Reverse remodeling and enhanced adrenergic reserve from passive external support in experimental dilated heart failure.
Reverse remodeling and enhanced adrenergic reserve from passive external support in experimental dilated heart failure.
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DOI：
10.1016/s0735-1097(02)01890-9
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发表时间：
2002-06
影响因子：
24
通讯作者：
W. F. Saavedra;R. Tunin;N. Paolocci;T. Mishima;G. Suzuki;C. Emala;P. Chaudhry;P. Anagnostopoulos
中科院分区：
文献类型：
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作者：
W. F. Saavedra;R. Tunin;N. Paolocci;T. Mishima;G. Suzuki;C. Emala;P. Chaudhry;P. Anagnostopoulos
ObjectivesWe试图测试被动弹性遏制设备的有效性，以扭转慢性室重构和肾上腺素能下调在衰竭的心脏，但仍保持preload reserve.BackgroundProgressive心脏重构由于心力衰竭被认为是加剧潜在的心肌功能障碍。在压力-容积分析中，我们测试了限制渐进式心脏扩张的影响，由外部应用的被动遏制设备上的基础和肾上腺素能刺激的功能，在失败的犬hearts.MethodsIschemic扩张型心肌病引起的反复冠状动脉内微栓塞在6只狗。在手术植入围绕两个心室的薄聚酯补片（心脏支持装置[CSD]）之前和之后3 - 6个月对动物进行研究。结果长期使用CSD使舒张末期和收缩末期容积分别降低了−19 ± 4%和−22 ± 8%（均p <0. 0001），收缩末期压力-容积关系向左偏移（p <0. 01），与逆向重构相一致。舒张末期压和室舒张刚度没有显著变化。CSD植入后对多巴酚丁胺的收缩反应明显改善（CSD后射血分数增加55 ± 8%，CSD前为-10 ± 8%，p < 0.05），同时腺苷酸环化酶对异丙肾上腺素的反应也增加。β-肾上腺素能受体的密度或亲和力没有变化。舒张压顺应性没有受到不利影响，并且通过CSD保留了预加载恢复功能，这与缺乏收缩一致。结论通过不产生舒张压收缩的被动外部支持，可以实现收缩期壁应力降低和肾上腺素能信号传导改善的反向重塑。这种方法可能被证明在治疗慢性心力衰竭方面是有用的。
ObjectivesWe sought to test the efficacy of a passive elastic containment device to reverse chronic chamber remodeling and adrenergic down-regulation in the failing heart, yet still maintaining preload reserve.BackgroundProgressive cardiac remodeling due to heart failure is thought to exacerbate underlying myocardial dysfunction. In a pressure–volume analysis, we tested the impact of limiting progressive cardiac dilation by an externally applied passive containment device on both basal and adrenergic-stimulated function in failing canine hearts.MethodsIschemic dilated cardiomyopathy was induced by repeated intracoronary microembolizations in six dogs. The animals were studied before and three to six months after surgical implantation of a thin polyester mesh (cardiac support device [CSD]) that surrounded both cardiac ventricles. Pressure–volume relations were measured by a conductance micromanometer catheter.ResultsLong-term use of the CSD lowered end-diastolic and end-systolic volumes by −19 ± 4% and −22 ± 8%, respectively (both p < 0.0001) and shifted the end-systolic pressure–volume relation to the left (p < 0.01), compatible with reverse remodeling. End-diastolic pressure and chamber diastolic stiffness did not significantly change. The systolic response to dobutamine markedly improved after CSD implantation (55 ± 8% rise in ejection fraction after CSD vs. −10 ± 8% before CSD, p < 0.05), in conjunction with a heightened adenylyl cyclase response to isoproterenol. There was no change in the density or affinity of beta-adrenergic receptors. Diastolic compliance was not adversely affected, and preload-recruitable function was preserved with the CSD, consistent with a lack of constriction.ConclusionsReverse remodeling with reduced systolic wall stress and improved adrenergic signaling can be achieved by passive external support that does not generate diastolic constriction. This approach may prove useful in the treatment of chronic heart failure.