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TOPIC OUTLINE

SUMMARY
INTRODUCTION
GENERAL ELECTROCARDIOGRAPHIC FINDINGS
Increased QRS voltage
Increased QRS duration
Left axis deviation
Repolarization abnormalities
Left atrial abnormality
ELECTROCARDIOGRAPHIC DIAGNOSIS
Sokolow-Lyon indices
Romhilt-Estes point score system
Cornell voltage criteria
Accuracy
SUMMARY
REFERENCES
GRAPHICS View All
TABLES
Romhilt Estes point score
WAVEFORMS
LVH tutorial
ECG ST-T changes with LVH tutorial
RELATED TOPICS
Clinical implications and treatment of left ventricular hypertrophy in hypertension
Left anterior fascicular block
Electrocardiographic diagnosis of left ventricular hypertrophy

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Electrocardiographic diagnosis of left ventricular hypertrophy
Author
Ary L Goldberger, MD
Section Editor
David M Mirvis, MD
Deputy Editor
Gordon M Saperia, MD, FACC
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2013. | This topic last updated: Nov 27, 2012.
INTRODUCTION Left ventricular hypertrophy (LVH) refers to an increase in the size of myocardial
fibers in the main cardiac pumping chamber. Such hypertrophy is usually the response to a chronic volume or
pressure load.
The two most important pressure overload states are systemic hypertension and aortic stenosis.
The major conditions associated with left ventricular volume overload are aortic or mitral valve
regurgitation and dilated cardiomyopathy.
Ventricular septal defects cause both right and left ventricular volume overload, while hypertrophic
cardiomyopathy is an example of an inherited condition in which LVH (usually with asymmetric septal
hypertrophy) occurs in the absence of any apparent hemodynamic pressure or volume overload. A
physiologic type of hypertrophy with increase in wall thickness and left ventricular and diastolic volume may
occur in trained athletes. The "athletic heart" is often associated with ECG voltage criteria for LVH.
LVH is not an acute condition. It takes weeks and usually months to years to develop. Patients with LVH
from any cause are at increased risk for major cardiovascular complications including congestive heart failure
and cardiac arrhythmias [ 1 ]. These pathophysiologies may be fostered by the development of myocardial
fibrosis in concert with LVH.
The electrocardiogram is a useful but imperfect tool for detecting LVH. The utility of the ECG relates to its
being relatively inexpensive and widely available. The limitations of the ECG relate to its moderate sensitivity
or specificity depending upon which of the many proposed sets of criteria are applied [ 2,3 ].
Echocardiography is the procedure of choice for diagnosing LVH. It can also permit quantitation of LV mass
and give important information about the etiology of LVH (such as aortic or mitral valve disease, or
hypertrophic cardiomyopathy). However, the ECG may be used when echocardiography is unavailable or
not cost effective [ 4 ].
GENERAL ELECTROCARDIOGRAPHIC FINDINGS Left ventricular hypertrophy and related
changes can produce five major ECG findings: increased QRS voltage; increased QRS duration; left axis
deviation; repolarization (ST-T) changes; and left atrial abnormality [ 2,5,6 ]:
Increased QRS voltage An increase in left ventricular mass predictably will augment the amplitude of
voltage generated by these fibers. This effect will, in turn, increase the amplitude of positive forces (R waves)
recorded over the left chest leads and negative forces (S waves) recorded over the right chest leads. LVH
will also increase the amplitude of R waves in those limb leads that record the projection of these positive
forces (typically I and aVL with a horizontal or leftward QRS axis) ( waveform 1 ).
Increased QRS duration An increase in LV mass is often associated with widening of the QRS duration.
This change may be subtle or may be associated with incomplete, or eventually complete, left bundle branch
block (LBBB). On the other hand, most patients with LBBB have underlying LVH. In addition, some causes
of LVH can lead to LBBB by other mechanisms such as calcification or fibrosis of the proximal ventricular
conduction system, which lies close to the valve ring, in calcific aortic stenosis.
Left axis deviation LVH is usually associated with a horizontal or frankly leftward (-30) QRS axis in the
frontal plane leads. However, LVH may occur with a vertical QRS axis (or even rightward axis), especially in
young adults or patients with biventricular hypertrophy. (See "Left anterior fascicular block" .)
Repolarization abnormalities Severe LVH, especially due to a pressure load, is often associated with ST
depressions and T wave inversions in leads with relatively tall R waves ( waveform 2 ). This pattern, formally
referred to as LV "strain" (but best referred to as "LVH with associated ST-T wave abnormalities"), may be
due to primary alteration in repolarization of hypertrophied muscle or to relative subendocardial ischemia.
In a review of 886 hypertensive patients with LVH, these ST-T wave changes were present in 15 percent,
were more common in those with coronary heart disease (29 versus 11 percent without coronary disease),
and were associated with a greater left ventricular mass [ 7 ]. In another report of patients without evidence
of coronary disease, increasing magnitude of ST depression correlated with increasing LV mass and with
increasing prevalence of LVH [ 8 ]. However, the sensitivity and specificity of ST segment depression alone
for detecting LVH were limited.
A cellular basis for T wave inversion was suggested from an animal model of LVH which found regional
differences in action potential characteristics [ 9 ]. There was prolongation of the early repolarization phase of
the action potential duration in the subepicardial and mid-myocardial layers; this phase was not altered in the
subendocardium, but the plateau phase of the action potential was shortened. The net effect was an
endocardial to epicardial sequence of repolarization, the reverse of normal.
In comparison, LVH with a volume load state, particularly due to mitral or aortic regurgitation, is sometimes
associated with prominent positive T waves in the lateral chest leads.
