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{{SK}} CPVT, bidirectional tachycardia induced by catecholamines, catecholamine-induced polymorphic ventricular tachycardia, familial polymorphic ventricular tachycardia, FPVT | {{SK}} CPVT, bidirectional tachycardia induced by catecholamines, catecholamine-induced polymorphic ventricular tachycardia, familial polymorphic ventricular tachycardia, FPVT | ||
==Overview== | ==Overview== | ||
Catecholaminergic Polymorphic Ventricular Tachycardia ([[CPVT]]) is a rare [[inherited]] [[arrhythmogenic]] disorder characterized by [[syncopal attacks]], [[ventricular arrhythmias]], and even [[sudden cardiac death]], mostly in [[young]] patients. It is caused by [[mutations]] in [[calcium]] handling proteins such as [[Ryanodine receptor 2|RyR2]] and [[Calsequestrin|CASQ2]] within the sarcoplasmic reticulum, which results in [[ventricular arrhythmias]] in the setting of a high [[adrenergic]] tone such as during physical exercise or strong emotions. There are no associated structural abnormalities of the [[heart]]. | Catecholaminergic Polymorphic Ventricular Tachycardia ([[CPVT]]) is a rare [[inherited]] [[arrhythmogenic]] disorder characterized by [[syncopal attacks]], [[ventricular arrhythmias]], and even [[sudden cardiac death]], mostly in [[young]] patients. It is caused by [[mutations]] in [[calcium]] handling proteins such as [[Ryanodine receptor 2|RyR2]] and [[Calsequestrin|CASQ2]] within the [[sarcoplasmic reticulum]], which results in [[ventricular arrhythmias]] in the setting of a high [[adrenergic]] tone such as during physical exercise or strong emotions. There are no associated structural abnormalities of the [[heart]]. | ||
==Historical Perspective== | ==Historical Perspective== | ||
Revision as of 17:32, 12 July 2020
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Ventricular tachycardia Microchapters |
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Differentiating Ventricular Tachycardia from other Disorders |
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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]
Synonyms and keywords: CPVT, bidirectional tachycardia induced by catecholamines, catecholamine-induced polymorphic ventricular tachycardia, familial polymorphic ventricular tachycardia, FPVT
Overview
Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a rare inherited arrhythmogenic disorder characterized by syncopal attacks, ventricular arrhythmias, and even sudden cardiac death, mostly in young patients. It is caused by mutations in calcium handling proteins such as RyR2 and CASQ2 within the sarcoplasmic reticulum, which results in ventricular arrhythmias in the setting of a high adrenergic tone such as during physical exercise or strong emotions. There are no associated structural abnormalities of the heart.
Historical Perspective
- Catecholaminergic polymorphic ventricular tachycardia (CPVT) was first described by Reid et al in 1975 and 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 (hRyR2) mutations were first identified in the pathogenesis of Catecholaminergic polymorphic ventricular tachycardia.[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]
Classification
| Type | OMIM | Gene | Protein | Mode of inheritance | Locus |
|---|---|---|---|---|---|
| CPVT1 | 604772 | RyR2 | Ryanodine receptor 2 | Autosomal dominant | 1q42.1-q43 |
| CPVT2 | 611938 | CASQ2 | Calsequestrin 2 | Autosomal recessive | 1p13.3-p11 |
| CPVT3 | 614021 | Unknown | - | Autosomal recessive | 7p14–p22 |
| CPVT4 | 614916 | CALM1 | Calmodulin 1 | Autosomal dominant | 14q32.11 |
| CPVT5 | 615441 | TRDN | Triadin | Autosomal recessive | 6q22.31 |
Pathophysiology
The voltage-gated ion channel mutation associated with CPVT intermittently causes the heart to develop polymorphic ventricular tachycardia in response to the natural release of catecholamines. Catecholaminergic polymorphic VT may have both autosomal dominant and autosomal recessive pattern of inheritance. The following genes are associated with CPVT:
- RYR2:
- Mutations in cardiac ryanodine receptor gene RyR2 accounts for CPVT 1, and majority of the cases (approximately 50-65%).[2][7]
- Genetic linkage studies revealed the disease-causing locus with an autosomal dominant inheritance pattern on chromosome 1q42–q43.[8]
- RyR2 is involved in intracellular calcium homeostasis and in the excitation-contraction coupling of the heart.
