From the Authors

We thank Dr Morphet for raising the infectious hypothesis as a potential mechanism contributing to calcification of the aortic valve. Calcific aortic stenosis (AS), a common heart valve disease, has long been attributed to a passive degenerative process. However, recent investigations have found striking similarities between vascular atherosclerosis and AS. Because AS shares similar risk factors with vascular atherosclerosis, most of the research activities have been focused on the lipid-driven hypothesis as a key mechanism involved into aortic valve calcification. As it is the case with vascular atherosclerosis, recent findings also suggest that bacterial infections may lead to aortic valve calcification. In this regard, nanobacterial-like structures have been found in calcified human aortic valves (1). In animals, inoculation of bacterial flora on the aortic valve may lead to large valvular calcification (2). Moreover, in humans, it is suspected that chronic indolent infections in other sites, such as periodontal disease, may be involved in atherosclerosis development (3). Thus, it appears that low-grade and recurrent episodes of endocarditis may contribute to valvular calcification. Of particular significance, it seems that the innate immune system evolved to sense the ‘danger signals’ coming from both internal and external sources (4). In this regard, a distinct set of receptors recognizing pathogen-associated molecular patterns have been discovered in the last decade. For instance, oxidized low-density lipoprotein (an important component of AS valves) and bacterial LPS are potent agonists of the toll-like receptors (5). Thus, signals coming from both internal and external sources are being discovered, and suggest that intricate and interconnected mechanisms may participate in a low-grade inflammatory state and the development of atherosclerosis. Hence, it is not excluded that a complex disease such as AS has, in some individuals, potentially overlapping mechanisms leading to valvular inflammation. However, currently, most of the evidence indicates that in a vast majority of patients, an atheroinflammatory process, which is largely modulated by the atherogenic dyslipidemia, is a key mechanism in aortic valve calcification (6). Nonetheless, it is likely that other proinflammatory signals, such as subacute chronic infections, may contribute to ectopic calcification of the aortic valve in selected individuals.

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