Epileptic Heart: Difference between revisions
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==Overview== | ==Overview== | ||
Chronic [[epileptic]] episodes and the subsequent [[catecholamine]] surges and [[hypoxia]] events may affect the [[heart]] and [[coronary]] [[vessels]] and result in the [[dysfunction]] of the [[heart]] | Chronic [[epileptic]] episodes and the subsequent [[catecholamine]] surges and [[hypoxia|hypoxic]] events may affect the [[heart]] and [[coronary]] [[vessels]] and result in the [[dysfunction]] of the [[heart]]. This [[condition]] is known as the "epileptic heart." This concept was first described by Dr. Richard L. Verrier and his colleagues in 2020. | ||
==Historical Perspective== | ==Historical Perspective== | ||
* | *Absence of [[cardiac]] activity during [[epilepsy|epileptic seizure]], first described by Dr. A.E. Russell, an English physician, in 1906.<ref name="Russell1906">{{cite journal|last1=Russell|first1=A.E.|title=CESSATION OF THE PULSE DURING THE ONSET OF EPILEPTIC FITS,|journal=The Lancet|volume=168|issue=4325|year=1906|pages=152–154|issn=01406736|doi=10.1016/S0140-6736(01)30477-4}}</ref> | ||
*The epileptic heart was first | *The epileptic heart was first described by Drs. Verrier, Pang, Nearing, and Schachter, in 2020.<ref name="VerrierPang2020">{{cite journal|last1=Verrier|first1=Richard L.|last2=Pang|first2=Trudy D.|last3=Nearing|first3=Bruce D.|last4=Schachter|first4=Steven C.|title=The Epileptic Heart: Concept and clinical evidence|journal=Epilepsy & Behavior|volume=105|year=2020|pages=106946|issn=15255050|doi=10.1016/j.yebeh.2020.106946}}</ref> | ||
==Classification== | ==Classification== | ||
| Line 17: | Line 17: | ||
==Pathophysiology== | ==Pathophysiology== | ||
*The exact mechanisms involved in the epileptic heart | |||
*The exact mechanisms involved in the epileptic heart are still being elucidated. However, the conceptual framework below provides helpful information on the development of [[heart disease]] in patients with [[epilepsy]].<ref name="VerrierSchachter2018">{{cite journal|last1=Verrier|first1=Richard L.|last2=Schachter|first2=Steven C.|title=Is heart disease in chronic epilepsy a consequence of seizures or a fellow traveler?|journal=Epilepsy & Behavior|volume=86|year=2018|pages=211–213|issn=15255050|doi=10.1016/j.yebeh.2018.06.027}}</ref> | |||
{{familytree/start}} | {{familytree/start}} | ||
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=== Epilepsy and Cardiac Arrhythmia === | ===Epilepsy and Cardiac Arrhythmia=== | ||
[[Cardiac]] [[arrhythmia]] have long been observed in [[patients]] with [[epilepsy]]. | [[Cardiac]] [[arrhythmia]] have long been observed in [[patients]] with [[epilepsy]]. Three different mechanisms explain this association:<ref name="Shmuelyvan der Lende2017">{{cite journal|last1=Shmuely|first1=S.|last2=van der Lende|first2=M.|last3=Lamberts|first3=R.J.|last4=Sander|first4=J.W.|last5=Thijs|first5=R.D.|title=The heart of epilepsy: Current views and future concepts|journal=Seizure|volume=44|year=2017|pages=176–183|issn=10591311|doi=10.1016/j.seizure.2016.10.001}}</ref> | ||
*Direct ( | |||
*Direct (causal) pathway | |||
*Co-existence of [[epilepsy]] and [[cardiac]] [[arrhythmia]] in the context of [[genetic]] [[disorders]]: | *Co-existence of [[epilepsy]] and [[cardiac]] [[arrhythmia]] in the context of [[genetic]] [[disorders]]: | ||
**[[Genes]] involved in [[epilepsy]]: [[SCN1A]], [[KCNA1]], and [[SCN8A]] | **[[Genes]] involved in [[epilepsy]]: [[SCN1A]], [[KCNA1]], and [[SCN8A]] | ||
**[[Genes]] involved in [[heart]] [[diseases]]: [[KCNQ1]], [[KCNH2]], [[SCN5A]], [[RYR2]] | **[[Genes]] involved in [[heart]] [[diseases]]: [[KCNQ1]], [[KCNH2]], [[SCN5A]], [[RYR2]] | ||
*Resultant association: | *Resultant association: | ||
