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THE CASE
A 56-year-old physician (CUL) visited a local seafood restaurant, after having fasted since the prior evening. He had a history of hypertension that was well controlled with lisinopril/hydrochlorothiazide.
The physician and his party were seated outside, where the temperature was in the mid-70s. The group ordered oysters on the half shell accompanied by mignonette sauce, cocktail sauce, and horseradish. The physician ate an olive-size amount of horseradish with an oyster. He immediately complained of a sharp burning sensation in his stomach and remarked that the horseradish was significantly stronger than what he was accustomed to. Within 30 seconds, he noted an increased heart rate, weakness, and intense sweating. There was no increase in nasal secretions. Observers noted that he was very pale.
About 5 minutes after eating the horseradish, the physician leaned his head back and briefly lost consciousness. His wife, while supporting his head and checking his pulse, instructed other diners to call for emergency services, at which point the physician regained consciousness and the dispatcher was told that an ambulance was no longer necessary. Within a matter of minutes, all symptoms had abated, except for some mild weakness.
THE DIAGNOSIS
Ten minutes after the event, the physician identified his symptoms as a horseradish-induced vasovagal syncope (VVS), based on a case report published in JAMA in 1988, which his wife found after he asked her to do an Internet search of his symptoms.1
THE DISCUSSION
Horseradish’s active component is isothiocyanate. Horseradish-induced syncope is also called Seder syncope after the Jewish Passover holiday dinner at which observant Jews are required to eat “bitter herbs.”1,2 This type of syncope is thought to occur when horseradish vapors directly irritate the gastric or respiratory tract mucosa.
VVS commonly manifests for the first time at around age 13 years; however, the timing of that first occurrence can vary significantly among individuals (as in this case)
The loss of consciousness may be caused by an emotional trigger (eg, sight of blood, cast removal,8 blood or platelet donations9,10), a painful event (eg, an injection11), an orthostatic trigger12 (eg, prolonged standing), or visceral reflexes such as swallowing.13 In approximately 30% of cases, loss of consciousness is associated with memory loss.14 Loss of consciousness with VVS may be associated with injury in 33% of cases.15
Continue to: The recovery with awareness
The recovery with awareness of time, place, and person may be a feature of VVS, which would differentiate it from seizures and brainstem vascular events. Autonomic prodromal symptoms—including abdominal discomfort, pallor, sweating, and nausea—may precede the loss of consciousness.8
An evolutionary response?
VVS may have developed as a trait through evolution, although modern medicine treats it as a disease. Many potential explanations for VVS as a body defense mechanism have been proposed. Examples include fainting at the sight of blood, which developed during the Old Stone Age—a period with extreme human-to-human violence—or acting like a “possum playing dead” as a tactic designed to confuse an attacker.16
Another theory involves clot production and suggests that VVS-induced hypotension is a defense against bleeding by improving clot formation.17
A psychological defense theory maintains that the fainting and memory loss are designed to prevent a painful or overwhelming experience from being remembered. None of these theories, however, explain orthostatic VVS.18
The brain defense theory could explain all forms of VVS. It postulates that hypotension causes decreased cerebral perfusion, which leads to syncope resulting in the body returning to a more orthostatic position with increased cerebral profusion.19
Continue to: The patient
The patient in this case was able to leave the restaurant on his own volition 30 minutes after the event and resume normal activities. Ten days later, an electrocardiogram was performed, with negative results. In this case, the use of a potassium-wasting diuretic exacerbated the risk of a fluid-deprived state, hypokalemia, and hypotension, possibly contributing to the syncope. The patient has since “gotten back on the horseradish” without ill effect.
THE TAKEAWAY
Consumers and health care providers should be aware of the risks associated with consumption of fresh horseradish and should allow it to rest prior to ingestion to allow some evaporation of its active ingredient. An old case report saved the patient from an unnecessary (and costly) emergency department visit.
ACKNOWLEDGEMENTS
The authors would like to thank Terry J. Hannan, MBBS, FRACP, FACHI, FACMI for his critical review of the manuscript.
