Catecholaminergic polymorphic ventricular tachycardia historical perspective: Difference between revisions
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{{Catecholaminergic polymorphic ventricular tachycardia}} | {{Catecholaminergic polymorphic ventricular tachycardia}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}}{{MRV}} | ||
==Overview== | ==Overview== | ||
Catecholaminergic polymorphic ventricular tachycardia ([[CPVT]]) was first described by [[Reid et al]] in 1975. It was described as a familial [[cardiac arrhythmia]] that occurs in patients with structurally normal [[heart]] and causes [[exercise]] or emotion triggered [[syncope]] and [[sudden death]] with a distinguishing pattern of [[ventricular arrhythmias|ventricular]] and [[supraventricular arrhythmias]]. In 2001, cardiac [[ryanodine receptor 2|Ryanodine Receptor]] gene ([[ryanodine receptor 2|RyR2]]) [[mutations]] were first implicated in the pathogenesis of catecholaminergic polymorphic ventricular tachycardia ([[CPVT]]). Subsequent experimental studies demonstrated that the abnormal [[calcium]] release from the [[sarcoplasmic reticulum]] caused [[arrhythmias]] mediated by delayed afterdepolarizations and triggered activity. | |||
==Historical Perspective== | ==Historical Perspective== | ||
=== | *Catecholaminergic polymorphic ventricular tachycardia ([[CPVT]]) was first described by [[Reid et al]] in 1975, followed by [[Coumel et al]] in 1978.<ref name="ReidTynan1975">{{cite journal|last1=Reid|first1=D S|last2=Tynan|first2=M|last3=Braidwood|first3=L|last4=Fitzgerald|first4=G R|title=Bidirectional tachycardia in a child. A study using His bundle electrography.|journal=Heart|volume=37|issue=3|year=1975|pages=339–344|issn=1355-6037|doi=10.1136/hrt.37.3.339}}</ref> | ||
* | *[[CPVT]] was described as a familial [[cardiac arrhythmia]] that occurs in patients with structurally normal [[heart]] and causes [[exercise]] or emotion triggered [[syncope]] and [[sudden death]] with a distinguishing pattern of [[ventricular arrhythmias|ventricular]] and [[supraventricular arrhythmias]]. | ||
*In 2001, Cardiac [[ryanodine receptor 2|Ryanodine Receptor]] Gene ([[ryanodine receptor 2|RyR2]]) [[mutations]] were first implicated in the pathogenesis of catecholaminergic polymorphic ventricular tachycardia ([[CPVT]]).<ref name="PrioriNapolitano2001">{{cite journal|last1=Priori|first1=Silvia G.|last2=Napolitano|first2=Carlo|last3=Tiso|first3=Natascia|last4=Memmi|first4=Mirella|last5=Vignati|first5=Gabriele|last6=Bloise|first6=Raffaella|last7=Sorrentino|first7=Vincenzo|last8=Danieli|first8=Gian Antonio|title= | |||
*[ | Mutations in the Cardiac Ryanodine Receptor Gene ( | ||
hRyR2 | |||
* | ) Underlie Catecholaminergic Polymorphic Ventricular Tachycardia | ||
*In [ | |journal=Circulation|volume=103|issue=2|year=2001|pages=196–200|issn=0009-7322|doi=10.1161/01.CIR.103.2.196}}</ref> | ||