- Mutations in RYR2 cause uncontrolled calcium leakage from the sarcoplasmic reticulum during electrical diastole, with a subsequent increase in the cytosolic calcium concentration.[5][2]
- CASQ2:
- Mutations in cardiac calsequestrin gene CASQ2 accounts for CPVT 2, for approximately 2–5% of the CPVT cases.[9]
- The chromosome involved is located on 1p13.3-p11 with an autosomal recessive pattern of inheritance.
- CASQ2 is a Ca2+ buffering protein within the sarcoplasmic reticulum that plays a role in the control of calcium release from the sarcoplasmic reticulum to the cytosol.
The genes encoding cardiac ryanodine-calcium release channel RyR2 or, infrequently, cardiac calsequestrin CASQ2 are thus involved in the release of calcium from the sarcoplasmic reticulum and mutations therein result in inappropriate calcium leak from the sarcoplasmic reticulum.[5][10][11] The cytosolic calcium overload activates the sodium-calcium exchanger, leading to a transient inward current, and delayed after-depolarizations that in turn can lead to triggered arrhythmias, particularly under conditions of high β-adrenergic tone.[12][13]
Other genes that have been associated with CPVT are:
- Unknown:
- CPVT 3 has been linked to chromosome 7p14–p22 with an autosomal recessive pattern of inheritance.[14]
- This novel phenotype is highly malignant form of CPVT, characterized by exercise-induced ventricular arrhythmia and a minor exercise-induced QT-prolongation.
- CALM1
- Mutations in Calmodulin 1 gene CALM1 accounts for CPVT 4, for approximately <1% of the CPVT cases.
- Mutation in the CALM1 gene was first identified in a Swedish family with a history of exercise-induced ventricular arrhythmias, syncope, and sudden death.[15]
- The chromosome involved is located on 14q32 with an autosomal dominant pattern of inheritance.
- Calmodulin is a calcium-binding protein that stabilizes RYR2 and controls its opening during diastole.[15]
- TRDN:
- Mutations in Triadin gene TRDN accounts for CPVT 5, for approximately 1-2% of the CPVT cases.[16]
- Mutations in the gene encoding Triadin (TRDN) were identified in the probands of 2 families in whom mutations for RYR2 and CASQ2 were not identified.[16]
- The chromosome involved is located on 6q22 with an autosomal recessive pattern of inheritance.
- Triadin is a protein within the sarcoplasmic reticulum, physically and functionally related to the ryanodine receptor that plays a role in the control of calcium release from the sarcoplasmic reticulum to the cytosol.
- TRDN mutations impair FKBP12.6–RYR2 interaction, thus destabilizing the RyR2 channel opening,[17] or by a reduction of CASQ2 protein levels.[16], thus affecting calcium release and resulting in a calcium leak during diastole similar to that observed for RyR2 mutants.
More recently, two other genes have been reported to cause CPVT-like phenotype (phenocopy):[18][19]
- KCNJ2- encoding for Inward-rectifier potassium ion channel - autosomal dominant - 17q24.3
- ANKB- encoding for ankyrin B, a cytoskeletal protein - autosomal dominant - 4q25
Differentiating Catecholaminergic polymorphic ventricular tachycardia from other Diseases
Catecholaminergic polymorphic ventricular tachycardia must be differentiated from other diseases that cause syncope, ventricular tachycardia, and sudden cardiac death, such as:
- Arrhythmogenic right ventricular dysplasia
- Short-coupled ventricular tachycardia (SC-torsade de pointes [TdP])
- Long QT syndrome
- Andersen-Tawil syndrome
Epidemiology and Demographics
- The prevalence of catecholaminergic polymorphic ventricular tachycardia is estimated to be 1 per 10,000 individuals. Although the true prevalence is unknown.[20]
Age
- Catecholaminergic polymorphic ventricular tachycardia onset is more commonly observed during childhood and adolescence with the mean age of onset of symptoms between age 7 and 12 years.[4][21][7]
- CPVT has also been reported in adults with onset as late as the fourth decade.[22]
Gender
- CPVT affects males and females equally;[23] although males are more likely to present at an earlier age (in childhood or adolescence), while females are more likely to present at an older age (20 years, mean).[4]
Race
- There is no racial predilection for CPVT.