CORRESPONDENCE
Christoph U. Lehmann, MD, Clinical Informatics Center, 5323 Harry Hines Boulevard, Dallas, TX 75390; [email protected]
1. Rubin HR, Wu AW. The bitter herbs of Seder: more on horseradish horrors. JAMA. 1988;259:1943. doi: 10.1001/jama.259.13.1943b
2. Seder syncope. The Free Dictionary. Accessed July 20, 2022. https://medical-dictionary.thefreedictionary.com/Horseradish+Syncope
3. Sheldon RS, Sheldon AG, Connolly SJ, et al. Age of first faint in patients with vasovagal syncope. J Cardiovasc Electrophysiol. 2006;17:49-54. doi: 10.1111/j.1540-8167.2005.00267.x
4. Wallin BG, Sundlöf G. Sympathetic outflow to muscles during vasovagal syncope. J Auton Nerv Syst. 1982;6:287-291. doi: 10.1016/0165-1838(82)90001-7
5. Jardine DL, Melton IC, Crozier IG, et al. Decrease in cardiac output and muscle sympathetic activity during vasovagal syncope. Am J Physiol Heart Circ Physiol. 2002;282:H1804-H1809. doi: 10.1152/ajpheart.00640.2001
6. Waxman MB, Asta JA, Cameron DA. Localization of the reflex pathway responsible for the vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol. Can J Physiol Pharmacol. 1992;70:882-889. doi: 10.1139/y92-118
7. Alboni P, Alboni M. Typical vasovagal syncope as a “defense mechanism” for the heart by contrasting sympathetic overactivity. Clin Auton Res. 2017;27:253-261. doi: 10.1007/s10286-017-0446-2
8. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009;30:2631-2671. doi: 10.1093/eurheartj/ehp298
9. Davies J, MacDonald L, Sivakumar B, et al. Prospective analysis of syncope/pre-syncope in a tertiary paediatric orthopaedic fracture outpatient clinic. ANZ J Surg. 2021;91:668-672. doi: 10.1111/ans.16664
10. Almutairi H, Salam M, Batarfi K, et al. Incidence and severity of adverse events among platelet donors: a three-year retrospective study. Medicine (Baltimore). 2020;99:e23648. doi: 10.1097/MD.0000000000023648
11. Coakley A, Bailey A, Tao J, et al. Video education to improve clinical skills in the prevention of and response to vasovagal syncopal episodes. Int J Womens Dermatol. 2020;6:186-190. doi: 10.1016/j.ijwd.2020.02.002
12. Thijs RD, Brignole M, Falup-Pecurariu C, et al. Recommendations for tilt table testing and other provocative cardiovascular autonomic tests in conditions that may cause transient loss of consciousness: consensus statement of the European Federation of Autonomic Societies (EFAS) endorsed by the American Autonomic Society (AAS) and the European Academy of Neurology (EAN). Auton Neurosci. 2021;233:102792. doi: 10.1016/j.autneu.2021.102792
13. Nakagawa S, Hisanaga S, Kondoh H, et al. A case of swallow syncope induced by vagotonic visceral reflex resulting in atrioventricular node suppression. J Electrocardiol. 1987;20:65-69. doi: 10.1016/0022-0736(87)90010-0
14. O’Dwyer C, Bennett K, Langan Y, et al. Amnesia for loss of consciousness is common in vasovagal syncope. Europace. 2011;13:1040-1045. doi: 10.1093/europace/eur069
15. Jorge JG, Raj SR, Teixeira PS, et al. Likelihood of injury due to vasovagal syncope: a systematic review and meta-analysis. Europace. 2021;23:1092-1099. doi: 10.1093/europace/euab041
16. Bracha HS, Bracha AS, Williams AE, et al. The human fear-circuitry and fear-induced fainting in healthy individuals—the paleolithic-threat hypothesis. Clin Auton Res. 2005;15:238-241. doi: 10.1007/s10286-005-0245-z
17. Diehl RR. Vasovagal syncope and Darwinian fitness. Clin Auton Res. 2005;15:126-129. doi: 10.1007/s10286-005-0244-0
18. Engel CL, Romano J. Studies of syncope; biologic interpretation of vasodepressor syncope. Psychosom Med. 1947;9:288-294. doi: 10.1097/00006842-194709000-00002
19. Blanc JJ, Benditt DG. Vasovagal syncope: hypothesis focusing on its being a clinical feature unique to humans. J Cardiovasc Electrophysiol. 2016;27:623-629. doi: 10.1111/jce.12945
THE CASE
A 56-year-old physician (CUL) visited a local seafood restaurant, after having fasted since the prior evening. He had a history of hypertension that was well controlled with lisinopril/hydrochlorothiazide.
