代偿性心肌肥厚患者心肌力学正常时收缩心室功能改善。

Katashi Okoshi, Henrique Barbosa Ribeiro, Marina Politi Okoshi, Beatriz Bojikian Matsubara, Giancarlo Gonçalves, Reginaldo Barros, Antonio Carlos Cicogna
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引用次数: 46

摘要

心肌收缩功能的变化与左室整体功能的关系在稳定型心性肥厚过程中仍存在争议。为了阐明这一点,我们分析了压力过载引起的心脏肥厚大鼠的左室功能和体外心肌力学。雄性Wistar大鼠(70 g)接受升主动脉狭窄8周(AAS组,n = 9)。麻醉下经胸超声心动图评估左室表现。研究了离体乳头肌制剂在等长收缩时的心肌功能。将数据与年龄和性别匹配的假手术大鼠(C组,n = 9)进行比较。LV体重与体重比(C: 2.13 +/- 0.14 mg/g;AAS: 3.24 +/- 0.44 mg/g), LV相对壁厚(C: 0.18 +/- 0.02;AAS: 0.33 +/- 0.09), LV分数缩短(C: 54 +/- 5%;AAS: 70 +/- 8%)升高(P < 0.05)。超声心动图分析也显示有显著相关性(r = 0.74;百分比分数缩短指数与左室相对壁厚之间的关系P < 0.001)。AAS离体肌肉的表现显示,主动张力(C: 6.6 +/- 1.7 g/mm2;AAS: 6.5 +/- 1.5 g/mm2)和最大张力发展速率(C: 69 +/- 21 g/mm2/s;AAS: 69 +/- 18 g/mm2/s),与C组无显著差异(P > 0.05)。总之,代偿性压力过载心肌肥厚与心肌功能保存和心室功能增加有关。左室功能的改善可能是由于以相对壁厚增加为特征的心室重构。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Improved systolic ventricular function with normal myocardial mechanics in compensated cardiac hypertrophy.

There is still controversy about the relation between changes in myocardial contractile function and global left ventricular (LV) performance during stable concentric hypertrophy. To clarify this, we analyzed LV function in vivo and myocardial mechanics in vitro in rats with pressure overload-induced cardiac hypertrophy. Male Wistar rats (70 g) underwent ascending aortic stenosis for 8 weeks (group AAS, n = 9). LV performance was assessed by transthoracic echocardiography under anesthesia. Myocardial function was studied in isolated papillary muscle preparations during isometric contraction. The data were compared with age- and sex-matched sham-operated rats (group C, n = 9). LV weight-to-body weight ratio (C: 2.13 +/- 0.14 mg/g; AAS: 3.24 +/- 0.44 mg/g), LV relative wall thickness (C: 0.18 +/- 0.02; AAS: 0.33 +/- 0.09), and LV fractional shortening (C: 54 +/- 5%; AAS: 70 +/- 8%) were increased in group AAS (P < 0.05). Echocardiographic analysis also indicated a significant association (r = 0.74; P < 0.001) between the percent fractional shortening index and LV relative wall thickness. The performance of AAS isolated muscle revealed that active tension (C: 6.6 +/- 1.7 g/mm2; AAS: 6.5 +/- 1.5 g/mm2) and maximum rate of tension development (C: 69 +/- 21 g/mm2/s; AAS: 69 +/- 18 g/mm2/s) were not significantly different from group C (P > 0.05). In conclusion, compensated pressure-overload myocardial hypertrophy is associated with preserved myocardial function and increased ventricular performance. The improved LV function might be due to the ventricular remodeling characterized by an increased relative wall thickness.

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