Mitral valve prolapse (MVP) has been described as the most common valvular abnormality contributing to mitral regurgitation [1
], accompanied by late systolic murmur and associated with 1 or both of the redundant, floppy mitral leaflets in the left atrium. With the steadily decreasing rate of rheumatic heart valve disease, mitral valve prolapse has become the leading cause of mitral valve surgery for isolated mitral insufficiency in industrialized countries [2
]. Several clinical studies have reported prevalence rates ranging from 5% to 15% and even as high as 35% [3
] among specific populations. The controversies have not ceased in spite of the introduction of echocardiography and the established guidelines for diagnosis of MVP. Nowadays, based on echocardiography, large sample database and more realistic representation, the prevalence of mitral valve prolapse was found to be less than 1% in a cohort of healthy teenage students, young athletes and patients undergoing echocardiography for clinical reasons [8
]. While the negative events associated with congestive heart failure, progressive mitral insufficiency, bacterial endocarditis, thromboembolism and even sudden death may emerge at the endpoint in the course of aging and occur far more frequently in patients with MVP compared to controls, which have been determined. However, the natural course of mitral valve prolapse is markedly heterogeneous, varying from benign with a normal lifespan to malignant manifestation with significant morbidity and mortality caused by the progressive valvular regurgitation. Hence, management of this potentially malignant entity should consider the underlying etiology and perform close follow-up to allow for early identification of the subjects requiring medical or surgical intervention. However, the underlying causative pathogenesis is incompletely understood. A view that mitral valve prolapse has a well-recognized concerning with heritable genetic connective tissue disorders [11
], is the most popular and feasible mechanism among the several putative hypotheses. A familial basis for this circumstance has long been established with an autosomal dominant mode of inheritance [14
]; nevertheless, the variable penetrance is probably influenced by age, sex and autonomic nervous state, manifesting a marked heterogeneity of clinical presentation even between affected members of the same family. Hence, we wondered whether there is any environmental factor that has a triggering role in the development of mitral valve prolapse.