The physician and his party were seated outside, where the temperature was in the mid-70s. The group ordered oysters on the half shell accompanied by mignonette sauce, cocktail sauce, and horseradish. The physician ate an olive-size amount of horseradish with an oyster. He immediately complained of a sharp burning sensation in his stomach and remarked that the horseradish was significantly stronger than what he was accustomed to. Within 30 seconds, he noted an increased heart rate, weakness, and intense sweating. There was no increase in nasal secretions. Observers noted that he was very pale.
About 5 minutes after eating the horseradish, the physician leaned his head back and briefly lost consciousness. His wife, while supporting his head and checking his pulse, instructed other diners to call for emergency services, at which point the physician regained consciousness and the dispatcher was told that an ambulance was no longer necessary. Within a matter of minutes, all symptoms had abated, except for some mild weakness.
THE DIAGNOSIS
Ten minutes after the event, the physician identified his symptoms as a horseradish-induced vasovagal syncope (VVS), based on a case report published in JAMA in 1988, which his wife found after he asked her to do an Internet search of his symptoms.1
THE DISCUSSION
Horseradish’s active component is isothiocyanate. Horseradish-induced syncope is also called Seder syncope after the Jewish Passover holiday dinner at which observant Jews are required to eat “bitter herbs.”1,2 This type of syncope is thought to occur when horseradish vapors directly irritate the gastric or respiratory tract mucosa.
VVS commonly manifests for the first time at around age 13 years; however, the timing of that first occurrence can vary significantly among individuals (as in this case)
The loss of consciousness may be caused by an emotional trigger (eg, sight of blood, cast removal,8 blood or platelet donations9,10), a painful event (eg, an injection11), an orthostatic trigger12 (eg, prolonged standing), or visceral reflexes such as swallowing.13 In approximately 30% of cases, loss of consciousness is associated with memory loss.14 Loss of consciousness with VVS may be associated with injury in 33% of cases.15
Continue to: The recovery with awareness
The recovery with awareness of time, place, and person may be a feature of VVS, which would differentiate it from seizures and brainstem vascular events. Autonomic prodromal symptoms—including abdominal discomfort, pallor, sweating, and nausea—may precede the loss of consciousness.8
An evolutionary response?
VVS may have developed as a trait through evolution, although modern medicine treats it as a disease. Many potential explanations for VVS as a body defense mechanism have been proposed. Examples include fainting at the sight of blood, which developed during the Old Stone Age—a period with extreme human-to-human violence—or acting like a “possum playing dead” as a tactic designed to confuse an attacker.16
Another theory involves clot production and suggests that VVS-induced hypotension is a defense against bleeding by improving clot formation.17
A psychological defense theory maintains that the fainting and memory loss are designed to prevent a painful or overwhelming experience from being remembered. None of these theories, however, explain orthostatic VVS.18
The brain defense theory could explain all forms of VVS. It postulates that hypotension causes decreased cerebral perfusion, which leads to syncope resulting in the body returning to a more orthostatic position with increased cerebral profusion.19
Continue to: The patient
The patient in this case was able to leave the restaurant on his own volition 30 minutes after the event and resume normal activities. Ten days later, an electrocardiogram was performed, with negative results. In this case, the use of a potassium-wasting diuretic exacerbated the risk of a fluid-deprived state, hypokalemia, and hypotension, possibly contributing to the syncope. The patient has since “gotten back on the horseradish” without ill effect.
THE TAKEAWAY
Consumers and health care providers should be aware of the risks associated with consumption of fresh horseradish and should allow it to rest prior to ingestion to allow some evaporation of its active ingredient. An old case report saved the patient from an unnecessary (and costly) emergency department visit.
ACKNOWLEDGEMENTS
The authors would like to thank Terry J. Hannan, MBBS, FRACP, FACHI, FACMI for his critical review of the manuscript.
CORRESPONDENCE
Christoph U. Lehmann, MD, Clinical Informatics Center, 5323 Harry Hines Boulevard, Dallas, TX 75390; [email protected]
THE CASE
A 56-year-old physician (CUL) visited a local seafood restaurant, after having fasted since the prior evening. He had a history of hypertension that was well controlled with lisinopril/hydrochlorothiazide.
