e167journal.publications.chestnet.org [ Correspondence ] Manifold Embryonic Ciliary Functions in the Genesis of Kartagener Syndrome and

To the Editor: Physicians have been acquainted with the seemingly incongruous association of situs inversus with bronchi-ectasis for a century. 1, 2 Primary ciliary dyskinesia has been identifi ed as the underlying cause of bronchiectasis and its accompanying maladies: sinusitis, hearing loss, and infertility in men and women (sperm and oviduct immotility) with Kartagener syndrome. Less well known is that a defi cit in embryonic ciliary motility may result in situs errors and heterotaxy as quantifi ed by Shapiro et al 3 in this issue of CHEST (see page 1176). Cartwright et al 4 demonstrated the mechanism whereby cilia determine left-right asymmetry. Slough et al 5 delin-eated their cardiac role in mouse embryos with absent cilia in which endocardial cushions failed to develop, leading to heterotaxy. Th ey suggested that cardiac cilia function as mechanosensors, integrating fl ow, cardiac function, and morphogenesis. Th is conceptual frame-work is both scientifi cally gratifying and a tribute to the generative power of natural selection, which has led to the varied and invaluable adaptive repurposing of the primitive mechanism of ciliary motility. Do the authors agree with this unifying formulation of the genesis of the multifarious features of Kartagener syndrome