Department of Cardiac Surgery, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PRC.
Med Sci Monit. 2011 Sep;17(9):HY27-31. doi: 10.12659/msm.881918.
Mitral valve prolapse is a common valvular abnormality that is caused by myxomatous degeneration, characterized macroscopically by leaflet thickening and redundancy accompanied with histologically marked proliferation of the spongiosa and mucopolysaccharide acid replacement of leaflet collagen in the prolapse leaflets. Nevertheless, the discrepant natural history and various concomitant syndromes cannot be explained completely by the current genetic autosomal dominant inheritance theory. In addition, autonomic dysregulation has been commonly reported in mitral valve prolapse, but has never been indicated as a major underlying cause. This article attempts to interpret the occurrence of primary pathology and progression in mitral valve prolapse on a common basis of improper autonomic tone. The imbalanced background of autonomic nervous firing leads to disharmonized synthetic/catabolism balance in the extracellular matrix, disrupted transition in the interstitial cellular component and invalided anti-inflammatory pathway in the endothelium, which trigger and accelerate the progression of this condition. Such a hypothesis not only unifies the seemingly disparate syndromes and valvular disorder, but also has implications for future biopharmaceutical and mechanical treatment.
二尖瓣脱垂是一种常见的瓣膜异常,由黏液样变性引起,其特征为肉眼可见的瓣叶增厚和冗余,同时伴有脱垂瓣叶的海绵状组织和黏多糖酸替代瓣叶胶原的组织学显著增生。然而,目前的常染色体显性遗传理论并不能完全解释这种疾病不一致的自然病史和各种伴随综合征。此外,自主神经失调在二尖瓣脱垂中很常见,但从未被认为是主要的潜在原因。本文试图在自主神经张力不当的共同基础上解释二尖瓣脱垂的原发性病理和进展。自主神经放电的不平衡背景导致细胞外基质中合成/分解代谢平衡失调,细胞间质成分的过渡紊乱以及内皮细胞中的抗炎途径失效,从而引发并加速了这种情况的进展。这种假设不仅统一了看似不同的综合征和瓣膜疾病,而且对未来的生物制药和机械治疗也具有重要意义。