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Left Ventricular Hypertrophy With Strain

Thu, 12/12/2013 - 10:38 -- Dawn

This ECG is from a man with left ventricular hypertrophy.  LVH causes taller-than-normal QRS complexes in leads oriented toward the left side of the heart, such as Leads I, II, aVL, V4, V5, and V6.  Leads on the opposite side, such as V1, V2, and V3, will have deeper-than-normal S waves.  A commonly-used criteria for determination of LVH is the  Sokolow-Lyon index:     S in V1 + R in V5 or V6 (whichever is larger) ≥ 35 mm (≥ 7 large squares);  and  R in aVL ≥ 11 mm.  There is no perfect ECG criteria for determining LVH. The most accurate way to evaluate the size and thickness of the chambers of the heart is echocardiogram (ultrasound).  Frequently, there is left axis deviation, especially if the hypertrophy is confined to the left ventricle.

The left ventricle can be enlarged for many reasons, some worse than others.  Athletes naturally enlarge the heart, as they work the muscle.  Pathological causes for LVH can include anything that strains the heart as it pushes against increased afterload, such as hypertension and aortic stenosis, and diseases of the myocardium, such as cardiac myopathies.

ECGs that show LVH often have signs of other problems, including enlargement of the atria and/or the right ventricle.  LVH does not preclude the diagnosis of acute coronary insufficiency or myocardial infarction, but it can make the signs of other problems more difficult to see.  When LVH is caused by a pathological condition, we often see the "strain" pattern, which is ST depression and T wave inversion in leads with upright QRS complexes (the lateral leads).  A reciprocal ST elevation can occur in the right-sided leads, which can be confusing to those looking for STEMI.

 Dr. Ed Burns, of Life In the Fast Lane, has a very good page describing the criteria and facts of LVH.     Dr. Ken Grauer discusses LVH Here, and in all of his publications and on his website.

If you look closely at this ECG, you will find other abnormalities, and clinical corelation is always warranted.

 

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Comments

ekgpress@mac.com's picture

     The Instructor Collection ECG for this week provides an excellent illustration of how it may be difficult with LVH to determine if there is more than just "strain" reflected by ST-T wave appearance. I think there is more than just LVH in this tracing. I'd interpret this ECG as follows:

  • Baseline artifact.
  • Sinus rhythm at ~80/minute.
  • Long PR (0.24 seconds). Slight QRS prolongation (to 0.11 sec). Normal QT 
  • LAD (Left Axis Deviation) - of about -20 degrees. This is not leftward enough to qualify for LAHB, which requires a left axis more negative than - 30 degrees. Remember it is area under the curve that counts - which is why I think there is slightly more net positive than negative area in lead II - therefore an axis less than -30 degrees.
  • Although there is a negative component to the P wave in lead V1 - it is not negative enough to qualify for left atrial enlargement (Click HERE for Review of Atrial enlargement criteria).
  • There is definite LVH - both from the very tall R wave in lead aVL - as well as from marked increased in precordial lead amplitude (Click HERE for Review of LVH criteria). 
  • QRST Changes: - Q in aVL - QS in V1,V2, but normal transition (between V3-to-V4). It is the ST-T waves that are abnormal ...
IMPRESSION - Sinus rhythm with 1st degree AV block. LAD. LVH with "strain" and/or ischemia. Urge cliical correlation.
 
DISCUSSION - First - there is QRS widening on this tracing. This does not look like the pattern of LBBB (not wide enough; Q in aVL; S in V6). Sometimes marked LVH may widen the QRS by 0.01 or 0.02 (a thicker ventricle takes longer to travel through) - and that is what I believe is happening here - though I can't rule out a component of incomplete LBBB. This is more than academic - because assessment of ST-T waves becomes much more difficult IF there is a conduction block. In this case however - I believe the slight QRS widening is most likely a reflection of this patient's thicker ventricle - which allows us to more confidently assess ST-T wave morphology.
  • Note the marked J-point depression in V4-thru-V6 (of 3-4 mm). This is more than what is usually seen with pure LV "strain".
  • Note how the inverted T waves look symmetric in V4-thru-V6 - with much sharper descent than the usuallly more gradual ST decline (seen in Figure 3 in the above LVH link). In addition - the upright T wave in lead V3 is quite peaked. This is not the reciprocal of pure "strain".
BOTTOM LINE: I interpret ECGs like this as showing "LVH and strain and/or ischemia". There is NO WAY on ECG to determine if strain - ischemia - or both are present. Clinical correlation in context of prior and follow-up ECGs is needed to know for sure.

 

Ken Grauer, MD  www.kg-ekgpress.com   [email protected] 

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