Typical vasovagal syncope as a "defense mechanism" for the heart by contrasting sympathetic overactivity.

Many observations suggest that typical (emotional or orthostatic) vasovagal syncope (VVS) is not a disease, but rather a manifestation of a non-pathological trait. Some authors have hypothesized this type of syncope as a "defense mechanism" for the organism and a few theories have been postulated. Under the human violent conflicts theory, the VVS evolved during the Paleolithic era only in the human lineage.

Vasovagal Syncope As A Manifestation Of An Evolutionary Selected Trait.

Some observations suggest that typical (emotional or orthostatic) vasovagal syncope (VVS) is not a disease, but rather a manifestation of a non-pathological trait. We conducted an extensive bibliographic research on the vasovagal reactions in animals, including humans, in order to investigate the possible factors that may explain the origin and evolution of VVS. We found two processes which appear relevant for the investigation of VVS evolution: fear/threat bradycardia (alarm bradycardia) in animals, mainly during tonic immobility and vasovagal reflex during hemorrhagic shock (thoracic hypovolemia) both in animals and humans.

Simultaneous occurrence of two independent vagal reflexes: a possible cause of vagal sudden death.

A vagal origin of sudden death has been hypothesised in humans, but it has not yet been clearly demonstrated. Two vagal reflexes have been widely investigated: the diving reflex and the fear-induced central reaction, which are responsible for diving bradycardia and alarm bradycardia, respectively. The latter occurs in humans mainly in the context of emotional presyncope/syncope.

Diving bradycardia: a mechanism of defence against hypoxic damage.

A feature of all air-breathing vertebrates, diving bradycardia is triggered by apnoea and accentuated by immersion of the face or whole body in cold water. Very little is known about the afferents of diving bradycardia, whereas the efferent part of the reflex circuit is constituted by the cardiac vagal fibres. Diving bradycardia is associated with vasoconstriction of selected vascular beds and a reduction in cardiac output.

[Origin and evolution of vasovagal syncope].

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.

The origin of vasovagal syncope: to protect the heart or to escape predation?

Major lines of evidence suggest that classical (emotional and orthostatic) vasovagal syncope (VVS) is not a disease, but rather a manifestation of a non-pathological trait. It is, therefore, reasonable to investigate the possible factors that may explain its origin and evolution. We reviewed the data available in the literature on the vasovagal reaction in humans and animals in order to identify possible similarities that might provide insight into the evolution of VVS.

[Psychosocial factors as predictors of atherosclerosis and cardiovascular events: contribution from animal models].

Conventional risk factors (abnormal lipids, hypertension, etc.) are independent predictors of atherosclerosis and cardiovascular events; however, these factors are not specific since about half patients with acute myocardial infarction paradoxically result at low cardiovascular risk. Recent prospective studies provide convincing evidence that some psychosocial factors are independent predictors of atherosclerosis and cardiovascular events, as well.