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首页> 外文期刊>American Journal of Physiology >Beneficial effects of delayed ivabradine treatment on cardiac anatomical and electrical remodeling in rat severe chronic heart failure.
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Beneficial effects of delayed ivabradine treatment on cardiac anatomical and electrical remodeling in rat severe chronic heart failure.

机译：伊伐布雷定延迟治疗对大鼠严重慢性心力衰竭的心脏解剖和电重构的有益作用。

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摘要

We tested the hypothesis that heart rate (HR) reduction, induced by the selective hyperpolarization-activated current inhibitor ivabradine (Iva), might improve left ventricular (LV) function, structure, and electrical remodeling in severe post-myocardial infarction (MI) chronic heart failure (HF). MI was produced in adult male Wistar rats. After 2 mo, echocardiography was performed before the randomization into MI and MI + Iva (10 mg x kg(-1) x day(-1)) groups. After 3 mo of treatment, echocardiography and 24-h telemetry were recorded. Cardiac collagen, mRNA, and protein expressions of angiotensin-converting enzyme (ACE) and ANG II type 1 (AT(1)) receptor were quantified. As a result, at 2 mo post-MI, all rats displayed severe congestive HF signs (ejection fraction < 30%). At 5 mo post-MI, body and heart weights were similar in the MI and MI + Iva groups. LV ejection fraction and LV end-diastolic pressure were worsened in the MI group, whereas both were improved with Iva. Iva reduced HR by 10.4% (P < 0.03 vs. MI) and ventricular premature complexes by 89% (P < 0.03) and improved HR variability (standard deviation of the RR interval) by 22% (P < 0.05). There were no effects of Iva on PR, QRS, and QT durations. Interstitial fibrosis in the MI-remote LV was markedly reduced by Iva (4.0 +/- 0.1 vs. 1.8 +/- 0.1%, P < 0.005). Increases in ventricular gene and protein expressions of ACE and AT(1) receptor in MI were completely blunted by Iva. In conclusion, these data indicated that HR reduction by Iva prevents the worsening of LV dysfunction and remodeling that may be related to a downregulation of cardiac renin-angiotensin-aldosterone system transcripts. Such beneficial effects of Iva on cardiac remodeling open new clinical perspectives for the treatment of severe HF.
机译：我们测试了以下假设：在严重的心肌梗死（MI）慢性患者中，选择性超极化激活电流抑制剂伊伐布雷定（Iva）引起的心率（HR）降低可能改善左心室（LV）功能，结构和电重构心力衰竭（HF）。 MI是在成年雄性Wistar大鼠中产生的。 2 mo后，进行超声心动图检查，然后随机分为MI和MI + Iva（10 mg x kg（-1）x day（-1））组。治疗3个月后，记录超声心动图和24小时遥测。定量血管紧张素转换酶（ACE）和ANG II 1型（AT（1））受体的心脏胶原，mRNA和蛋白质表达。结果，在心梗后2个月，所有大鼠均表现出严重的充血性HF征象（射血分数<30％）。 MI后5个月，MI和MI + Iva组的体重和心脏重量相似。 MI组左室射血分数和左室舒张末期压恶化，而Iva组均改善。 Iva使HR降低10.4％（相对于MI的P <0.03），使室性早搏复合物降低89％（P <0.03），并使HR变异性（RR间隔的标准差）提高22％（P <0.05）。 Iva对PR，QRS和QT持续时间没有影响。 Iva可显着降低MI远端LV的间质纤维化（4.0 +/- 0.1与1.8 +/- 0.1％，P <0.005）。 Iva完全抑制了MI患者ACE和AT（1）受体的心室基因和蛋白质表达增加。总之，这些数据表明Iva降低HR可以防止LV功能障碍和重塑恶化，这可能与心脏肾素-血管紧张素-醛固酮系统转录物的下调有关。 Iva对心脏重塑的这种有益作用为重症HF的治疗开辟了新的临床前景。

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