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1


Lateral STEMI clinical significance

        The lateral wall of the LV is supplied by branches of the left anterior descending (LAD) and left circumflex (LCx) arteries.
        Infarction of the lateral wall usually occurs as part of a larger territory infarction, e.g. anterolateral STEMI.
        Isolated lateral STEMIs are less common, but may be produced by occlusion of smaller branch arteries that supply the lateral wall, e.g. the first diagonal branch (D1) of the LAD, the obtuse marginal branch (OM) of the LCx, or the ramus intermedius.
        Lateral STEMI is a stand-alone indication for emergent reperfusion.
        Lateral extension of an anterior, inferior or posterior MI indicates a larger territory of myocardium at risk with consequent worse prognosis.

2

ECG diagnostics of LATERAL STEMI

  •         ST elevation in the lateral leads (I, aVL, V5-6).
  •         Reciprocal ST depression in the inferior leads (III and aVF).

 

  •     ST elevation primarily localised to leads I and aVL is referred to as a high lateral STEMI.

NB. Reciprocal change in the inferior leads is only seen when there is ST elevation in leads I and aVL. This reciprocal change may be obliterated when there is concomitant inferior ST elevation (i.e an inferolateral STEMI)

3

categories of lateral infarctions

  1.         Anterolateral STEMI due to LAD occlusion.
  2.         Inferior-posterior-lateral STEMI due to LCx occlusion.
  3.         Isolated lateral infarction due to occlusion of smaller branch arteries such as the D1, OM or ramus intermedius.

4

Anterior STEMI significance

  •         Anterior STEMI results from occlusion of the left anterior descending artery (LAD).
  •         Anterior myocardial infarction carries the worst prognosis of all infarct locations, mostly due to larger infarct size.
  •         A study comparing outcomes from anterior and inferior infarctions (STEMI + NSTEMI) found that on average, patients with anterior MI had higher incidences of in-hospital mortality (11.9 vs 2.8%), total mortality (27 vs 11%), heart failure (41 vs 15%) and significant ventricular ectopic activity (70 vs 59%) and a lower ejection fraction on admission (38 vs 55%) compared to patients with inferior MI.
  •         In addition to anterior STEMI, other high-risk presentations of anterior ischaemia include left main coronary artery (LMCA) occlusion and Wellens’ syndrome.

5

Anterior STEMI on ECG

  •         ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).
  •         Reciprocal ST depression in the inferior leads (mainly III and aVF).

6

important ecg changes to be aware of

  •         Anterior-inferior STEMI due to occlusion of a “wraparound” LAD: simultaneous ST elevation in the precordial and inferior leads due to occlusion of a variant (“type III”) LAD that wraps around the cardiac apex to supply both the anterior and inferior walls of the left ventricle.
  •         Left main coronary artery occlusion: widespread ST depression with ST elevation in aVR ≥ V1
  •         Wellens’ syndrome: deep precordial T wave inversions or biphasic T waves in V2-3, indicating critical proximal LAD stenosis (a warning sign of imminent anterior infarction)

7

Inferior STEMI significance

  •         Inferior MIs account for 40-50% of all myocardial infarctions.
  •         Generally have a more favourable prognosis than anterior myocardial infarction (in-hospital mortality only 2-9%), however certain factors indicate a worse outcome.
  •         Up to 40% of patients with an inferior STEMI will have a concomitant right ventricular infarction. These patients may develop severe hypotension in response to nitrates and generally have a worse prognosis.
  •         Up to 20% of patients with inferior STEMI will develop significant bradycardia due to second- or third-degree AV block. These patients have an increased in-hospital mortality (>20%).
  •         Inferior STEMI may also be associated with posterior infarction, which confers a worse prognosis due to increased area of myocardium at risk.

8

inferior STEMI on ECG

  •         ST elevation in leads II, III and aVF
  •         Progressive development of Q waves in II, III and aVF
  •         Reciprocal ST depression in aVL (± lead I)

9

Right ventricular infarction

  •         Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon.
  •         Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.
  •         Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.

In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:

  •         ST elevation in V1 - the only standard ECG lead that looks directly at the right ventricle.
  •         ST elevation in lead III > lead II  - because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.

10

Wellens syndrome

  •         Wellens’ syndrome is a pattern of inverted or biphasic T waves in V2-3 (in patients presenting with ischaemic chest pain) that is highly specific for critical stenosis of the left anterior descending artery.
  •         Patients may be pain free by the time the ECG is taken and have normally or minimally elevated cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next 2-3 weeks.

There are two patterns of T-wave abnormality in Wellens’ syndrome:

  •         Type A Wellens’ T-waves are deeply and symmetrically inverted
  •         Type B Wellens’ T-waves are biphasic, with the initial deflection positive and the terminal deflection negative

11

Posterior STEMI

  •         Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.
  •         Isolated posterior MI is less common (3-11% of infarcts).
  •         Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death.
  •         Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed.

Posterior MI is suggested by the following changes in V1-3:

  •         Horizontal ST depression
  •         Tall, broad R waves (>30ms)
  •         Upright T waves
  •         Dominant R wave (R/S ratio > 1) in V2