Professor Emeritus, Kyoto University, Nishiiru Karasuma Shimochojamachi-dori, Kamikyo-ku, Kyoto, 602-8002, Japan,
Heart Fail Rev. 2013 Nov;18(6):703-14. doi: 10.1007/s10741-013-9401-z.
Dilated cardiomyopathy is characterized by dilatation of the left or right ventricle, or both ventricles. The degree of myocardial dysfunction is not attributable to abnormal loading conditions. The infectious-immune theory has long been hypothesized to explain the pathogenesis of many etiologically unrecognized dilated cardiomyopathies. Inflammations followed by immune reactions, which may be excessive, in the myocardium, evoked by external triggers such as viral infections and/or autoimmune antibodies, continue insidiously, and lead to the process of cardiac remodeling with ventricular dilatation and systolic dysfunction. This ultimately results in dilated cardiomyopathy. Hepatitis C virus-associated heart diseases are good examples of cardiac lesions definitely induced by viral infections in humans that progress to a chronic stage through complicated immune mechanisms. Therapeutic strategies for myocarditis and dilated cardiomyopathy have been obtained through analyses of the acute, subacute, and chronic phases of experimental viral myocarditis in mice. The appropriate modulation of excessive immune reactions during myocarditis, rather than their complete elimination, appears to be a key option in the prevention and treatment of dilated cardiomyopathy. The clinical application of an NF-κB decoy and immune adsorption of IgG3 cardiac autoantibodies have been used as immunomodulating therapies and may provide novel approaches for the treatment of refractory patients with dilated cardiomyopathy. Conventional therapeutic agents for chronic heart failure such as β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists in particular should be re-evaluated on the basis of their anti-inflammatory properties in the treatment of dilated cardiomyopathy.
扩张型心肌病的特征是左心室、右心室或两者均扩张。心肌功能障碍的程度不能归因于异常的负荷条件。感染免疫理论长期以来一直被用来解释许多病因不明的扩张型心肌病的发病机制。炎症后继发的免疫反应，可能是过度的，在心肌中，由外部触发因素如病毒感染和/或自身抗体引起，持续潜伏，并导致心室扩张和收缩功能障碍的心脏重构过程。这最终导致扩张型心肌病。丙型肝炎病毒相关性心脏病就是人类心脏病变肯定是由病毒感染引起的很好的例子，通过复杂的免疫机制进展为慢性阶段。通过对实验性病毒性心肌炎的急性期、亚急性期和慢性期的分析，已经获得了心肌炎和扩张型心肌病的治疗策略。在心肌炎期间，适当调节过度的免疫反应，而不是完全消除，似乎是预防和治疗扩张型心肌病的关键选择。NF-κB 诱饵和 IgG3 心脏自身抗体的免疫吸附已被用作免疫调节治疗方法，可能为治疗难治性扩张型心肌病患者提供新的方法。基于其在扩张型心肌病治疗中的抗炎特性，应重新评估慢性心力衰竭的常规治疗药物，如β受体阻滞剂、血管紧张素转换酶抑制剂、血管紧张素受体阻滞剂和醛固酮拮抗剂。