The physician and his party were seated outside, where the temperature was in the mid-70s. The group ordered oysters on the half shell accompanied by mignonette sauce, cocktail sauce, and horseradish. The physician ate an olive-size amount of horseradish with an oyster. He immediately complained of a sharp burning sensation in his stomach and remarked that the horseradish was significantly stronger than what he was accustomed to. Within 30 seconds, he noted an increased heart rate, weakness, and intense sweating. There was no increase in nasal secretions. Observers noted that he was very pale.
About 5 minutes after eating the horseradish, the physician leaned his head back and briefly lost consciousness. His wife, while supporting his head and checking his pulse, instructed other diners to call for emergency services, at which point the physician regained consciousness and the dispatcher was told that an ambulance was no longer necessary. Within a matter of minutes, all symptoms had abated, except for some mild weakness.
THE DIAGNOSIS
Ten minutes after the event, the physician identified his symptoms as a horseradish-induced vasovagal syncope (VVS), based on a case report published in JAMA in 1988, which his wife found after he asked her to do an Internet search of his symptoms.1
THE DISCUSSION
Horseradish’s active component is isothiocyanate. Horseradish-induced syncope is also called Seder syncope after the Jewish Passover holiday dinner at which observant Jews are required to eat “bitter herbs.”1,2 This type of syncope is thought to occur when horseradish vapors directly irritate the gastric or respiratory tract mucosa.
VVS commonly manifests for the first time at around age 13 years; however, the timing of that first occurrence can vary significantly among individuals (as in this case)
The loss of consciousness may be caused by an emotional trigger (eg, sight of blood, cast removal,8 blood or platelet donations9,10), a painful event (eg, an injection11), an orthostatic trigger12 (eg, prolonged standing), or visceral reflexes such as swallowing.13 In approximately 30% of cases, loss of consciousness is associated with memory loss.14 Loss of consciousness with VVS may be associated with injury in 33% of cases.15
Continue to: The recovery with awareness
The recovery with awareness of time, place, and person may be a feature of VVS, which would differentiate it from seizures and brainstem vascular events. Autonomic prodromal symptoms—including abdominal discomfort, pallor, sweating, and nausea—may precede the loss of consciousness.8
An evolutionary response?
VVS may have developed as a trait through evolution, although modern medicine treats it as a disease. Many potential explanations for VVS as a body defense mechanism have been proposed. Examples include fainting at the sight of blood, which developed during the Old Stone Age—a period with extreme human-to-human violence—or acting like a “possum playing dead” as a tactic designed to confuse an attacker.16
Another theory involves clot production and suggests that VVS-induced hypotension is a defense against bleeding by improving clot formation.17
A psychological defense theory maintains that the fainting and memory loss are designed to prevent a painful or overwhelming experience from being remembered. None of these theories, however, explain orthostatic VVS.18
The brain defense theory could explain all forms of VVS. It postulates that hypotension causes decreased cerebral perfusion, which leads to syncope resulting in the body returning to a more orthostatic position with increased cerebral profusion.19
Continue to: The patient
The patient in this case was able to leave the restaurant on his own volition 30 minutes after the event and resume normal activities. Ten days later, an electrocardiogram was performed, with negative results. In this case, the use of a potassium-wasting diuretic exacerbated the risk of a fluid-deprived state, hypokalemia, and hypotension, possibly contributing to the syncope. The patient has since “gotten back on the horseradish” without ill effect.
THE TAKEAWAY
Consumers and health care providers should be aware of the risks associated with consumption of fresh horseradish and should allow it to rest prior to ingestion to allow some evaporation of its active ingredient. An old case report saved the patient from an unnecessary (and costly) emergency department visit.
ACKNOWLEDGEMENTS
The authors would like to thank Terry J. Hannan, MBBS, FRACP, FACHI, FACMI for his critical review of the manuscript.
