title: [Origin and evolution of vasovagal syncope].
abstract: Vasovagal syncope (VVS) is characterized by sudden hypotension and bradycardia, due to inhibition of the sympathetic system and activation of the vagal system, respectively. Major lines of evidence suggest that classical (emotional and orthostatic) VVS is not a disease, but a characteristic of the individual. It is, therefore, interesting to investigate the factors that can explain its origin and evolution and, to this purpose, we investigated the available literature data on the vasovagal reflex in animals, including humans. We found two processes in vertebrates, which appear relevant to the investigation of VVS evolution: fear and threat bradycardia in animals and vasovagal reflex during hemorrhagic shock, both in animals and humans. The trigger of the latter is thoracic hypovolemia, the same of the vasovagal reflex occurring in humans during orthostatic stress (prolonged standing, tilt testing). During thoracic hypovolemia, the vasovagal reflex in humans seems to share physiological mechanisms similar to those observed in other mammals, that is an activation of the vagal system and an inhibition of the sympathetic system, preceded by an activation of the same system. Even emotional VVS in humans seems to share physiological mechanisms similar to those observed in other vertebrates during fear/threat bradycardia. Therefore, the vasovagal reflex appears to be predisposed in humans and other vertebrates with the same mechanisms and this may indicate a common evolutionary root. If the vasovagal reflex persisted for millions of years along the vertebrates evolutionary history, we can reasonably assume that it has (or it maybe had in the past) a function. Also, since this reflex is sporadically displayed, a role as a "defense mechanism" appears likely. The most likely hypothesis is a defense mechanism of the heart during stressful and possible dangerous heart conditions. The slowing of heart rate induced by the vasovagal reflex may constitute a beneficial break of cardiac pump (thereby reducing myocardial oxygen consumption) and permit better diastolic filling and coronary perfusion.
authors.affiliation: Divisione di Cardiologia, Ospedale Civile, Cento, FE. p.alboni@ausl.fe.it
authors.forename: Paolo
authors.initials: P
authors.lastname: Alboni
authors.forename: Marco
authors.initials: M
authors.lastname: Alboni
authors.forename: Giorgio
authors.initials: G
authors.lastname: Bertorelle
mesh_terms: D000465:Algorithms; D000818:Animals; D005075:Biological Evolution; D001919:Bradycardia / Q000503:physiopathology*; D005239:Fear; D006801:Humans; D007022:Hypotension / Q000503:physiopathology; D007024:Hypotension, Orthostatic / Q000503:physiopathology*; D020896:Hypovolemia / Q000503:physiopathology; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D019462:Syncope, Vasovagal / Q000209:etiology / Q000503:physiopathology*; D014630:Vagus Nerve / Q000503:physiopathology*