Risk factors
There has been no risk stratification for CPVT so far, but the possible risk factors in the development of catecholaminergic polymorphic ventricular tachycardia (CPVT) are:
- Physical activity such as exercise,
- Stress,
- Young age,
- Family history of syncope or sudden death, and
- Family history of CPVT
Screening
Natural History, Complications, Prognosis
Natural History
- The symptoms of CPVT usually develop during childhood and adolescence, in the first and second decades of life, and start with symptoms such as episodes of syncope.
- More than 30% of affected individuals will experience symptoms before the age of 10 years and the majority (60% to 80%) of the patients will have one or more symptomatic arrhythmia episodes before age 40.[3] [4] [22] [24]
- If left untreated, the disease is highly lethal, as approximately 30% of patients experience at least one cardiac arrest and up to 80% one or more syncopal spells.[3][4]
- The polymorphic ventricular tachycardia may self-terminate or it may degenerate into ventricular fibrillation, causing sudden cardiac death.
Complications
Common complications of catecholaminergic polymorphic ventricular tachycardia include:
Prognosis
- Prognosis is generally poor, and the 10-year mortality of patients with CPVT is approximately 40%.[22]
- Studies show that there is a correlation between the age of the first syncope and the severity of the disease, with a worse prognosis in the case of early occurrence.[3]
- If left untreated, patients with CPVT have a mortality rate of 30% before age 40.[4][23]
Diagnosis
Diagnostic Criteria
- The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
- [criterion 1]
- [criterion 2]
- [criterion 3]
- [criterion 4]
Symptoms
- Clinical presentation of CPVT is variable, including asymptomatic patients identified as a part of familial screening.
- Among the symptomatic patients,
- Other symptoms include:
Laboratory findings
- There are no specific laboratory findings associated with catecholaminergic polymorphic ventricular tachycardia.
- However, to exclude electrolyte abnormalities as the cause of ventricular tachycardia, ionized calcium, magnesium and phosphate levels should be obtained.[27][28]
Electrocardiogram
The resting electrocardiogram is usually unremarkable but can show sinus bradycardia and a prominent U wave.
Exercise Stress Testing
CPVT is a diagnosis based on reproducing ventricular arrhythmias during exercise stress testing, syncope occurring during physical activity and acute emotion, and a history of exercise or emotion-related palpitations and dizziness with an absence of structural cardiac abnormalities.
Imaging
Other diagnostic studies
Genetic testing is available in some locations and may be useful in diagnosing the presence of the genetic disorder among related individuals before the onset of aborted sudden death or sudden cardiac death.
Treatment
CPVT is treated with beta blockers, verapamil or an ICD (implantable cardiac defibrillator).
Pharmacotherapy
Medications to treat CPVT include beta blockers and verapamil.[29]
According to recent research published in Nature Medicine, flecainide inhibits the release of the cardiac ryanodine receptor–mediated Ca2+, and is therefore believed to medicate the underlying molecular cause of CPVT in both mice and humans.[30]
Implantable cardioverter-defibrillator
Implantable cardioverter-defibrillators are used to prevent sudden death.
Sympathectomy
In recent reports, left cardiac sympathetic denervation and bilateral thoracoscopic sympathectomy have shown promising results in individuals whose symptoms cannot be controlled by beta blockers.[31]
ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (DO NOT EDIT) [32]
| Class I |
| "1. Beta blockers are indicated for patients who are clinically diagnosed with CPVT on the basis of the presence of spontaneous or documented stress-induced ventricular arrhythmias. (Level of Evidence: C)" |
| "2. Implantation of an ICD with use of beta blockers is indicated for patients with CPVT who are survivors of cardiac arrest and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)" |
| Class IIa |
| "1. Beta blockers can be effective in patients without clinical manifestations when the diagnosis of CPVT is established during childhood based on genetic analysis. (Level of Evidence: C)" |
| "2. Implantation of an ICD with the use of beta blockers can be effective for affected patients with CPVT with syncope and/or documented sustained VT while receiving beta blockers and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)" |
| Class IIb |
| "1. Beta blockers may be considered for patients with CPVT who were genetically diagnosed in adulthood and never manifested clinical symptoms of tachyarrhythmias. (Level of Evidence: C)" |
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.
