The highest value for the QRS voltage in left ventricular hypertrophy

The highest value for the QRS voltage in left ventricular hypertrophy

J. ELECTROCARDIOLOGY, 6 (3)259-262, 1973 The Highest Value for the QRS Voltage in Left Ventricular Hypertrophy BY PAUL J. IOANNIDIS, M.D.,* CHRIST AR...

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J. ELECTROCARDIOLOGY, 6 (3)259-262, 1973

The Highest Value for the QRS Voltage in Left Ventricular Hypertrophy BY PAUL J. IOANNIDIS, M.D.,* CHRIST ARAVANIS, M.D.,** CONSTANTINE KOUROUKLIS, M.D., AND ADRIAN CORCONDILAS, M.D.***

and hemodynamic data of a case with idiopathic hypertrophic myocardiopathy with QRS voltages higher than in any other previously reported case of LVH and the follow-up of the electrocardiogram (ECG) and VCG.

SUMMARY

The electrocardiogram (ECG) of a patient with idiopathic hypertrophic myocardiopathy without obstruction presented giant voltage for the QRS complex, reaching 10.85 mV in lead V 5 (SokolowLyon's index 14.85 mV). The veetoreardiogram (VCG) showed the maximum spatial QRS vector reaching 7.2 mV. The repolarization pattern was that of left ventricular "strain". Review of the literature showed that in no other reported ease of left ventricular hypertrophy was such extreme voltage present. For this reason, it is assumed that the QRS voltage of this case represents the upper limits for left ventricular hypertrophy. The ECG and VCG after a twoyear follow-up showed, in addition, the gradual development of right ventrieular hypertrophy.

CASE REPORT The patient, a 30-year-old white male, a house painter, was in good health up to a year prior to his hospital admission when he started feeling tired; at the same time he had episodes of tachycardia and shortness of breath upon exertion. His condition gradually became worse to the point that he couldn't climb more than two flights of stairs without considerable dyspnea. The patient used to smoke 20 cigarettes daily but was abstaining from alcohol. Five years earlier he had a virus hepatitis. From the family history his father died of "heart failure". Upon admission, physical examination showed a well developed, well nourished man; his height was 1.56 m and his weight 57 Kg. From the physical examination, the point of maximum cardiac impulse was on the 4th and 5th left intercostal spaces and the midclavicular line. On auscultation, a fourth heart sound and a mid-tolate systolic ejection murmur were heard on the apical area. The pulses were normal and the blood pressure 130/80 mm Hg. Routine blood tests, urinalysis and blood chemistry were within normal limits. Chest x-ray examination showed the cardiothoracic ratio to be within normal limits (14:28.2), but the left ventricular border was sharply delineated and more than usually curved. Cardiac catheterization showed normal pressures in the right atrium, right ventricle, pulmonary artery and the aorta; mean pulmonary capillary pressure was 12 mm Hg and with an "a" wave of 20 mm Hg. Left ventricular end-diastolic pressure was elevated, up to 20 mm Hg. No pressure gradient was found across the aortic and pulmonic valves or across their outflow tracts, at rest or after Isuprel injection. The cardiac output was estimated according to the Fick principle to 4.58 Lt/min and the pulmonary, and peripheral resistances were within normal limits.

One of the basic criteria in the electrocardiographic diagnosis of left ventricular hypertrophy (LVH) has been the voltage of the QRS complex in the left precordial leads. Furthermore, in the vectorcardiogram (VCG), the spatial magnitude of the maximum QRS vector was faithfully correlated with the degree of anatomic hypertrophy I as well as with the systolic pressure in the left ventricle2 in cases of LVH due to systolic overload. Although the lower limits for many electro- or vectorcardiographic voltage criteria employed in the diagnosis of LVH are overlapping the upper limits of normal, the upper limits for the voltage criteria in the presence of LVH are still undetermined. The purpose of this paper is to present the clinical electrocardiographic, vectorcardiographic

From the Department of Cardiology, Athens National University, Hippocrateion Hospital, Athens, Greece. *Consultant in Cardiology, 2nd Dept. of Surgery, Athens National University, Associate Director, Cardiology Division, Aretaeion Hospital, Athens, Greece. **Associate Professor in Cardiology. **Chief of Cardiopulmonary Laboratory. Address for reprints: Paul J. Ioannidis, M.D., Ifikratous St., 9, Athens 506, Greece. 259

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The ECG (Fig. 1), recorded on photo-sensitive paper with an Electronics for Medicine apparatus, showed giant QRS voltage in most of the leads with the highest QRS voltage present in lead V 5 (10.85 mV). The Sokolow-Lyon's index (SV~ + RVs) was 14.85 mV. Q waves were absent in leads I, II, V5 and V 6. The S-T segment was depressed in leads V4 - V6 and it was followed by an inverted T wave (2 mV deep in lead Vs). While the QRS duration was within normal limits (0.075 sec), the Q-T duration was prolonged (0.46 - 0.48 sec). According to the above findings the diagnosis of LVH with "strain" was obvious. The VCG (Fig. 2) was recorded with the Frank lead system.3 Its morphologic analysis showed no abnormalities regarding the P loops. The initial QRS vectors were deviated anteriorly and leftwards. The initial part of the QRS loop was bulging anteriorly and leftwards up to its 35th msec, thus giving the impression of a coexisting slight right ventricular hypertrophy (RVH). The middle time-area of the QRS loop was presenting a "folding" in its course and a markedly high amplitude of its vectors; the space orientation of the vectors in this time-area was posteriorly, leftwards and inferiorly. The appearance of the maximum QRS vector was delayed (50th msec) and its spatial voltage measured4 7.2 inV. The terminal part of the QRS loop ended into a rightwards deviated J point. The T loop was elongated with a

