The Initial Stage of Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats is Manifested by a Decrease in the QRS Amplitude/Left Ventricular Mass Ratio

Abstract

In this study we tested the hypothesis of the relative voltage deficit, i.e. the discrepancy between increased left ventricular mass (LVM) and QRS amplitudes, in an experimental model of spontaneously hypertensive rats (SHR) during the period of a moderate increase in blood pressure. To address this issue we recorded orthogonal electrocardiograms of male SHR at the age of 12 and 20 weeks. During this period the systolic blood pressure (sBP) increased from 165 ± 3 mmHg to 195 ± 1 mmHg (p < 0.001). Age and sex matched WKY rats were used as control groups. The sBP values in WKY normotensive control groups were within normal limits (122 ± 8 mmHg and 130 ± 4mmHg, respectively). The maximum QRS spatial vector magnitude (QRSmax) was calculated from X, Y, Z amplitudes of the orthogonal electrocardiograms. The animals were sacrificed and the left ventricular mass was weight. The specific potential of myocardium (SP) was calculated as a ratio of QRSmax to LVM. The LVM in SHR (0.86 ± 0.05 g and 1.05 ± 0.07 g, respectively) was significantly higher as compared to WKY (0.65 ± 0.07 g and 0.70 ± 0.02 g), and the increase of LVM closely correlated with the sBP increase. On the other hand, QRSmax in SHR did not follow either the increase of sBP, or LVM. The QRSmax values in SHR did not differ from those of WKY at the age of 12 weeks (0.59 ± 0.14 mV compared to 0.46 ± 0.05 mV), and they were even lower in SHR at the age of 20 weeks (0.74 ± 0.08 mV compared to 0.44 ± 0.05 mV, p < 0.001). The values of SP, quantifying the relative voltage deficit, were significantly lower in SHR as compared to the WKY control. The values decreased significantly in SHR with increasing age, sBP and LVM, i.e., with the progression of hypertrophic remodeling of the left ventricle. The results of this study support the hypothesis of the relative voltage deficit in LVH. These results are consistent with the finding of a high number of false negative ECG results in clinical ECG diagnostics of LVH, and could contribute to an understanding of the diagnostic importance of the false negative ECG results, their re‐evaluation and utilization for clinical diagnosis and prognosis.