** | **Certain [[anti-epileptic]] [[medications|medications with sodium channel blocking properties]] have been known to cause [[arrhythmia]]. | ||
**[[Seizure]] may also | **[[Seizure]] may also cause [[arrhythmia]]. | ||
***[[Ictal]] phase may be associated with [[tachycardia]], [[asystole]], [[bradycardia]], and [[AV block]]. | ***[[Ictal]] phase may be associated with [[tachycardia]], [[asystole]], [[bradycardia]], and [[AV block]]. | ||
***Postictal phase may be associated with [[asystole]], [[AV block]], [[atrial flutter]] or [[atrial fibrillation|fibrillation]], and [[ventricular fibrillation]]. | ***Postictal phase may be associated with [[asystole]], [[AV block]], [[atrial flutter]] or [[atrial fibrillation|fibrillation]], and [[ventricular fibrillation]]. | ||
=== Epilepsy and Structural Heart Disease === | |||
===Epilepsy and Structural Heart Disease=== | |||
Three mechanisms have been suggested to explain the association between [[epilepsy]] and [[structural heart disease]]:<ref name="Shmuelyvan der Lende2017">{{cite journal|last1=Shmuely|first1=S.|last2=van der Lende|first2=M.|last3=Lamberts|first3=R.J.|last4=Sander|first4=J.W.|last5=Thijs|first5=R.D.|title=The heart of epilepsy: Current views and future concepts|journal=Seizure|volume=44|year=2017|pages=176–183|issn=10591311|doi=10.1016/j.seizure.2016.10.001}}</ref> | Three mechanisms have been suggested to explain the association between [[epilepsy]] and [[structural heart disease]]:<ref name="Shmuelyvan der Lende2017">{{cite journal|last1=Shmuely|first1=S.|last2=van der Lende|first2=M.|last3=Lamberts|first3=R.J.|last4=Sander|first4=J.W.|last5=Thijs|first5=R.D.|title=The heart of epilepsy: Current views and future concepts|journal=Seizure|volume=44|year=2017|pages=176–183|issn=10591311|doi=10.1016/j.seizure.2016.10.001}}</ref> | ||
*Direct ( | |||
*Direct (causal) pathway in which [[structural heart disease]] may result in [[stroke]] and subsequent [[epilepsy]]. | |||
*Common [[risk factors]] contribute to the development of both [[epilepsy]] and [[structural heart disease]]. | *Common [[risk factors]] contribute to the development of both [[epilepsy]] and [[structural heart disease]]. | ||
*Resultant pathway: | *Resultant pathway: | ||
**[[Epilepsy]] may stimulate [[myocardial ischemia]] and [[Takotsubo syndrome]]. | **[[Epilepsy]] may stimulate [[myocardial ischemia]] and [[Takotsubo syndrome|a Takotsubo-like syndrome]]. | ||
**[[Anti-epileptic]] [[medications]] contribute to the development of [[arteriosclerosis]], [[weight]] gain, [[non alcoholic fatty liver disease]] and [[metabolic syndrome]] and result in poorer [[cardiovascular]] risk profile. | **[[Anti-epileptic|Certain anti-epileptic]] [[medications]] contribute to the development of [[arteriosclerosis]], [[weight]] gain, [[non alcoholic fatty liver disease|non-alcoholic fatty liver disease]] and [[metabolic syndrome]] and result in a poorer [[cardiovascular]] risk profile. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 21:06, 12 January 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sahar Memar Montazerin, M.D.[2]
Synonyms and keywords:
Overview
Chronic epileptic episodes and the subsequent catecholamine surges and hypoxic events may affect the heart and coronary vessels and result in the dysfunction of the heart. This condition is known as the "epileptic heart." This concept was first described by Dr. Richard L. Verrier and his colleagues in 2020.