Fig. 2. Initial vectorcardiogram and orthogonal electrocardiogram (Frank lead system). H: horizontal plane projection, F: frontal plane, and LS: left sagittal. J, ELECTROCARDIOLOGY, VOL. 6, NO. 3. 1973

H I G H E S T QRS V O L T A G E IN LVH

delayed inscription of its initial limb and a rapid return of its terminal. The T loop was oriented straight to the right. During the next two years the repeated electrocardiographic and vectorcardiographic studies showed the following changes. The E C G (Fig. 3) presented a gradual increase of the R wave amplitude in leads V~ and Vz while the Q R S amplitude decreased to 9.8 mV in lead V 5. The V C G (Fig. 4) demonstrated more impressive changes. Almost all of its instantaneous vectors shifted slightly anteriorly and so the maximum Q R S vector came closer to the axis of the X coordinate. As a result of this shift the vectors up to the 47th msec are now located anteriorly and leftwards. These vectors maintained their initial voltage but the maximum vector lost voltage and subsided to 5.90 mV. The T loop vectors shifted slightly posteriorly but their orientation remained rightwards and always opposite to those of the Q R S loop. These evolutions are suggestive that R V H has been developed in the meantime on top of the existing LVH.

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DISCUSSION The reported case obviously represents an idiopathic hypertrophic myocardiopathy without obstruction. It seems that the hypertrophy involved mainly the left ventricle but gradually areas of the right ventricle were affected as well. The most impressive electrocardiographic finding was the presence of the highest Q R S voltages ever reported for left ventricular hypertrophy; the Q R S in lead V 5 measured 10.85 mV and the SokolowLyon's index 14.85 mV. Up to now the greatest voltage has been reported by Morgan 5 in a case of hypertrophic subaortic stenosis where the Q R S in lead V 5 was 5.3 mV high and the Sokolow-Lyon's i n d e x summed 14.6 mV. The Frank V C G displayed also the highest voltage reported up to date for the spatial maximum QRS vector, which was estimated 4 to 7.2 mV. Hugenholtz 6 in his study of 100 cases with LVH due to aortic valve stenosis and coorctation of the aorta, reported that the upper limits for the spatial maximum Q R S vector were 6.00 mV. Ellison and Restieaux 7 from over 300 patients with valvular aortic stenosis reported that the higher spatial maximum Q R S vector of their series was 6.9 inV. Regarding our patient the observed ventricular hypertrophy was existing without additional factors which would favor an increase of the surface potential. His weight was normal for his age and height; Chest deformities were not present and the cardiac silhouette did not show a hypertrophy of such a degree as to consider a proximity J. ELECTROCARDIOLOGY, VOL. 6, NO. 3, 1973

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effect of voltage amplification. On the other hand, no hemodynamic findings of systolic or diastolic left ventricular overload were shown on catheterization. So, it appears that the height of the voltages found initially in the Q R S vectors of this case is independent of the usual provoking or amplifying factors and thus it should represent the presently known upper limits for LVH.

REFERENCES 1. Hugenholtz, P. G., Ellison, R. C., and Miettinen, O. S.: Spatial voltages in the assessment of left ventricular hypertrophy (Frank system). J. Electrocardiol. 1: 77, 1968. 2. Hugenholtz, P. G., and Gamboa, R.: Effect of chronically increased ventricular pressure on electrical forces of the heart. A correlation between hemodynamic and vectorcardiographic data (Frank system in 90 patients with aortic or pulmonic stenosis). Circulation 30:511, 1964. 3. Frank, E;: An accurate, clinically practical system for spatial vectorcardiography. Circulation 13: 737, 1956. 4. Ioannidis, P. J., Lekos, D., and Ioannidis, E. J.: Orthogonal versus planar vector electrocardio graphy. Cardiology 57: 150, 1972. 5. Morgan, J. R., and Forker, A. D.: The electrocardiogram in hypertrophic subaortic stenosis. Milit. Med: 137: 115, 1972.

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Fig. 4. Vectorcardiogram and orthogonal electrocardiogram two years later (Frank lead system). Twofold amplification of the P and T loops is shown in the bottom of each planar projection. H: horizontal plane projection, F: frontal plane, and LS: left sagittal.

6. Hugenhohz, P. G.: The accuracy of vectorcardiographic criteria as related to the hemodynamic state. In: Vectorcardiography 1965. Hoffman, I., ed. North Holland Publishing Co., Amsterdam, 1966, p. 163.

7. Ellison, R. C., and Restieaux, N. J.: Vectorcardiography in Congenital Heart Disease. A Method for Estimating Severity. W. B. Saunders Co., Philadel phia, 1972, p. 47.

J. ELECTROCARDIOLOGY, VOL. 6, NO. 3, 1973