Download Electrocardiographic Evidence for Left Ventricular Hypertrophy

VOLUME 22, NO. 3 FALL 1990
JOURNAL OF INSURANCE MEDICINE
Interesting Electrocardiogram
ELECTROCARDIOGRAPHIC EVIDENCE FOR LEFT
VENTRICULAR HYPERTROPHY
M. IRENI~ FERRER, MD
Consultant in Cardiology
Metropolitan Life Insurance Company
Professor Emeritus of Clinical Medicine,
College of Physicians and Surgeons, Columbia University
Consultant Electrocardiographer,
Presbyterian Hospital, Columbia Presbyterian
Medical Center, New York, NY
interventricular septum, may result in obstruction to blood
Hypertrophy of the left ventricle usually involves both the free
flow from the left ventricle during systole as the septum abuts
wall and the interventricular septum. The papillary muscles
and trabeculae are thickened and may reduce the luminal against the anterior leaflets of the mitral valve. This leaflet
dimensions of the chambers. In the hypertrophied myocaroften shows endocardial thickening. The obstructive syndium the cardiac cells increase in diameter and length, but do drome caused by this lesion has been termed idiopathic hynot increase in number. The thickening of the cells results from pertrophic subaortic stenosis, idiopathic hypertrophic
an increase in the number of sarcomeres and mitochondria. subvalvular aortic stenosis, hypertrophic obstructive cardioDepending upon the stimulus to hypertrophy, the proportion
myopathy and muscular subaortic stenosis. This type of hyof the cell occupied by either mitochondria or contractile units
pertrophy can occur early in life and in some instances seems
becomes disturbed so that one population of organelles hyperto be of familial or congenital origin. Left ventriculography
trophies out of proportion to the rest of the cellular composhows impingement of the hypertrophied septum on the left
nents. The cell, for example, that has enlarged in response to ventricular outflow tract and variations in the contour of the
a volume overload has an increased number of mitochondria, left ventricular cavity. The electrocardi~)gram may show unusually prominent Q waves in addition to left ventricular
compared to the normal; the cell that hypertrophies in response to a pressure overload responds by an increase in
hypertrophy. Diagnosis of this type of hypertrophy requires
sarcomeric units. Connective tissue cells often increase in demonstration of obstruction to left ventricular outflow below
number. When hypertrophy exists without dilatation, it is
the level of the aortic valve. Here, echocardiography has besometimes called concentric hypertrophy.
come extremely important in demonstrating increased septal
thickness and systolic anterior motion (SAM) of the anterior
Hypertrophy of the left ventricle can be caused by increases in
leaflet of the mitral valve. The latter may not be present at test,
pressure of volume load. Dilatation of the left ventricle is but because of the dynamic nature of the obstruction, may be
usually accompanied by hypertrophy and can result from left
brought out by provocation with the Valsalva maneuver, amyl
ventricular failure, sustained arrhythmias, aortic and mitral nitrite, inotropic agents or premature beats.
regurgitation, ventricular septal defect and patient ductus
Marked hypertrophy decreases the compliance of the left venarteriosus.
tricle and elevates the end-diastolic pressure in the chamber.
In certain persons, marked hypertrophy of the left ventricle,
with or without ventricular dilatation, occurs in the absence When dilatation accompanies hypertrophy, it produces what
of a generally accepted cause. Although the primary alteration is sometimes termed eccentric hypertrophy. General enlargement of the ventricle occurs, and the apical portion of the
in these cases may be hypertrophy of the myofibers, varying
degrees of muscle necrosis and patchy fibrosis are also usually chamber becomes conspicuous. The trabeculae carneae and
papillary muscles are flattened and less prominent than in
found in the myocardium. These latter alterations tend to be
subendocardial in location and are frequently associated with pure hypertrophy.
mural thrombosis. Within the myocyte itself, accumulations
The use of the electrocardiogram to diagnose left ventricular
of Z substance are a prominent feature; they may be involved
in the generation of new sarcomeric units in the cell. These hypertrophy (LVH) can be helpful if its limitations are recognized. First of all, mild to moderate hypertrophy may not alter
types of cardiomyopathy have been termed idiopathic myothe electrocardiogram. However, marked hypertrophy of the
cardial hypertrophy, idiopathic of primary myocardial disease
left ventricle can cause changes in the electrocardiogram
and familial cardiomegaly.
which are due to a change in the position of the heart in the
thorax and an increase in muscle mass, with a consequent shift
In some instances, marked hypertrophy, particularly of the
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VOLUME 22,
No. 3 FALL 1990
ELECTROCARDIOGRAPHIC EVIDENCE FOR LEFT VENTRICULAR HYPERTROPHY
in orientation of the vector of depolarization. The mean electrical axis of the QRS may be shifted considerably to the left
(left axis deviation is present when angle alpha lies between
+29° and -90°), but in thin-chested persons and those with a
vertical heart, this may not occur. Increased QRS voltage is
often seen and is considered significant when the largest
positive or negative deflection in the limb leads (at normal
standardization) is greater than 20 mm (2.0 mv); or when S in
V1, V2 or V3 is more than 30 mm (3.0 mv); or when R in V5 or
V6 is more than 30 mm (3.0 mv); or when the sum of R in V5
or V6 and the deeper of the S waves in V1, V2 or V3 is 40 mm
or more. The duration of the QRS complex is often, but not
always, prolonged and may range between 0.10 and 0.12 sec.
The intrinsicoid deflection, or time from the onset of the QRS
complex to the peak of R, in V6 may be delayed (longer than
0.045 sec.). Secondary changes in depolarization (S-T segment
and T wave) may occur with marked hypertrophy and are
manifested by depression of S-T segments and negative T
waves in leads I, aVL, and V4-V6.
Hence to diagnose hypertrophy from the electrocardiogram
there should be a moderate degree of left axis deviation or
increased QRS voltage, or both, coupled with depression of ST
segments and negative T waves in leads I, aVL, V4-V6.
The importance of having more than one criterion for LVH on
the electrocardiogram is illustrated by this electrocardiogram.
It was done on a 41-year-old woman with uncontrolled hypertension despite three drugs (catapres, capotin and tenormin)o
This tracing meets the minimal criterion for LVH since the
voltage of QRS in lead aVL is increased, measuring 1.4 mv or
14 mm. The upper limits of normal for QRS is 13 mm. in aVL.
There is no V lead evidence of LVH. The previous day the QRS
in aVL was normal (12 mm.). The suggestion from this tracing
is that the criteria for LVH on the electrocardiogram, must be
carefully sought and if the electrocardiogram alone presents
evidence for LVH we should probably insist on ST-T abnoro
malities being present on the tradng. With the ease of obtaining echocardiograms today, this modality may well be a better
criterion than the electrocardiogram in our evaluation of LVH.
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