- ↑ 2.0 2.1 2.2 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) - ↑ 3.0 3.1 3.2 3.3 3.4 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.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 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.
- ↑ 5.0 5.1 5.2 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.
- ↑ 7.0 7.1 Ackerman, M. J.; Priori, S. G.; Willems, S.; Berul, C.; Brugada, R.; Calkins, H.; Camm, A. J.; Ellinor, P. T.; Gollob, M.; Hamilton, R.; Hershberger, R. E.; Judge, D. P.; Le Marec, H.; McKenna, W. J.; Schulze-Bahr, E.; Semsarian, C.; Towbin, J. A.; Watkins, H.; Wilde, A.; Wolpert, C.; Zipes, D. P. (2011). "HRS/EHRA Expert Consensus Statement on the State of Genetic Testing for the Channelopathies and Cardiomyopathies: This document was developed as a partnership between the Heart Rhythm Society (HRS) and the European Heart Rhythm Association (EHRA)". Europace. 13 (8): 1077–1109. doi:10.1093/europace/eur245. ISSN 1099-5129.
- ↑ Swan, Heikki; Piippo, Kirsi; Viitasalo, Matti; Heikkilä, Päivi; Paavonen, Timo; Kainulainen, Katariina; Kere, Juha; Keto, Pekka; Kontula, Kimmo; Toivonen, Lauri (1999). "Arrhythmic disorder mapped to chromosome 1q42–q43 causes malignant polymorphic ventricular tachycardia in structurally normal hearts". Journal of the American College of Cardiology. 34 (7): 2035–2042. doi:10.1016/S0735-1097(99)00461-1. ISSN 0735-1097.
- ↑ Lahat, Hadas; Pras, Elon; Olender, Tsviya; Avidan, Nili; Ben-Asher, Edna; Man, Orna; Levy-Nissenbaum, Etgar; Khoury, Asad; Lorber, Avraham; Goldman, Boleslaw; Lancet, Doron; Eldar, Michael (2001). "A Missense Mutation in a Highly Conserved Region of CASQ2 Is Associated with Autosomal Recessive Catecholamine-Induced Polymorphic Ventricular Tachycardia in Bedouin Families from Israel". The American Journal of Human Genetics. 69 (6): 1378–1384. doi:10.1086/324565. ISSN 0002-9297.
- ↑ di Barletta, Marina Raffaele; Viatchenko-Karpinski, Serge; Nori, Alessandra; Memmi, Mirella; Terentyev, Dmitry; Turcato, Federica; Valle, Giorgia; Rizzi, Nicoletta; Napolitano, Carlo; Gyorke, Sandor; Volpe, Pompeo; Priori, Silvia G. (2006). "Clinical Phenotype and Functional Characterization of
CASQ2
Mutations Associated With Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation. 114 (10): 1012–1019. doi:10.1161/CIRCULATIONAHA.106.623793. ISSN 0009-7322. line feed character in
|title=at position 54 (help) - ↑ Lehnart, Stephan E.; Wehrens, Xander H.T.; Laitinen, Päivi J.; Reiken, Steven R.; Deng, Shi-Xiang; Cheng, Zhenzhuang; Landry, Donald W.; Kontula, Kimmo; Swan, Heikki; Marks, Andrew R. (2004). "Sudden Death in Familial Polymorphic Ventricular Tachycardia Associated With Calcium Release Channel (Ryanodine Receptor) Leak". Circulation. 109 (25): 3208–3214. doi:10.1161/01.CIR.0000132472.98675.EC. ISSN 0009-7322.
