Ultrasonic tissue characterization identifies early myocardial changes in a genetic animal model of hypertension and heart failure

Left ventricular hypertrophy (LVH) is characterized by a period of compensated functional state, followed by hemodynamic decompensation. To characterize the physical properties of the myocardium in LVH, ultrasonic tissue characterization was performed in a polygenic animal model of hypertensive heart disease, the SHHF/Mcc-fa^cp (SHHF) rat. These animals develop LVH and CHF in a genetically determined, reproducible fashion. 2-D guided transthoracic M-mode echocardiograms and transmitral Doppler spectra were recorded for assessment of LV geometry and systolic and diastolic function in two different age groups of rats (13 and 22 months). Measurements of the cyclic variation of integrated backscatter (CVIB) were made in vivo from 2-D parasternal long-axis views of the LV posterior wall. Subsequently, hemodynamic measurements were obtained in isolated, retrogradely perfused hearts performing isovolumic work. Control(n=4) SHHF(n=8) Conlrol(n=5) SHHF(n=5) Age (months) 12±1.4 13.4±1 23±0.5 21.7±1.6 LVMass (g) 0.9±.04 1.19±.07*0.87±.02 1.2±.07*FS (%) 48±2.6 50±1.4 49±2.7 52±3.8 Vcfc 2.6±0.3 2.4±0.2 2.6±0.3 2.6±0.3 Mitral E/A 1.9±0.12 1.83±0.22 1.58±0.16# 1.75±0.16 LV Dev. Press(mmHg) 148±11 175±8# N/A 162±13# Peak +dP/dt (mmHg/s) 4505±595 5332±578# N/A 5240±668#*p < 0.0001 vs control # p<0.01vs cont. Compared to controls, SHHF animals developed LVH to a similar degree in both age groups. Despite well preserved systolic and diastolic function, the SHHF rats showed a marked decrease in CVIB with aging. In conclusion, these experiments demonstrate that 1) non invasive CVIB measurements are feasible in small animal models of heart disease, 2) changes in the physical properties of the myocardium precede the development of heart failure, and 31 these abnormalities in physical properties may not be directly related to the severity of LVH.