The association between mitral valve prolapse and skeletal abnormalities has been the focus of several previous studies, almost all of which have concentrated on back or thoracic skeletal abnormalities. Notably, Movahed and colleagues reported an association between kyphosis and MVP. Indeed, straight back was coexistent in 27% of patients with myxomatous mitral valve degeneration .
Several former studies by Salomon et al., and Peh et al. have reported an association between thoracic skeletal abnormalities such as pectus excavatum and mitral valve prolapse. To date, the etiology of the close association between skeletal abnormalities and MVP has not been investigated. Although it has been postulated that this association might constitute an attenuated form of Marfan syndrome, this speculation remains elusive in the absence of any genetic study to prove it [9, 10].
To our knowledge, no study to date has investigated the association between pes planus and MVP, despite the fact that they might be caused by similar connective tissue dysfunction.
Our study notes an unexpectedly high prevalence of MVP in patients with flat foot (88%). This association suggests a common genetic background between both anomalies. This coincides with Raj and Kiel’s report about the prevalence of PP and its genetic background, where MVP prevalence in the general population ranges from 1 to 37% . The mean age of our patients was 8.2 ± 0.9, which excludes the entity of transient pes planus that usually disappears before the age of 6 years .
There is a reported 2.5% risk of sudden death with mitral valve prolapse, mostly due to associated Long QT syndrome. Furthermore, there are speculations that the tension on the chordae and subvalvular apparatus caused by the prolapsing valve results in myocardial degeneration and fibrosis, with the subsequent creation of a substrate for arrhythmias. The mentioned risk has prompted a remarkable need for the development of a screening policy for MVP. Three-generational screening of families in the case of a diagnosed family member with MVP has been recently proposed, but the cost-effectiveness of this strategy remains elusive [11, 12].
Alternatively, our study offers a new screening policy for MVP, where we suggest the determination of MA in patients with PP. MA angle in lateral foot xray is a routine procedure in such types of patients and will not add a non-required investigation among them. An angle greater than 5 degrees, according to our findings, has a 100% sensitivity in pointing to the concurrent presence of MVP, which is a justified diagnostic accuracy for performing echocardiography in this high-risk group.
To conclude, the tight relationship between pes planus and MVP illustrated in this study warrants the screening of patients with pes planus for the presence of MVP. Meary angle, an easy and cheap radiographic measure, can serve as a good predictor of MVP. Nonetheless, the generalization of the results of this study needs a larger sample size to consolidate the revealed results.