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Xiang Hu, Qiang Zhao
Med Sci Monit 2011; 17(9): HY27-31
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.