*In [ | *In 1995 and 2002, the clinical studies by [[Leenhardt et al]] and [[Priori et al]], respectively, have contributed to the understanding of the natural history of [[CPVT]].<ref name="LeenhardtLucet1995">{{cite journal|last1=Leenhardt|first1=Antoine|last2=Lucet|first2=Vincent|last3=Denjoy|first3=Isabelle|last4=Grau|first4=Francis|last5=Ngoc|first5=Dien Do|last6=Coumel|first6=Philippe|title=Catecholaminergic Polymorphic Ventricular Tachycardia in Children|journal=Circulation|volume=91|issue=5|year=1995|pages=1512–1519|issn=0009-7322|doi=10.1161/01.CIR.91.5.1512}}</ref><ref name="PrioriNapolitano2002">{{cite journal|last1=Priori|first1=Silvia G.|last2=Napolitano|first2=Carlo|last3=Memmi|first3=Mirella|last4=Colombi|first4=Barbara|last5=Drago|first5=Fabrizio|last6=Gasparini|first6=Maurizio|last7=DeSimone|first7=Luciano|last8=Coltorti|first8=Fernando|last9=Bloise|first9=Raffaella|last10=Keegan|first10=Roberto|last11=Cruz Filho|first11=Fernando E.S.|last12=Vignati|first12=Gabriele|last13=Benatar|first13=Abraham|last14=DeLogu|first14=Angelica|title=Clinical and Molecular Characterization of Patients With Catecholaminergic Polymorphic Ventricular Tachycardia|journal=Circulation|volume=106|issue=1|year=2002|pages=69–74|issn=0009-7322|doi=10.1161/01.CIR.0000020013.73106.D8}}</ref> | ||
*In 2004, studies showed that [[Ryanodine receptor 2|RyR2]] mutations reduced the threshold for Store-Overload-Induced [[Calcium|Ca2+]] Release (SOICR) and increased the tendency for triggered [[arrhythmia]]. Thus it appeared evident that catecholaminergic polymorphic ventricular tachycardia was caused by uncontrolled [[Calcium|Ca2+]] release from the [[sarcoplasmic reticulum]].<ref name="JiangXiao2004">{{cite journal|last1=Jiang|first1=D.|last2=Xiao|first2=B.|last3=Yang|first3=D.|last4=Wang|first4=R.|last5=Choi|first5=P.|last6=Zhang|first6=L.|last7=Cheng|first7=H.|last8=Chen|first8=S. R. W.|title=RyR2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca2+ release (SOICR)|journal=Proceedings of the National Academy of Sciences|volume=101|issue=35|year=2004|pages=13062–13067|issn=0027-8424|doi=10.1073/pnas.0402388101}}</ref> | |||
=== | *In 2006, subsequent experimental studies demonstrated that the abnormal [[calcium]] release caused [[arrhythmias]] mediated by delayed [[afterdepolarizations]] and triggered activity.<ref name="LiuColombi2006">{{cite journal|last1=Liu|first1=Nian|last2=Colombi|first2=Barbara|last3=Memmi|first3=Mirella|last4=Zissimopoulos|first4=Spyros|last5=Rizzi|first5=Nicoletta|last6=Negri|first6=Sara|last7=Imbriani|first7=Marcello|last8=Napolitano|first8=Carlo|last9=Lai|first9=F. Anthony|last10=Priori|first10=Silvia G.|title=Arrhythmogenesis in Catecholaminergic Polymorphic Ventricular Tachycardia|journal=Circulation Research|volume=99|issue=3|year=2006|pages=292–298|issn=0009-7330|doi=10.1161/01.RES.0000235869.50747.e1}}</ref> | ||
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=== | |||
==References== | ==References== | ||
Latest revision as of 15:27, 23 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mounika Reddy Vadiyala, M.B.B.S.[2]
Overview
Catecholaminergic polymorphic ventricular tachycardia (CPVT) was first described by Reid et al in 1975. It was described as a familial cardiac arrhythmia that occurs in patients with structurally normal heart and causes exercise or emotion triggered syncope and sudden death with a distinguishing pattern of ventricular and supraventricular arrhythmias. In 2001, cardiac Ryanodine Receptor gene (RyR2) mutations were first implicated in the pathogenesis of catecholaminergic polymorphic ventricular tachycardia (CPVT). Subsequent experimental studies demonstrated that the abnormal calcium release from the sarcoplasmic reticulum caused arrhythmias mediated by delayed afterdepolarizations and triggered activity.
