG, the repolarization phase starts at the junction, or j point, and continues until the T wave. The ST segment is normally at or near the baseline.

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 likely some genetic 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 repolarization between the endocardial and epicardial layers of the left ventricle. The endocardial myocytes need a little more time to repolarize (about 22 msec). This difference causes an electrical current from the endocardium to the epicardium, which reads as a positive signal on the ECG.[1]

[edit] ST elevation

ST elevatie is measured at the junctional or j-point.[2]
Examples of normal ST elevation
Examples of pathologic ST elevation. LVH, LBBB, Pericarditis, Hyperkalemia, Anterior AMI

The most important cause of ST segment elevation is acute Ischemia. Other causes are [3][4]:

In a study by Otto et al., among 123 patients with chest pain and ST segment elevation of >1mm, 63 patients did not have a myocardial infarction. Diagnoses in patients who did not have a myocardial infarction were LVH (33%) and LBBB (21%). [5] In daily practice this means that in these patients the diagnosis of myocardial infarction has to depend on other diagnostic means, such as laboratory tests, echocardiography and coronary angiography.

An important clue for the diagnosis of ischemia is the presence of reciprocal ST segment depression.

Characteristics of early repolarization

Early repolarization is a term used for ST segment elevation without underlying disease. It probably has nothing to do with actual early repolarization. It is commonly seen in young men. It is important to discern early repolarization from ST segment elevation from other causes such as ischemia. Characteristics of early repolarization are:[6]

Early repolarization in inferior leads (II, III en AVF) has recently been found to be associated with an increased risk of cardiac death (1 mm of ST elevation carried an OR of 1.3 and 2 mm an OR of 3.0 )[7]

[edit] ST depression

The most important cause of ST segment depression is Ischemia. Other causes of ST segment depression are:

[edit] T wave changes

Different forms of T wave morphology

The T wave is quite 'labile' and long lists of possible causes of T wave changes exist. A changing T wave can be a sign that 'something' is abnormal, but it doesn't say much about the severity. T waves can be peaked, normal, flat, or negative. Flat and negative T waves are defined as:

flat T wave
< 0.5 mm negative or positive T wave in leads I, II, V3, V4, V5 or V6
negative T wave
> 0.5 mm negative T wave in leads I, II, V3, V4, V5 or V6

A concise list of possible causes of T wave changes:


References

  1. edited by Douglas P. Zipes... [et al.]. Braunwald's heart disease. Philadelphia, Pa.: Elsevier Saunders, 2005. isbn:0808923056.
  2. Gibbons RJ, Balady GJ, Bricker JT, Chaitman BR, Fletcher GF, Froelicher VF, Mark DB, McCallister BD, Mooss AN, O'Reilly MG, Winters WL Jr, Gibbons RJ, Antman EM, Alpert JS, Faxon DP, Fuster V, Gregoratos G, Hiratzka LF, Jacobs AK, Russell RO, and Smith SC Jr. 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 2002 Oct 1; 106(14) 1883-92. pmid:12356646. PubMed 12356646 HubMed 12356646
  3. Wang K, Asinger RW, and Marriott HJ. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003 Nov 27; 349(22) 2128-35. doi:10.1056/NEJMra022580 pmid:14645641. PubMed 14645641 HubMed 14645641
  4. Van de Werf F, Ardissino D, Betriu A, Cokkinos DV, Falk E, Fox KA, Julian D, Lengyel M, Neumann FJ, Ruzyllo W, Thygesen C, Underwood SR, Vahanian A, Verheugt FW, and Wijns W. Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J 2003 Jan; 24(1) 28-66. pmid:12559937. PubMed 12559937 HubMed 12559937
  5. Otto LA and Aufderheide TP. Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis fo acute myocardial infarction. Ann Emerg Med 1994 Jan; 23(1) 17-24. pmid:8273952. PubMed 8273952 HubMed 8273952
  6. Kambara H and Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976 Aug; 38(2) 157-6. pmid:133604. PubMed 133604 HubMed 133604
  7. Tikkanen JT, Anttonen O, Junttila MJ, Aro AL, Kerola T, Rissanen HA, Reunanen A, and Huikuri HV. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med 2009 Dec 24; 361(26) 2529-37. doi:10.1056/NEJMoa0907589 pmid:19917913. PubMed 19917913 HubMed 19917913
All Medline abstracts: PubMed HubMed
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