Power John M, Byrne Melissa, Raman Jai, Alferness Clif
Baker Medical Research Institute, P.O. Box 6492, St Kilda Road Central, Victoria 8008, Melbourne, Australia.
Prog Biophys Mol Biol. 2003 May-Jul;82(1-3):197-206. doi: 10.1016/s0079-6107(03)00016-6.
Heart failure (HF) is a progressive degenerative and malignant syndrome with a large number of aetiologies including coronary artery disease, chronic hypertension, exposure to toxins, bacteria and viruses and in a significant percentage of HF patients, the causal mechanism is unclear. The HF trail of morbidity and mortality is well documented and is characterised by step-like periods of relative symptomatic stability, compensation, separated by decompensatory episodes. The homeostatic response to the decline in cardiac function is diverse and involves most organs. There is an increase in resting rate, intra-cardiac hormone production (catecholamines, aldosterone, etc.) and in particular structural changes occur with increased mass and dilatation (dilated cardiomyopathy, DCM). DCM is associated with decreased cardiac output, contractility and energy efficiency and an increase in pro-arrhythmia and conduction defects. Kass et al. (Circulation 91(9) (1995) 2314) first demonstrated in patients who had undergone a dynamic cardio-myoplasty procedure, that, preventing further dilatation in DCM was beneficial and that the improved cardiovascular status was largely independent of muscle stimulation. We hypothesised that this outcome could be achieved by implanting a fabric cardiac support device around both ventricles to the AV junction. Subsequently, it was shown by us and others (Kass et al., 1995) (Cardiovasc. Res. 44(3) (1999) 549); (Ann. Thorac. Surg. 70(4) (2000) 1275) (in different animal models of DCM) that passive ventricular constraint prevented further dilatation, initiated left ventricular volume reduction and reversed the decline in ejection fraction, mitral valve integrity and left ventricular contractility, when compared with untreated controls. Subsequent European and North American clinical trials in patients with DCM of varying aetiologies have shown equal promise and an absence of device related complications (Circulation 104(12 Suppl. 1) (2001) I270); (Ann. Thorac. Cardiovasc. Surg. 7(5) (2001) 278). The mechanisms behind this improvement have yet to be fully clarified however the support generated by the device upon the right and ventricular freewall would lower wall tension. Not only is passive ventricular constraint a very promising treatment modality for heart failure and DCM it should provide a useful research tool for the study of the role of ventricular dilatation in the progression of heart failure.
心力衰竭（HF）是一种进行性退行性恶性综合征，病因众多，包括冠状动脉疾病、慢性高血压、接触毒素、细菌和病毒等，且相当一部分HF患者的病因机制尚不清楚。HF的发病和死亡轨迹有充分记录，其特征是相对症状稳定、代偿的阶梯状时期，中间穿插失代偿发作。机体对心功能下降的稳态反应多种多样，涉及大多数器官。静息心率、心内激素分泌（儿茶酚胺、醛固酮等）增加，特别是会出现心肌质量增加和扩张等结构变化（扩张型心肌病，DCM）。DCM与心输出量减少、收缩力和能量效率降低以及心律失常和传导缺陷增加有关。卡斯等人（《循环》91(9)（1995年）2314）首次在接受动态心肌成形术的患者中证明，防止DCM进一步扩张是有益的，且心血管状况的改善在很大程度上与肌肉刺激无关。我们假设通过在两个心室周围至房室交界处植入一个织物心脏支撑装置可以实现这一结果。随后，我们和其他人（卡斯等人，1995年）（《心血管研究》44(3)（1999年）549）；（《胸外科年鉴》70(4)（2000年）1275）（在不同的DCM动物模型中）表明，与未治疗的对照组相比，被动心室约束可防止进一步扩张，启动左心室容积减少，并逆转射血分数、二尖瓣完整性和左心室收缩力的下降。随后在不同病因的DCM患者中进行的欧洲和北美临床试验显示出同样的前景，且没有与装置相关的并发症（《循环》104(12增刊1)（2001年）I270）；（《胸心血管外科年鉴》7(5)（2001年）278）。然而，这种改善背后的机制尚未完全阐明，但该装置对右心室和心室游离壁产生的支撑会降低壁张力。被动心室约束不仅是一种非常有前景的心力衰竭和DCM治疗方式，还应为研究心室扩张在心力衰竭进展中的作用提供一个有用的研究工具。