- ↑ Cerrone, Marina; Noujaim, Sami F.; Tolkacheva, Elena G.; Talkachou, Arkadzi; O’Connell, Ryan; Berenfeld, Omer; Anumonwo, Justus; Pandit, Sandeep V.; Vikstrom, Karen; Napolitano, Carlo; Priori, Silvia G.; Jalife, José (2007). "Arrhythmogenic Mechanisms in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation Research. 101 (10): 1039–1048. doi:10.1161/CIRCRESAHA.107.148064. ISSN 0009-7330.
- ↑ Knollmann, B. C. (2006). "Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia". Journal of Clinical Investigation. doi:10.1172/JCI29128. ISSN 0021-9738.
- ↑ Bhuiyan, Zahurul A.; Hamdan, Mohamed A.; Shamsi, Eman T.A.; Postma, Alex V.; Mannens, Marcel M.A.M.; Wilde, Arthur A. M.; Al-Gazali, Lihadh (2007). "A Novel Early Onset Lethal Form of Catecholaminergic Polymorphic Ventricular Tachycardia Maps to Chromosome 7p14-p22". Journal of Cardiovascular Electrophysiology. 18 (10): 1060–1066. doi:10.1111/j.1540-8167.2007.00913.x. ISSN 1045-3873.
- ↑ 15.0 15.1 Nyegaard, Mette; Overgaard, Michael T.; Søndergaard, Mads T.; Vranas, Marta; Behr, Elijah R.; Hildebrandt, Lasse L.; Lund, Jacob; Hedley, Paula L.; Camm, A. John; Wettrell, Göran; Fosdal, Inger; Christiansen, Michael; Børglum, Anders D. (2012). "Mutations in Calmodulin Cause Ventricular Tachycardia and Sudden Cardiac Death". The American Journal of Human Genetics. 91 (4): 703–712. doi:10.1016/j.ajhg.2012.08.015. ISSN 0002-9297.
- ↑ 16.0 16.1 16.2 Roux-Buisson, Nathalie; Cacheux, Marine; Fourest-Lieuvin, Anne; Fauconnier, Jeremy; Brocard, Julie; Denjoy, Isabelle; Durand, Philippe; Guicheney, Pascale; Kyndt, Florence; Leenhardt, Antoine; Le Marec, Hervé; Lucet, Vincent; Mabo, Philippe; Probst, Vincent; Monnier, Nicole; Ray, Pierre F.; Santoni, Elodie; Trémeaux, Pauline; Lacampagne, Alain; Fauré, Julien; Lunardi, Joël; Marty, Isabelle (2012). "Absence of triadin, a protein of the calcium release complex, is responsible for cardiac arrhythmia with sudden death in human". Human Molecular Genetics. 21 (12): 2759–2767. doi:10.1093/hmg/dds104. ISSN 0964-6906.
- ↑ "Catecholaminergic Polymorphic Ventricular Tachycardia - GeneReviews® - NCBI Bookshelf".
- ↑ Tristani-Firouzi, Martin; Jensen, Judy L.; Donaldson, Matthew R.; Sansone, Valeria; Meola, Giovanni; Hahn, Angelika; Bendahhou, Said; Kwiecinski, Hubert; Fidzianska, Anna; Plaster, Nikki; Fu, Ying-Hui; Ptacek, Louis J.; Tawil, Rabi (2002). "Functional and clinical characterization of KCNJ2 mutations associated with LQT7 (Andersen syndrome)". Journal of Clinical Investigation. 110 (3): 381–388. doi:10.1172/JCI15183. ISSN 0021-9738.
- ↑ Mohler, Peter J.; Splawski, Igor; Napolitano, Carlo; Bottelli, Georgia; Sharpe, Leah; Timothy, Katherine; Priori, Silvia G.; Keating, Mark T.; Bennett, Vann (2004). "A cardiac arrhythmia syndrome caused by loss of ankyrin-B function". Proceedings of the National Academy of Sciences. 101 (24): 9137–9142. doi:10.1073/pnas.0402546101. ISSN 0027-8424.
- ↑ "Catecholaminergic Polymorphic Ventricular Tachycardia - GeneReviews® - NCBI Bookshelf".