CORRESPONDENCE
Christoph U. Lehmann, MD, Clinical Informatics Center, 5323 Harry Hines Boulevard, Dallas, TX 75390; [email protected]
1. Rubin HR, Wu AW. The bitter herbs of Seder: more on horseradish horrors. JAMA. 1988;259:1943. doi: 10.1001/jama.259.13.1943b
2. Seder syncope. The Free Dictionary. Accessed July 20, 2022. https://medical-dictionary.thefreedictionary.com/Horseradish+Syncope
3. Sheldon RS, Sheldon AG, Connolly SJ, et al. Age of first faint in patients with vasovagal syncope. J Cardiovasc Electrophysiol. 2006;17:49-54. doi: 10.1111/j.1540-8167.2005.00267.x
4. Wallin BG, Sundlöf G. Sympathetic outflow to muscles during vasovagal syncope. J Auton Nerv Syst. 1982;6:287-291. doi: 10.1016/0165-1838(82)90001-7
5. Jardine DL, Melton IC, Crozier IG, et al. Decrease in cardiac output and muscle sympathetic activity during vasovagal syncope. Am J Physiol Heart Circ Physiol. 2002;282:H1804-H1809. doi: 10.1152/ajpheart.00640.2001
6. Waxman MB, Asta JA, Cameron DA. Localization of the reflex pathway responsible for the vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol. Can J Physiol Pharmacol. 1992;70:882-889. doi: 10.1139/y92-118
7. Alboni P, Alboni M. Typical vasovagal syncope as a “defense mechanism” for the heart by contrasting sympathetic overactivity. Clin Auton Res. 2017;27:253-261. doi: 10.1007/s10286-017-0446-2
8. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009;30:2631-2671. doi: 10.1093/eurheartj/ehp298
9. Davies J, MacDonald L, Sivakumar B, et al. Prospective analysis of syncope/pre-syncope in a tertiary paediatric orthopaedic fracture outpatient clinic. ANZ J Surg. 2021;91:668-672. doi: 10.1111/ans.16664
10. Almutairi H, Salam M, Batarfi K, et al. Incidence and severity of adverse events among platelet donors: a three-year retrospective study. Medicine (Baltimore). 2020;99:e23648. doi: 10.1097/MD.0000000000023648
11. Coakley A, Bailey A, Tao J, et al. Video education to improve clinical skills in the prevention of and response to vasovagal syncopal episodes. Int J Womens Dermatol. 2020;6:186-190. doi: 10.1016/j.ijwd.2020.02.002
12. Thijs RD, Brignole M, Falup-Pecurariu C, et al. Recommendations for tilt table testing and other provocative cardiovascular autonomic tests in conditions that may cause transient loss of consciousness: consensus statement of the European Federation of Autonomic Societies (EFAS) endorsed by the American Autonomic Society (AAS) and the European Academy of Neurology (EAN). Auton Neurosci. 2021;233:102792. doi: 10.1016/j.autneu.2021.102792
13. Nakagawa S, Hisanaga S, Kondoh H, et al. A case of swallow syncope induced by vagotonic visceral reflex resulting in atrioventricular node suppression. J Electrocardiol. 1987;20:65-69. doi: 10.1016/0022-0736(87)90010-0
14. O’Dwyer C, Bennett K, Langan Y, et al. Amnesia for loss of consciousness is common in vasovagal syncope. Europace. 2011;13:1040-1045. doi: 10.1093/europace/eur069
15. Jorge JG, Raj SR, Teixeira PS, et al. Likelihood of injury due to vasovagal syncope: a systematic review and meta-analysis. Europace. 2021;23:1092-1099. doi: 10.1093/europace/euab041
16. Bracha HS, Bracha AS, Williams AE, et al. The human fear-circuitry and fear-induced fainting in healthy individuals—the paleolithic-threat hypothesis. Clin Auton Res. 2005;15:238-241. doi: 10.1007/s10286-005-0245-z
17. Diehl RR. Vasovagal syncope and Darwinian fitness. Clin Auton Res. 2005;15:126-129. doi: 10.1007/s10286-005-0244-0
18. Engel CL, Romano J. Studies of syncope; biologic interpretation of vasodepressor syncope. Psychosom Med. 1947;9:288-294. doi: 10.1097/00006842-194709000-00002
19. Blanc JJ, Benditt DG. Vasovagal syncope: hypothesis focusing on its being a clinical feature unique to humans. J Cardiovasc Electrophysiol. 2016;27:623-629. doi: 10.1111/jce.12945
