Electrocardiographic Evidence for Left Ventricular Hypertrophy

JOURNAL OF INSURANCE MEDICINE

VOLUME 22, NO. 3 FALL 1990

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

Hypertrophy of the left ventricle usually involves both the free wall and the interventricular septum. The papillary muscles and trabeculae are thickened and may reduce the luminal dimensions of the chambers. In the hypertrophied myocardium the cardiac cells increase in diameter and length, but do not increase in number. The thickening of the cells results from an increase in the number of sarcomeres and mitochondria. Depending upon the stimulus to hypertrophy, the proportion of the cell occupied by either mitochondria or contractile units becomes disturbed so that one population of organelles hypertrophies out of proportion to the rest of the cellular components. The cell, for example, that has enlarged in response to a volume overload has an increased number of mitochondria, compared to the normal; the cell that hypertrophies in response to a pressure overload responds by an increase in sarcomeric units. Connective tissue cells often increase in number. When hypertrophy exists without dilatation, it is sometimes called concentric hypertrophy.

Hypertrophy of the left ventricle can be caused by increases in pressure of volume load. Dilatation of the left ventricle is usually accompanied by hypertrophy and can result from left ventricular failure, sustained arrhythmias, aortic and mitral regurgitation, ventricular septal defect and patient ductus arteriosus.

In certain persons, marked hypertrophy of the left ventricle, with or without ventricular dilatation, occurs in the absence of a generally accepted cause. Although the primary alteration in these cases may be hypertrophy of the myofibers, varying degrees of muscle necrosis and patchy fibrosis are also usually found in the myocardium. These latter alterations tend to be subendocardial in location and are frequently associated with mural thrombosis. Within the myocyte itself, accumulations of Z substance are a prominent feature; they may be involved in the generation of new sarcomeric units in the cell. These types of cardiomyopathy have been termed idiopathic myocardial hypertrophy, idiopathic of primary myocardial disease and familial cardiomegaly.

In some instances, marked hypertrophy, particularly of the

interventricular septum, may result in obstruction to blood flow from the left ventricle during systole as the septum abuts against the anterior leaflets of the mitral valve. This leaflet often shows endocardial thickening. The obstructive syndrome caused by this lesion has been termed idiopathic hypertrophic subaortic stenosis, idiopathic hypertrophic subvalvular aortic stenosis, hypertrophic obstructive cardiomyopathy and muscular subaortic stenosis. This type of hypertrophy can occur early in life and in some instances seems to be of familial or congenital origin. Left ventriculography shows impingement of the hypertrophied septum on the left ventricular outflow tract and variations in the contour of the left ventricular cavity. The electrocardi~)gram may show unusually prominent Q waves in addition to left ventricular hypertrophy. Diagnosis of this type of hypertrophy requires demonstration of obstruction to left ventricular outflow below the level of the aortic valve. Here, echocardiography has become extremely important in demonstrating increased septal thickness and systolic anterior motion (SAM) of the anterior leaflet of the mitral valve. The latter may not be present at test, but because of the dynamic nature of the obstruction, may be brought out by provocation with the Valsalva maneuver, amyl nitrite, inotropic agents or premature beats.

Marked hypertrophy decreases the compliance of the left ventricle and elevates the end-diastolic pressure in the chamber.

When dilatation accompanies hypertrophy, it produces what is sometimes termed eccentric hypertrophy. General enlargement of the ventricle occurs, and the apical portion of the chamber becomes conspicuous. The trabeculae carneae and papillary muscles are flattened and less prominent than in pure hypertrophy.

The use of the electrocardiogram to diagnose left ventricular hypertrophy (LVH) can be helpful if its limitations are recognized. First of all, mild to moderate hypertrophy may not alter the electrocardiogram. However, marked hypertrophy of the left ventricle can cause changes in the electrocardiogram 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

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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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