Endovascular reversal of renovascular hypertension blunts cardiac dysfunction and deformation in swine.
Endovascular reversal of renovascular hypertension blunts cardiac dysfunction and deformation in swine.
复制标题
血管内逆转肾血管性高血压可钝化猪的心脏功能障碍和畸形。
DOI：
10.1097/hjh.0000000000002654
复制
发表时间：
2021-03-01
影响因子：
4.9
通讯作者：
Lerman LO
中科院分区：
文献类型：
--
作者：
Yu S;Jiang K;Zhu XY;Ferguson CM;Krier JD;Lerman A;Lerman LO
肾血管性高血压（RVH）可引起血流动力学和体液畸变，可能损害心脏功能、结构和力学，包括心脏扭曲和变形。狭窄肾动脉的血运重建可以降低血压（BP），但其恢复RVH心脏力学的能力尚不清楚。我们假设经皮腔内肾血管成形术（PTRA）可以改善猪RVH的心脏功能和左心室（LV）变形。对17头家猪进行了16周的研究：RVH、RVH+PTRA和正常对照（每组n=5-6）。通过多探测器计算机断层扫描评估整体LV功能，并通过心电图触发的磁共振成像标记在心尖、中间和基底LV水平评估LV变形。离体评价心肌细胞肥大、心肌毛细血管密度和纤维化。RVH组血压和室壁厚度升高，PTRA组血压和室壁厚度降低，但仍高于对照组。RVH猪的LV心肌质量增加，也出现舒张功能障碍，而心输出量增加。此外，与对照组相比，RVH的心尖旋转和峰值扭转角均增加。离体，RVH诱导心肌纤维化和血管稀疏。PTRA恢复了心脏功能，减轻了肥大、血管稀疏和纤维化。与RVH相比，PTRA还使心尖旋转和峰值扭转角标准化，并升高基底峰值径向应变和心尖峰值径向应变。除了心脏LV适应性肥大和舒张功能障碍外，短期RVH还导致心脏变形。尽管仅部分改善BP，PTRA有效地恢复了心脏功能，逆转了异常力学。因此，肾血运重建可能是一个有用的策略，以保护RVH的心功能。
Renovascular hypertension (RVH) induces hemodynamic and humoral aberrations that may impair cardiac function, structure and mechanics, including cardiac twist and deformation. Revascularization of a stenotic renal artery can decrease blood pressure (BP), but its ability to restore cardiac mechanics in RVH remains unclear. We hypothesized that percutaneous transluminal renal angioplasty (PTRA) would improve cardiac function and left ventricular (LV) deformation in swine RVH. Seventeen domestic pigs were studied for 16 weeks: RVH, RVH+PTRA and normal controls (n=5–6 each). Global LV function was estimated by multidetector computed-tomography, and LV deformation by electrocardiographically-triggered magnetic resonance imaging tagging at the apical, mid, and basal LV levels. Cardiomyocyte hypertrophy, myocardial capillary density, and fibrosis were evaluated ex-vivo. BP and wall thickness were elevated in RVH and decreased by PTRA, yet remained higher than in controls. LV myocardial muscle mass increased in RVH pigs, which also developed diastolic dysfunction, whereas cardiac output increased. Furthermore, both apical rotation and peak torsion angle increased in RVH compared with controls. Ex-vivo, RVH induced myocardial fibrosis and vascular rarefaction. PTRA restored cardiac function and alleviated hypertrophy, vascular rarefaction, and fibrosis. PTRA also normalized apical rotation and peak torsion angle, and elevated basal peak radial strain and apical peak radial strain compared to RVH. Besides cardiac LV adaptive hypertrophy and diastolic dysfunction, short-term RVH causes cardiac deformation. Despite only partial improvement in BP, PTRA effectively restored cardiac function and reversed abnormal mechanics. Hence, renal revascularization may be a useful strategy to preserve cardiac function in RVH.