1. Rubin HR, Wu AW. The bitter herbs of Seder: more on horseradish horrors. JAMA. 1988;259:1943. doi: 10.1001/jama.259.13.1943b
2. Seder syncope. The Free Dictionary. Accessed July 20, 2022. https://medical-dictionary.thefreedictionary.com/Horseradish+Syncope
3. Sheldon RS, Sheldon AG, Connolly SJ, et al. Age of first faint in patients with vasovagal syncope. J Cardiovasc Electrophysiol. 2006;17:49-54. doi: 10.1111/j.1540-8167.2005.00267.x
4. Wallin BG, Sundlöf G. Sympathetic outflow to muscles during vasovagal syncope. J Auton Nerv Syst. 1982;6:287-291. doi: 10.1016/0165-1838(82)90001-7
5. Jardine DL, Melton IC, Crozier IG, et al. Decrease in cardiac output and muscle sympathetic activity during vasovagal syncope. Am J Physiol Heart Circ Physiol. 2002;282:H1804-H1809. doi: 10.1152/ajpheart.00640.2001
6. Waxman MB, Asta JA, Cameron DA. Localization of the reflex pathway responsible for the vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol. Can J Physiol Pharmacol. 1992;70:882-889. doi: 10.1139/y92-118
7. Alboni P, Alboni M. Typical vasovagal syncope as a “defense mechanism” for the heart by contrasting sympathetic overactivity. Clin Auton Res. 2017;27:253-261. doi: 10.1007/s10286-017-0446-2
8. Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009;30:2631-2671. doi: 10.1093/eurheartj/ehp298
9. Davies J, MacDonald L, Sivakumar B, et al. Prospective analysis of syncope/pre-syncope in a tertiary paediatric orthopaedic fracture outpatient clinic. ANZ J Surg. 2021;91:668-672. doi: 10.1111/ans.16664
10. Almutairi H, Salam M, Batarfi K, et al. Incidence and severity of adverse events among platelet donors: a three-year retrospective study. Medicine (Baltimore). 2020;99:e23648. doi: 10.1097/MD.0000000000023648
11. Coakley A, Bailey A, Tao J, et al. Video education to improve clinical skills in the prevention of and response to vasovagal syncopal episodes. Int J Womens Dermatol. 2020;6:186-190. doi: 10.1016/j.ijwd.2020.02.002
12. Thijs RD, Brignole M, Falup-Pecurariu C, et al. Recommendations for tilt table testing and other provocative cardiovascular autonomic tests in conditions that may cause transient loss of consciousness: consensus statement of the European Federation of Autonomic Societies (EFAS) endorsed by the American Autonomic Society (AAS) and the European Academy of Neurology (EAN). Auton Neurosci. 2021;233:102792. doi: 10.1016/j.autneu.2021.102792
13. Nakagawa S, Hisanaga S, Kondoh H, et al. A case of swallow syncope induced by vagotonic visceral reflex resulting in atrioventricular node suppression. J Electrocardiol. 1987;20:65-69. doi: 10.1016/0022-0736(87)90010-0
14. O’Dwyer C, Bennett K, Langan Y, et al. Amnesia for loss of consciousness is common in vasovagal syncope. Europace. 2011;13:1040-1045. doi: 10.1093/europace/eur069
15. Jorge JG, Raj SR, Teixeira PS, et al. Likelihood of injury due to vasovagal syncope: a systematic review and meta-analysis. Europace. 2021;23:1092-1099. doi: 10.1093/europace/euab041
16. Bracha HS, Bracha AS, Williams AE, et al. The human fear-circuitry and fear-induced fainting in healthy individuals—the paleolithic-threat hypothesis. Clin Auton Res. 2005;15:238-241. doi: 10.1007/s10286-005-0245-z
17. Diehl RR. Vasovagal syncope and Darwinian fitness. Clin Auton Res. 2005;15:126-129. doi: 10.1007/s10286-005-0244-0
18. Engel CL, Romano J. Studies of syncope; biologic interpretation of vasodepressor syncope. Psychosom Med. 1947;9:288-294. doi: 10.1097/00006842-194709000-00002
19. Blanc JJ, Benditt DG. Vasovagal syncope: hypothesis focusing on its being a clinical feature unique to humans. J Cardiovasc Electrophysiol. 2016;27:623-629. doi: 10.1111/jce.12945
