Echocardiographic evidence for early left ventricular hypertrophy in dogs with renal hypertension

To investigate the rate of development of left ventricular hypertrophy, left ventricular wall thickness was measured with M mode echocardiography in 12 unanesthetized dogs for several weeks before and for 8 weeks after the induction of hypertension. Hypertension was produced by wrapping one kidney in silk and performing contralateral nephrectomy 2 weeks later. Echocardiographic measurements were performed two to three times weekly and were averaged. The intraobserver and Interobserver variability of left ventricular posterior wall thickness measurements was, respectively, 3.9 percent (correlation coefficient [r] = 0.96, n = 27) and 5.4 percent (r = 0.93, n = 14). Left ventricular wall thickness during the baseline period was 7.8 ± 0.2 mm (mean ± standard deviation) with a coefficient of variation of 2.9 percent. After the wrapping of one kidney in silk, the mean arterial pressure increased by 10 mm Hg during week 1 (difference not significant) and by 12 mm Hg during week 2 (p < 0.05). After contralateral nephrectomy, mean arterial pressure increased by 46 mm Hg (p < 0.001) in 1 week and remained near that level for the rest of the study. In contrast, a significant increase in left ventricular wall thickness occurred during week 1 after wrapping (p < 0.05). A gradual increase in left ventricular wall thickness continued during the entire study.

Sequential M mode echocardiography in dogs is a sensitive and reproducible method of detecting small changes in left ventricular wall thickness. The early increase in left ventricular wall thickness in hypertensive dogs with only minimal increase in mean arterial pressure and the dissociation between the rate of development of hypertension and of left ventricular hypertrophy suggest that factors other than the pressure overload also may contribute to the initiation and evolution of cardiac hypertrophy.