- ↑ "Catecholaminergic Polymorphic Ventricular Tachycardia - GeneReviews® - NCBI Bookshelf".
- ↑ 22.0 22.1 22.2 22.3 Sumitomo, N (2003). "Catecholaminergic polymorphic ventricular tachycardia: electrocardiographic characteristics and optimal therapeutic strategies to prevent sudden death". Heart. 89 (1): 66–70. doi:10.1136/heart.89.1.66. ISSN 0007-0769.
- ↑ 23.0 23.1 Hayashi, Meiso; Denjoy, Isabelle; Extramiana, Fabrice; Maltret, Alice; Buisson, Nathalie Roux; Lupoglazoff, Jean-Marc; Klug, Didier; Hayashi, Miyuki; Takatsuki, Seiji; Villain, Elisabeth; Kamblock, Joël; Messali, Anne; Guicheney, Pascale; Lunardi, Joël; Leenhardt, Antoine (2009). "Incidence and Risk Factors of Arrhythmic Events in Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation. 119 (18): 2426–2434. doi:10.1161/CIRCULATIONAHA.108.829267. ISSN 0009-7322.
- ↑ Postma, A V (2005). "Catecholaminergic polymorphic ventricular tachycardia: RYR2 mutations, bradycardia, and follow up of the patients". Journal of Medical Genetics. 42 (11): 863–870. doi:10.1136/jmg.2004.028993. ISSN 1468-6244.
- ↑ Napolitano, Carlo (May 2007). "Diagnosis and treatment of catecholaminergic polymorphic ventricular tachycardia" (PDF). Heart Rhythm. 4 (5): 675–8. doi:10.1016/j.hrthm.2006.12.048. PMID 17467641. Retrieved 2008-12-17. Unknown parameter
|coauthors=ignored (help) [dead link] - ↑ Tester, David J.; Spoon, Daniel B.; Valdivia, Hector H.; Makielski, Jonathan C.; Ackerman, Michael J. (2004). "Targeted Mutational Analysis of the RyR2-Encoded Cardiac Ryanodine Receptor in Sudden Unexplained Death: A Molecular Autopsy of 49 Medical Examiner/Coroner's Cases". Mayo Clinic Proceedings. 79 (11): 1380–1384. doi:10.4065/79.11.1380. ISSN 0025-6196.
- ↑ Tchou P, Young P, Mahmud R, Denker S, Jazayeri M, Akhtar M (January 1988). "Useful clinical criteria for the diagnosis of ventricular tachycardia". Am. J. Med. 84 (1): 53–6. doi:10.1016/0002-9343(88)90008-3. PMID 3337132.
- ↑ Lown B, Temte JV, Arter WJ (June 1973). "Cardiac arrhythmias. 6. Ventricular tachyarrhythmias. Clinical aspects". Circulation. 47 (6): 1364–81. doi:10.1161/01.cir.47.6.1364. PMID 4709549.
- ↑ Sumitomo, Naokata (January 2003). "Catecholaminergic polymorphic ventricular tachycardia: electrocardiographic characteristics and optimal therapeutic strategies to prevent sudden death". Heart. 89 (1): 66–70. doi:10.1136/heart.89.1.66. PMC 1767500. PMID 12482795. Unknown parameter
|coauthors=ignored (help) - ↑ Watanabe, Hiroshi (2009-04-01). "Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans". Nature Medicine. 15 (4): 380–383. doi:10.1038/nm.1942. PMC 2904954. PMID 19330009. Retrieved 2009-05-04. Unknown parameter
|coauthors=ignored (help) - ↑ Scott, P.A. (October 2008). "Successful treatment of catecholaminergic polymorphic ventricular tachycardia with bilateral thoracoscopic sympathectomy". Heart Rhythm. 5 (10): 1461–1463. doi:10.1016/j.hrthm.2008.07.007. PMID 18760972. Unknown parameter
|coauthors=ignored (help) - ↑ Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M; et al. (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (10): e385–484. doi:10.1161/CIRCULATIONAHA.106.178233. PMID 16935995.
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