ECG Interpretation Review #73 (LVH – Hypertrophy – Voltage for LVH - Chamber Enlargement)

The 12-lead ECG shown below in Figure-1 was obtained from a healthy 29 year-old male in for an “insurance physical”.

• Interpret this 12-lead ECG.
• Is there voltage for LVH?
• Would voltage criteria for LVH be satisfied IF this patient was 40 years old?
• When voltage criteria for LVH are satisfied — What ECG finding best predicts that true chamber thickening/enlargement is likely?

Figure-1: 12-lead ECG obtained from a healthy 29-year old man. Is there LVH? 

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Interpretation of Figure 1:

There is sinus arrhythmia with a rate range between 65-75/minute. Intervals (PR/QRS/QT) are normal — and the mean QRS axis is normal (+50 degrees).

• Whether or not voltage criteria for LVH are satisfied on this tracing depends on the age of the patient.
• QRST Changes: A small q wave is seen in leads I and V6. R wave progression is normal (with transition between V2-to-V3). Other than minimal ST-T wave flattening in leads III, aVF — ST-T waves are unremarkable. There are no acute changes.

Voltage Criteria for LVH: Which Criteria to Use?

The ECG in Figure-1 provides an excellent example for illustrating two important concepts: 

• i) Many criteria exist for assessment of LVH; and, 
• ii) Some of these criteria are age-dependent.

   

Universal agreement on how to assess for LVH on ECG is lacking. How can there be agreement? — when more than 50 sets of criteria for LVH have been published in the literature. Practically speaking — none of these 50-plus criteria are optimally accurate. All suffer from imperfect sensitivity, which is no better than 55% by even the best of electrocardiographers. This means that up to half of the time when LV (Left Ventricular) thickening or LV chamber enlargement is present beyond the normal adult range — that it will not be detectable based on ECG assessment. BOTTOM Line: IF you truly need to know clinically about chamber enlargement — then get an Echo.

• Despite the poor sensitivity of ECG for picking up true chamber enlargement — specificity of the ECG may be excellent (ie, >90%) — IF in addition to adequate voltage for LVH, the patient also manifests ST-T wave abnormalities consistent with LV “strain” (See below).

Which of the 50 Criteria for LVH to Use?

Our answer as to which LVH criteria are best admittedly reflects our bias, which is based on our years of experience aiming to optimize sensitivity/specificity in ECG assessment. We feel LVH criteria can be greatly simplified by just remembering two numbers = “35” and “12”. Use of these 2 numbers readily identifies up to 90% of patients with LVH when it is possible to do so on 12-lead ECG (Figure-2):

Figure-2: Simplified voltage criteria for LVH.

Regarding Figure-2:

• Only one voltage criterion (ie, 35 or 12 ) — needs to be satisfied for ECG diagnosis of LVH.
• Use of the criterion for R in aVL ≥12mm is likely to be most helpful when there is left axis deviation (Use of this criterion with an R wave ≥12 in aVL may diagnose LVH despite minimal voltage in V1,V2 and V5,V6).
• Note that voltage criteria for LVH may not be valid for younger patients. This is because younger adults (in their 20’s) often manifest increased QRS amplitude without true chamber enlargement. We suggest not using these criteria for patients less than 35 years old.
• The accuracy (specificity) for the ECG diagnosis of LVH can be greatly increased — IF in addition to satisfying one or more voltage criteria, ST-T wave changes of "LV strain" are also present (See Figure-3 below).
• The Clinical History helps in assessing for LVH. It is good to know that even before looking at the ECG itself — the chance of true chamber enlargement is greatly increased IF the tracing is from a middle-aged, African-American man with longterm hypertension. A history of underlying heart disease (heart failure, hypertension, cardiomyopathy, valvular disease, coronary artery disease) clearly increases the likelihood of LVH in any given patient. On the other hand, the history in this case of a healthy, asymptomatic 29 year-old male — makes true LV chamber enlargement far less likely.

