Typical vasovagal syncope as a "defense mechanism" for the heart by contrasting sympathetic overactivity
- PMID: 28669087
- DOI: 10.1007/s10286-017-0446-2
Typical vasovagal syncope as a "defense mechanism" for the heart by contrasting sympathetic overactivity
Abstract
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. In this evolutionary period, a predominant cause of death was wounding by a sharp object. This theory could explain the occurrence of emotional VVS, but not of the orthostatic one. The clot production theory suggests that the vasovagal reflex is a defense mechanism against hemorrhage in mammals. This theory could explain orthostatic VVS, but not emotional VVS. The brain self-preservation theory is mainly based on the observation that during tilt testing a decrease in cerebral blood flow often precedes the drop in blood pressure and heart rate. The faint causes the body to take on a gravitationally neutral position, and thereby provides a better chance of restoring brain blood supply. However, a decrease in cerebral blood flow has not been demonstrated during negative emotions, which trigger emotional VVS. Under the heart defense theory, the vasovagal reflex seems to be a protective mechanism against sympathetic overactivity and the heart is the most vulnerable organ during this condition. This appears to be the only unifying theory able to explain the occurrence of the vasovagal reflex and its associated selective advantage, during both orthostatic and emotional stress.
Keywords: Bradycardia; Evolution; Tilt testing; Vasovagal syncope.
Comment in
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The target of vasovagal syncope is hemostasis and not heart protection.Clin Auton Res. 2017 Aug;27(4):215-217. doi: 10.1007/s10286-017-0450-6. Epub 2017 Jul 11. Clin Auton Res. 2017. PMID: 28699049 No abstract available.
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