Abstract

It has been found by Toyoshima and ramada that when the activation process of human heart ventricle was known, the ECG and VCG could be reconstructed from their tables of potential calculation, in which the potentials of ventricular unit areas were obtained by measuring the solid angle at many lead points of ECG and VCG.So, I tried the analysis of the electrocardiographic and vectorcardiographic changes in the ventricular hypertrophy by means of reconstruction of ECG and VCG under the next three conditions.First condition : Enlargement of the ventricular surface of either side. Second condition : Delay of activation of subepicardial muscle in hypertrophied ventricular wall. Third condition : Combined condition of the first and second one. Under the first condition, I could obtain ECG and VCG resembled closely in configuration to those practically recorded from patients with ventricular hypertrophy. I found also that the earlier onset of intrinsicoid deflection in V1 and V2 in the left ventricular hypertrophy, which was described in the text book of ECG by Hecht, could be attributed to the effect of dilated left ventricular endocardium. Under the second condition, I could obtain ECG and VCG resembled in configuration to those in ventricular hypertrophy, too, but I could find neither enlargement of QRS-complex nor earlier onset of intrinsicoid deflection in V1 and V2 in the left ventricular hypertrophy. Under the third condition, I could obtain the most resembled ECG and VCG to those in hypertrophy and could find also the enlargement of QRS-complex and the earlier onset of intrinsicoid deflection in V1 and V2 in left ventricular hypertrophy. In some cases of right ventricular hypertrophy, the QRS-loop was inscribed in a contrary direction to the normal in the horizontal and sagittal plane. Under any condition of these three, especially under the third condition, the middle portion of QRS-loop was displaced to the left-posterior in the left ventricular hypertrophy and to the right-anterior in the right ventricular hypertrophy. In the right ventricular hypertrophy, the R-wave in right precordial lead became large and the S-wave in left precordial lead became deep. In the left ventricular hypertrophy, the R-wave in right precordial lead and the S-wave in left procordial lead became small and V1 and V2 were often inscribed with QS-wave, but the S-wave in right precordial lead and the R-wave in left precordial lead became large. From these findings in reconstruction of ECG and VCG, I could find that the cause of characteristic changes of ECG and VCG in the ventricular hypertrophy could be attributed not only to the rotation of the heart around its long axis but also to the dilatation of ventricle or the delay of the arrival of the activation in the subepicardial muscle of the hypertrophied ventricular wall.

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