Additional Voltage Criteria:

No single voltage criterion will identify all patients with LVH. As a result — we occasionally turn to additional voltage criteria. We favor any of the following:

• A deep S wave (≥20-25 mm) in lead V1 or V2.
• A tall R wave (≥25 mm in V5 — or ≥18-20 mm in V6 ).
• An R wave ≥20 in any inferior lead (II, III, or aVF ).
• Cornell Criteria — LVH is present IF sum of R wave in lead aVL + S in V3 is ≥20mm (female) or  ≥28mm (male).
• Peguero Criteria — LVH is present IF sum of deepest S in any chest lead + S in V4 ≥ 23mm (female) or ≥28mm (male). NOTE: If the deepest S is in V4, then double this value.
• Bottom Line: In our experience, IF all you remember are the numbers ‘35’ and ‘12’ for LVH voltage criteria — then ~90% of the time when it is possible to diagnose LVH on the ECG of an adult, you will be able to do so!
• Satisfying any of the above additional criteria should help to pick up most of the remaining ~10%.
• Incorporating Clinical History and looking for “strain” or a strain “equivalent” — will further refine and increase accuracy (specificity) of your diagnosis.
• Keep in mind that competing conditions (ie, hyperkalemia, acute infarction, conduction defects, pulmonary disease) — may mask ECG diagnosis of LVH.
• IF you really need to know about chamber size — Get an Echo. The ECG is simply not optimally accurate.

LV “Strain” — Recognition/Use in Diagnosing LVH

It is difficult to define “strain”. We describe it as — a pattern of asymmetric ST-T depression (Panel C in Figure-3). Perhaps “strain” simply reflects that point of anatomic ventricular enlargement at which increased demand (from chamber thickening) outstrips blood supply — with resultant ST‑T wave repolarization changes from suboptimal perfusion. Or perhaps not … That said — What counts clinically is ECG recognition of a “strain” pattern.

• Note how downslope of the ST segment is slower with “strain” (arrow in Panel C of Figure-3) — compared to more rapid return of the ST segment to baseline. There may or may not be some associated J-point ST depression with LV "strain" (Not shown in Panel C).

Figure-3: ST-T wave appearance of normal (A) — vs “strain” (C) or a strain “equivalent” (B) — vs ischemia (D). 

   

LV “strain” is most commonly seen in one (or more) leads that look at the left ventricle.

• These include lateral leads I,aVL; V4,V5,V6.
• Less often — LV “strain” may be seen in the inferior leads (especially if the patient has an inferior axis).
• LV “strain” — is generally not seen in anterior leads (V1,V2,V3). In contrast, RV “strain” (as may occur with RVH or acute pulmonary embolus) — typically is seen in either anterior or inferior leads.

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• NOTE (Advanced Concept): Occasionally, you may see LV "strain" in anterior leads with deep S waves appearing as a reciprocal pattern — in which instead of ST-T wave depression, one or more anterior leads may show ST elevation with a mirror-image of the ST-T wave pattern that is usually seen with LV "strain" in lateral leads. (For an example of this — please see My Comment at the bottom of the December 27, 2018 post in Dr. Smith's ECG Blog.)

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The concept of pattern recognition is essential to ECG diagnosis. Consider the following:

• With ischemia (seen in Panel D of Figure-3) — there will often be symmetric T wave inversion in two or more leads in a general lead area.
• As one traces the path from a normal ST-T wave (Panel A in Figure-3) — to the asymmetric ST-T wave typical of LV “strain” (seen in Panel C) — one passes through an intermediate stage, where the ST-T wave flattens with beginning ST depression (Panel B). We designate this intermediate stage as a strain equivalent”.

   

The reason it is important to recognize “strain” — is that this finding greatly increases the accuracy of the ECG diagnosis of LVH.

• The presence of increased voltage without “strain” — has low specificity (<50%) for true chamber enlargement (especially if there is no underlying heart disease). We interpret the finding of increased voltage without ST-T wave changes of “strain as “Voltage for LVH”. This designation serves to acknowledge that despite voltage — statistical likelihood of true chamber enlargement is low.
• Clinical implications of LVH voltage plus a “strain equivalent” (ie, nonspecific ST-T wave flattening, as seen in Panel B of Figure-3) — are the same as they are for “strain” (greatly increased specificity for LVH — and an up to 8-fold increased morbidity/mortality as was shown in patients with longstanding hypertension in the Framingham study).

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• NOTE (Advanced Concept): Occasionally, you may see an ST-T wave pattern in one or more left-sided leads that looks very much like LV "strain", but without meeting LVH voltage criteria on the ECG. Given the poor overall sensitivity of the ECG for detecting LVH (ie, ≤55%, as noted above) — IF this patient almost meets voltage criteria — and — has a clinical history predisposing to LVH (ie, heart failure, longstanding hypertension) — then, it is still more likely than not that true chamber enlargement on Echo will be present. In such cases — I often write, "Probable LVH" in my interpretation of the ECG. Clearly, electrocardiography is an "art" — and the ECG is far from perfect as a diagnostic tool.
• PEARL: On occasion — the finding of either LV "strain" or ischemic-looking ST-T wave changes may mask the other! When this happens — it may be difficult (if not impossible) to distinguish between marked LVH (ie, from longstanding hypertension and/or cardiomyopathy) — vs LVH in a patient who also has acute ischemia/ongoing infarction. In such cases — I often write, "LVH and 'strain' and/or ischemia. Urge clinical correlation!" More information (ie, serial tracings, troponin, stat Echo, etc.) will often be needed to determine IF anything acute is ongoing.

