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. 2017 Feb 1;2(1):22–35. doi: 10.1016/j.jacbts.2016.09.007

Figure 1.

Figure 1

Renal Denervation Significantly Delayed Disease Progression in Both Animal Models

RD reduced significant pulmonary vascular resistance (A: MCT model; B: SuHx model). In addition, RD delayed the RV hypertrophy (C: MCT; D: SuHx). No changes were observed in RV end-diastolic diameter (E: MCT; F: SuHx) and in RV function (G: MCT; H: SuHx) or in cardiac output (I: MCT; J: SuHx). On the right side: Control: n = 5, MCT-sham: n = 9, and MCT-RD: n = 9. On the left side: Control: n = 6, SuHx-sham: n = 10, and SuHx-RD: n = 10. Data presented as mean ± SEM. Two-way ANOVA for repeated measurements followed by Bonferroni correction. Arrows indicate the interaction from 2-way ANOVA. ANOVA = analysis of variance; CO = cardiac output; MCT = monocrotaline; PVR = pulmonary vascular resistance; RD = renal denervation; RV = right ventricular; RVEDD = right ventricle end-diastolic diameter; RVWT= right ventricle wall thickness; SuHx = sugen + hypoxia; TAPSE = tricuspid annular plane systolic excursion.