Historical Perspective
- Absence of cardiac activity during epileptic seizure, first described by Dr. A.E. Russell, an English physician, in 1906.[1]
- The epileptic heart was first described by Drs. Verrier, Pang, Nearing, and Schachter, in 2020.[2]
Classification
- There is no established system for the classification of the epileptic heart.
Pathophysiology
- The exact mechanisms involved in the epileptic heart are still being elucidated. However, the conceptual framework below provides helpful information on the development of heart disease in patients with epilepsy.[3]
| Epilepsy | |||||||||||||||||||||||||||||||||||||||
| Cardiac effects | |||||||||||||||||||||||||||||||||||||||
| Repeated hypoxia and subsequent myocardial ischemia | Cathecholamines-induced cardiotoxicity | ||||||||||||||||||||||||||||||||||||||
| Accelerated atherosclerosis | Myocardial stunning | Vacuolization of myocytes and fibrosis | |||||||||||||||||||||||||||||||||||||
Epilepsy and Cardiac Arrhythmia
Cardiac arrhythmia have long been observed in patients with epilepsy. Three different mechanisms explain this association:[4]
- Direct (causal) pathway
- Co-existence of epilepsy and cardiac arrhythmia in the context of genetic disorders:
- Resultant association:
- Certain anti-epileptic medications with sodium channel blocking properties have been known to cause arrhythmia.
- Seizure may also cause arrhythmia.
- Ictal phase may be associated with tachycardia, asystole, bradycardia, and AV block.
- Postictal phase may be associated with asystole, AV block, atrial flutter or fibrillation, and ventricular fibrillation.
Epilepsy and Structural Heart Disease
Three mechanisms have been suggested to explain the association between epilepsy and structural heart disease:[4]
- Direct (causal) pathway in which structural heart disease may result in stroke and subsequent epilepsy.
- Common risk factors contribute to the development of both epilepsy and structural heart disease.
- Resultant pathway:
- Epilepsy may stimulate myocardial ischemia and a Takotsubo-like syndrome.
- Certain anti-epileptic medications contribute to the development of arteriosclerosis, weight gain, non-alcoholic fatty liver disease and metabolic syndrome and result in a poorer cardiovascular risk profile.
References
- ↑ Russell, A.E. (1906). "CESSATION OF THE PULSE DURING THE ONSET OF EPILEPTIC FITS,". The Lancet. 168 (4325): 152–154. doi:10.1016/S0140-6736(01)30477-4. ISSN 0140-6736.
- ↑ Verrier, Richard L.; Pang, Trudy D.; Nearing, Bruce D.; Schachter, Steven C. (2020). "The Epileptic Heart: Concept and clinical evidence". Epilepsy & Behavior. 105: 106946. doi:10.1016/j.yebeh.2020.106946. ISSN 1525-5050.
- ↑ Verrier, Richard L.; Schachter, Steven C. (2018). "Is heart disease in chronic epilepsy a consequence of seizures or a fellow traveler?". Epilepsy & Behavior. 86: 211–213. doi:10.1016/j.yebeh.2018.06.027. ISSN 1525-5050.
- ↑ 4.0 4.1 Shmuely, S.; van der Lende, M.; Lamberts, R.J.; Sander, J.W.; Thijs, R.D. (2017). "The heart of epilepsy: Current views and future concepts". Seizure. 44: 176–183. doi:10.1016/j.seizure.2016.10.001. ISSN 1059-1311.