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RETURN to this Case:
The patient in this case was a healthy, asymptomatic 29 year-old man in for an “insurance physical”. In Figure 4 — We blow-up precordial leads V1,V2 and V5,V6 from Figure-1 to illustrate how we assess to determine if voltage criteria for LVH are present. We focus on precordial leads in this case — since lead aVL in Figure-1 was clearly below the required 12mm amplitude.

Figure-4: Blow-up from Figure-1 to illustrate how QRS amplitude is counted. 

Regarding Figure-4:

• The deepest S wave in V1,V2 is in V1 (20) + the tallest R wave in V5, V6 (= 23 in V5) is >35 — so voltage criteria for LVH would be satisfied IF the patient was older than 35 (Figure-2). But because the patient is less than 35 years of age — voltage for LVH is not present.
• Regardless of whether the patient in this case is 29 or 40 years old — there is no indication of “strain” in any of the lateral leads in Figure-1. Thus, even IF the patient was over 35 — true LV chamber enlargement would be unlikely in this asymptomatic individual without ECG indication of “strain” or a “strain equivalent”.

LV “Strain” — It’s Effect on Specificity for LVH Diagnosis
Once “strain” and voltage for LVH are both present — specificity for LVH dramatically increases (up to ~90% — and >95% if the patient has underlying heart disease). This is seen in the precordial leads shown in Figure-5:

Figure-5: Illustrative precordial leads obtained from an older adult with long-standing hypertension. QRS amplitude is markedly increased — easily satisfying voltage criteria for LVH (Figure-2). In addition — Note ST-T wave changes consistent with LV "strain" in leads V4, V5, V6 (Figure-3). Specificity for LVH is virtually 100%.

Advanced Point: LV “Strain”?  — Ischemia?  — or both?

As alluded to earlier — Confusion often arises as to whether associated ST-T wave changes that are seen in a patient with increased QRS amplitude represent ischemia or “strain” — or both? The best way to explore this concept is by side-to-side comparison of a clinical example (Figure-6):

• In both Panel A and Panel B of Figure-6 — deepest S wave in V1,V2 + tallest R wave in V5,V6 easily satisfy voltage criteria for LVH.
• In Panel A — ST-T wave appearance in leads V5,V6 strongly suggests LV “strain” (there is asymmetric ST depression with slow sagging downslope). While we could not exclude the possibility of ischemia (there is after all, some J-point ST depression — especially in lead V4) — in the absence of a history of chest pain, we would suspect the changes in Panel A predominantly represent LVH with “strain”.
• In contrast, for Panel B — ST segments are coved in V3-through-V6. In addition, there is 1-2 mm of J‑point ST depression (below the PR segment baseline) in leads V4,V5,V6 — with T wave inversion that is deep and appears to be much more symmetric (especially in leads V4,V5). This appearance is more suggestive of ischemia.
• In particular — lead V3 in Panel B looks ischemic (pure LV “strain” virtually never produces ST coving and symmetric T inversion this far anterior).
• Lead V6 in Panel B — has an intermediate appearance between “strain” and/or ischemia. Given that this patient is “older” and has a history of heart disease and decidedly meets voltage criteria for LVH — We would interpret this ECG as being consistent with (if not highly suggestive of “LVH and “strain” and/or ischemia.” Clinical correlation and comparison with prior tracings would be needed to determine IF an acute ischemic process might be ongoing.

Figure-6: Comparison of the precordial lead sequence from 2 older patients with heart disease and obvious voltage for LVH. Voltage criteria for LVH are easily satisfied in each tracing. ST-T wave changes in Panel A look more like LV “strain”. On the other hand — ST-T wave changes in Panel B are more suggestive of LVH with possible ischemia as well as “strain”.

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- For more information – GO TO:

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• See also ECG Blog #75 - for review of Atrial Enlargement / Abnormality -
• See ECG Blog #77 - for review of RVH criteria -
• See also ECG Blog #92 ( = Basic Concepts #5) — for another approach to LVH.

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ADDENDUM (2019): To consolidate the criteria for LVH that I favor — I am adding Figure-7:

Figure-7: The criteria I favor for ECG diagnosis of LVH (See above text).