Historical Perspective
- Catecholaminergic polymorphic ventricular tachycardia (CPVT) was first described by Reid et al in 1975, followed by Coumel et al in 1978.[1]
- CPVT was described as a familial cardiac arrhythmia that occurs in patients with structurally normal heart and causes exercise or emotion triggered syncope and sudden death with a distinguishing pattern of ventricular and supraventricular arrhythmias.
- In 2001, Cardiac Ryanodine Receptor Gene (RyR2) mutations were first implicated in the pathogenesis of catecholaminergic polymorphic ventricular tachycardia (CPVT).[2]
- In 1995 and 2002, the clinical studies by Leenhardt et al and Priori et al, respectively, have contributed to the understanding of the natural history of CPVT.[3][4]
- In 2004, studies showed that RyR2 mutations reduced the threshold for Store-Overload-Induced Ca2+ Release (SOICR) and increased the tendency for triggered arrhythmia. Thus it appeared evident that catecholaminergic polymorphic ventricular tachycardia was caused by uncontrolled Ca2+ release from the sarcoplasmic reticulum.[5]
- In 2006, subsequent experimental studies demonstrated that the abnormal calcium release caused arrhythmias mediated by delayed afterdepolarizations and triggered activity.[6]
References
- ↑ Reid, D S; Tynan, M; Braidwood, L; Fitzgerald, G R (1975). "Bidirectional tachycardia in a child. A study using His bundle electrography". Heart. 37 (3): 339–344. doi:10.1136/hrt.37.3.339. ISSN 1355-6037.
- ↑ Priori, Silvia G.; Napolitano, Carlo; Tiso, Natascia; Memmi, Mirella; Vignati, Gabriele; Bloise, Raffaella; Sorrentino, Vincenzo; Danieli, Gian Antonio (2001). "Mutations in the Cardiac Ryanodine Receptor Gene (
hRyR2
) Underlie Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation. 103 (2): 196–200. doi:10.1161/01.CIR.103.2.196. ISSN 0009-7322. line feed character in
|title=at position 51 (help) - ↑ Leenhardt, Antoine; Lucet, Vincent; Denjoy, Isabelle; Grau, Francis; Ngoc, Dien Do; Coumel, Philippe (1995). "Catecholaminergic Polymorphic Ventricular Tachycardia in Children". Circulation. 91 (5): 1512–1519. doi:10.1161/01.CIR.91.5.1512. ISSN 0009-7322.
- ↑ Priori, Silvia G.; Napolitano, Carlo; Memmi, Mirella; Colombi, Barbara; Drago, Fabrizio; Gasparini, Maurizio; DeSimone, Luciano; Coltorti, Fernando; Bloise, Raffaella; Keegan, Roberto; Cruz Filho, Fernando E.S.; Vignati, Gabriele; Benatar, Abraham; DeLogu, Angelica (2002). "Clinical and Molecular Characterization of Patients With Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation. 106 (1): 69–74. doi:10.1161/01.CIR.0000020013.73106.D8. ISSN 0009-7322.
- ↑ Jiang, D.; Xiao, B.; Yang, D.; Wang, R.; Choi, P.; Zhang, L.; Cheng, H.; Chen, S. R. W. (2004). "RyR2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca2+ release (SOICR)". Proceedings of the National Academy of Sciences. 101 (35): 13062–13067. doi:10.1073/pnas.0402388101. ISSN 0027-8424.
- ↑ Liu, Nian; Colombi, Barbara; Memmi, Mirella; Zissimopoulos, Spyros; Rizzi, Nicoletta; Negri, Sara; Imbriani, Marcello; Napolitano, Carlo; Lai, F. Anthony; Priori, Silvia G. (2006). "Arrhythmogenesis in Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation Research. 99 (3): 292–298. doi:10.1161/01.RES.0000235869.50747.e1. ISSN 0009-7330.