RENOVASCULAR HYPERTENSION-INDUCED CARDIAC CHANGES IN A RAT MODEL: FEASIBILITY OF CONVENTIONAL AND RECENT ECHOCARDIOGRAPHY

Abstract

Objective: Renovascular hypertension (RH) is a major cause of secondary hypertension, and hypertension eventually led to cardiac remodeling in patients. Hypertension leads to concentric left ventricle hypertrophy, while hypervolemia originated from renal failure leads to eccentric hypertrophy. Both mechanisms occur in RH which results in complex cardiac remodeling. Uraemic cardiomyopathy results from RH is characterized by diastolic dysfunction, but traditional echocardiography was limited in evaluating the diastolic function due to unknown hemodynamic and morphologic status. Recently, non-invasive intraventricular pressure gradient (IVPG), a preload-independent diastolic function parameter, was established and showed higher sensitivity to evaluate diastolic dysfunctions, particularly during cardiomyopathy. However, no previous studies highlighted the feasibility of the IVPG in the diagnosis of RH. Design and method: Twelve rats were received subtotal nephrectomy in 1 week to produce progressive renal failure as the RH group. The other twelve rats were sham-operated as a control group. Conventional and color M-mode echocardiography was performed for isoflurane-anesthetized rats at 2nd, 4th, 6th, and 8th weeks post-operation. IVPG was evaluated based on the Euler equation. Results: Hypertension, polyuria and hypervolemia were observed in RH group from the 2nd, 4th, and 8th week, respectively. Marked left ventricle hypertrophy was evidenced at 6th (1.32 ± 0.28 vs 1.09 ± 0.09, p = 0.016) and 8th-week post-operation (1.34 ± 0.28 vs 1.16 ± 0.09, p = 0.014) that was more prominent in the posterior papillary muscle. Peak mitral E velocity in RH rats was higher than control at the 8th week (106.35 ± 16.04 vs 91.23 ± 10.82, p = 0.031). In contrast, tissue Doppler index, total IVPG, basal IVPG, and mid-to-apical IVPG showed no difference between groups throughout the experiment. Conclusions: Hypervolemia and RH lead to unclassified geometry in RH-associated cardiac remodeling. Blood pressure change precedes the change of preload during the development of RH cardiac remodeling.