Saavedra W Federico, Tunin Richard S, Paolocci Nazareno, Mishima Takayuki, Suzuki George, Emala Charles W, Chaudhry Pervaiz A, Anagnostopoulos Petros, Gupta Ramesh C, Sabbah Hani N, Kass David A
Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287, USA.
J Am Coll Cardiol. 2002 Jun 19;39(12):2069-76. doi: 10.1016/s0735-1097(02)01890-9.
We 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.
Progressive 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.
Ischemic 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.
Long-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.
Reverse 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.
我们试图测试一种被动弹性容纳装置在逆转衰竭心脏的慢性心室重塑和肾上腺素能下调方面的疗效，同时仍保持前负荷储备。
心力衰竭导致的进行性心脏重塑被认为会加剧潜在的心肌功能障碍。在压力-容积分析中，我们测试了通过外部应用的被动容纳装置限制进行性心脏扩张对衰竭犬心脏的基础功能和肾上腺素能刺激功能的影响。
通过对六只犬反复进行冠状动脉内微栓塞诱导缺血性扩张型心肌病。在手术植入围绕两个心室的薄聚酯网（心脏支持装置[CSD]）之前和之后三到六个月对动物进行研究。通过电导微压计导管测量压力-容积关系。
长期使用CSD可使舒张末期和收缩末期容积分别降低-19±4%和-22±8%（均p<0.0001），并使收缩末期压力-容积关系向左移位（p<0.01），与逆向重塑一致。舒张末期压力和心室舒张硬度没有显著变化。CSD植入后，对多巴酚丁胺的收缩反应明显改善（CSD植入后射血分数升高55±8%，而CSD植入前为-10±8%，p<0.05），同时对异丙肾上腺素的腺苷酸环化酶反应增强。β-肾上腺素能受体的密度或亲和力没有变化。舒张顺应性未受到不利影响，并且CSD保留了前负荷可募集功能，这与没有收缩一致。
通过不产生舒张期收缩的被动外部支持可以实现降低收缩壁应力和改善肾上腺素能信号传导的逆向重塑。这种方法可能被证明对慢性心力衰竭的治疗有用。
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