Left atrial abnormality Most patients with LVH develop abnormalities in left atrial depolarization due to
conduction delay or actual atrial enlargement. The two major markers of left atrial abnormal are increased
duration of P waves (120 ms) in the limb leads and/or biphasic P waves with a prominent negative
component (40 ms in duration and/or 1 mV in depth) in V1. Biphasic P waves with a very prominent
negative component may be a subtle but important clue to major abnormalities such as severe mitral
regurgitation or dilated cardiomyopathy.
The presence of a left atrial abnormality may be particularly helpful in the setting of a left bundle branch block.
In a series of 220 patients with and without a left bundle branch block, 92 percent of those with a left atrial
abnormality had LVH as established by echocardiography; the sensitivity, specificity, predictive valve, and
accuracy were 80, 89, 88, and 78 percent, respectively [ 10 ].
ELECTROCARDIOGRAPHIC DIAGNOSIS The electrocardiographic diagnosis of LVH is quite
reliable when very prominent voltage is seen in conjunction with left atrial and ST-T abnormalities, leftward
axis, or widening of the QRS. As noted above, however, false negative and false positive diagnoses are not
uncommon. Patients with LVH may fail to show voltage criteria, especially if they have only mild hypertrophy
or underlying obstructive lung disease. The sensitivity is also reduced in women and in subjects with obesity [
11 ]. Right bundle branch block, when associated with decreased S waves in leads V1 and V2, may
decrease the sensitivity of some voltage criteria for LVH. On the other hand, increased voltage is a common
normal variant, particularly in young adult males [ 2 ].
The question of whether left anterior fascicular block (hemiblock) can simulate LVH in the limb leads (ie, tall
R waves in I and aVL) is somewhat controversial among electrocardiographers and requires further study.
Since arterial hypertension is one of the most common causes of left anterior fascicular block [ 12 ] and also a
major cause of LVH, these two findings often co-exist.
Commonly used criteria are given below with estimates of their accuracy. Given the intrinsic limitations of the
ECG and the many extracardiac factors which affect QRS voltage (eg, body habitus, pulmonary status, age,
etc), it is not realistic to expect more than moderate accuracy from the ECG in diagnosing LVH [ 3 ].
The following are the major criteria used in the electrocardiographic diagnosis of LVH [ 5 ]. More complex
mathematical models based upon the ECG are of limited use in predicting echocardiographic LV mass [ 13 ].
Sokolow-Lyon indices There are two criteria with these widely used indices:
Sum of S wave in V1 and R wave in V5 or V6 3.5 mV (35 mm)
and/or
R wave in aVL 1.1 mV (11 mm); sometimes 1.3 mV (13 mm) is used.
Romhilt-Estes point score system This index gives different weights to specific findings ( table 1 ). A
score of 5 or more indicates "definite" LVH; a score of 4 indicates "probable" LVH. The upper limits of the
QRS duration used in this system (90 ms) was from the pre-computerized measurement era. The upper limits
of QRS duration by computerized measurements in adults is 100-110 ms.
Cornell voltage criteria These more recent criteria are based upon echocardiographic correlative studies
designed to detect a left ventricular mass index >132 g/m2 in men and >109 g/m2 in women [ 14 ].
For men: S in V3 plus R in aVL >2.8 mV (28 mm)
For women: S in V3 + R in aVL >2.0 mV (20 mm)
Accuracy The sensitivity and specificity of these criteria vary widely depending upon the populations
studied, the "gold standard" employed (echocardiographic or magnetic resonance imaging LV mass versus
necropsy measurements), and the severity of LVH. Overall, conservative estimates of the sensitivity of the
various criteria for moderate to severe LVH is in the 30 to 60 percent range, with specificities in the 80 to 90
percent range [ 5,15 ]. Although it is relatively insensitive, the ECG does have prognostic significance.
Hypertensive patients with echocardiographically proven LVH who also meet ECG criteria have a greater left
ventricular mass than those without the expected ECG changes [ 16 ]. The left ventricular mass is highest in
those with associated ST-T abnormalities (the formally termed so-called "strain" pattern).
Serial monitoring of ECG voltage also may be helpful. In particular, changes in ECG voltage over time may
reflect changes in left ventricular mass and correlate with cardiovascular risk (eg, regression of LVH with
effective antihypertensive therapy). However, "loss" of LVH voltage criteria may also be due to alterations in
lead placement or to factors that may be associated with decreased QRS voltage such as anasarca, pleural or
pericardial effusion, weight gain, and increased severity of chronic obstructive pulmonary disease. Thus,
regression of LVH is most accurately determined by echocardiography. (See "Clinical implications and
treatment of left ventricular hypertrophy in hypertension", section on 'Effect of antihypertensive therapy' .)
SUMMARY
Left ventricular hypertrophy (LVH) is an important finding since it usually reflects pressure and/or
volume loads, or a hypertrophic cardiomyopathy variant.
The ECG is relatively specific, but lacks sensitivity in diagnosing LVH. False positives are more
common in young or thin individuals, whose voltage may exceed conventional thresholds. False
negatives may occur with right bundle branch block, obesity, or chronic obstructive pulmonary disease.
Different sets of criteria for LVH have been proposed, all with advantages and disadvantages. None is
ideal.
In addition to increasing QRS voltages, LVH may be associated with increased QRS duration
(sometimes culminating in left bundle branch block), left atrial abnormality, leftward QRS axis and ST-
T alterations (formerly called strain.)
Because of its association with hypertension, cardiomyopathy, aortic or mitral valve disease, and
myocardial fibrosis, the finding of LVH on ECG has adverse prognostic implications related to heart
failure and atrial arrhythmogenesis.
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REFERENCES
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