Catecholaminergic polymorphic ventricular tachycardia: Difference between revisions
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==Diagnosis== | ==Diagnosis== | ||
[[Catecholaminergic polymorphic ventricular tachycardia diagnostic study of choice|Diagnostic study of choice]] | [[Catecholaminergic polymorphic ventricular tachycardia history and symptoms|History and Symptoms]] | [[Catecholaminergic polymorphic ventricular tachycardia physical examination|Physical Examination]] | [[Catecholaminergic polymorphic ventricular tachycardia laboratory findings|Laboratory Findings]] | [[Catecholaminergic polymorphic ventricular tachycardia electrocardiogram|Electrocardiogram]] | [[Catecholaminergic polymorphic ventricular tachycardia x ray|X-Ray Findings]] | [[Catecholaminergic polymorphic ventricular tachycardia echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Catecholaminergic polymorphic ventricular tachycardia CT scan|CT-Scan Findings]] | [[Catecholaminergic polymorphic ventricular tachycardia MRI|MRI Findings]] | [[Catecholaminergic polymorphic ventricular tachycardia other imaging findings|Other Imaging Findings]] | [[Catecholaminergic polymorphic ventricular tachycardia other diagnostic studies|Other Diagnostic Studies]] | |||
===Symptoms=== | ===Symptoms=== | ||
Revision as of 09:59, 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]
Synonyms and keywords: CPVT, bidirectional tachycardia induced by catecholamines, catecholamine-induced polymorphic ventricular tachycardia, familial polymorphic ventricular tachycardia, FPVT, polymorphic ventricular tachycardia.
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Catecholaminergic polymorphic ventricular tachycardia from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
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.[6][7]
Electrocardiogram
- Resting ECG:
- CPVT patients usually have a normal resting 12-lead-ECG, and the QT interval is usually not prolonged.[1][8][5]
- However, sinus bradycardia has been reported in approximately 20% of patients, as another consequence of the diastolic calcium leakage facilitated by either RyR2 or CASQ2 mutations.[9][10]
- In addition, prominent U-waves are observed in a subset of patients, which may also be related to altered intracellular calcium handling. However, its clinical significance is unknown.[11]
- Supraventricular arrhythmias, including isolated atrial ectopic beats, non-sustained supraventricular tachycardia and bursts of atrial fibrillation, are present in 16-26% of CPVT patients, maybe related to co-existing sinus node dysfunction.[1][12][13][14][15][16][17]
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.
- It has been observed that arrhythmias in CPVT often appear in a uniform and reproducible pattern that facilitates the recognition of affected patients.[1]
- Exercise Stress Testing is the primary diagnostic test and the most helpful clinical tool in diagnosing CPVT as it can reproducibly evoke the typical ventricular tachycardia during acute adrenergic activation (e.g., exercise, acute emotion).
- It may also be useful in monitoring the response to beta-blocker therapy of affected individuals in reproducible conditions.
- During exercise testing, sinus rhythm accelerates and beyond a heart rate of 120-130 beats per minute, isolated and often monomorphic ventricular premature beats (VPBs) typically occur first and then increase with heart rate to quadrigeminy, trigeminy, and bigeminy.
- Subsequently, the VPBs become polymorphic, and as the exercise increase, they form bursts of non-sustained polymorphic ventricular tachycardia (VT).
- If the activity is stopped, the arrhythmia disappears in the reverse order without clinical symptoms.
- However, when the activity is continued, the arrhythmia persists and becomes more rapid, eventually assuming the appearance of polymorphic ventricular tachycardia (VT), which is very fast, fibrillation-like and leads to syncope.
- Of note, in a subset of patients the ventricular arrhythmias already disappear with ongoing exercise.[18]
- Another type of polymorphic VT observed in CPVT patients is the bidirectional VT, which is a peculiar form of polymorphic VT characterized by 180° rotation of the QRS complex from beat to beat
- The occurrence of a bidirectional ventricular tachycardia (VT), which is the hallmark sign of CPVT is highly specific but not present in all patients.
- The bidirectional VT seen in CPVT are thought to originate from the His-Purkinje system from the alternating activation of the purkinje fibers of the two ventricles.[19][20][21]
| Exercise stress testing | |||||||||||||||||||||||||||||||||||
| Increase in sinus rhythm | |||||||||||||||||||||||||||||||||||
| Monomorphic premature ventricular contractions (PVCs) | |||||||||||||||||||||||||||||||||||
| Polymorphic PVC Bigeminy | Bidirectional PVC Bigeminy | ||||||||||||||||||||||||||||||||||
| Polymorphic VT | Bidirectional VT | ||||||||||||||||||||||||||||||||||
Epinephrine Infusion
- Epinephrine infusion is an alternative to establish the diagnosis CPVT in patients who cannot perform an exercise stress test.[22]
- In a study of 36 CPVT patients and 45 unaffected relatives, reported doses of epinephrine escalated from 0.05 mcg/kg/min to 0.1 mcg/kg/min to a maximum of 0.20 mcg/kg/min; and the mean maximum heart rate was significantly lower than the maximum heart rate achieved during exercise testing.[23]
- Epinephrine test appears to be highly specific (98%), but not as sensitive as the exercise test for provoking arrhythmia in CPVT patients.[23]
- Patients undergoing an epinephrine infusion should have continuous ECG monitoring.
Holter monitoring
- Exercise stress testing and epinephrine infusion should be complemented by 24-hours Holter recordings.
- In individuals unable to perform an exercise test, especially infants and children or patients whose symptoms are more emotion-related rather than exercise-related, Holter monitoring can be performed.
- Holter monitoring is also useful to detect the presence of supraventricular arrhythmias.
- Holter monitoring is less sensitive than exercise testing.[15]
Imaging
- There are no echocardiographic, CT and MRI findings associated with CPVT.
- However, cardiac imaging including MRI or CT helps in excluding structural abnormalities such as hypertrophic cardiomyopathy, coronary artery diseases, and arrhythmogenic right ventricular dysplasia, that may present similar to CPVT.
Genetic testing
- Genetic testing helps in the confirmation of the diagnosis of CPVT.
- Genetic screening allows the identification of mutations in up to 65% of patients with a clinical diagnosis of CPVT.
- Identification of heterozygous pathogenic variants in RYR2 or CALM1 or of biallelic pathogenic variants in CASQ2 or TRDN can also establish the diagnosis of CPVT.
- Recommendations for genetic testing are:[24][25]
- Comprehensive or CPVT1 and CVPT2 (RYR2 and CASQ2) targeted CPVT genetic testing is recommended for any patient in whom a clinical index of suspicion for CPVT has been established based on examination of the patient's clinical history, family history, and expressed electrocardiographic phenotype during exercise stress testing or catecholamine infusion.
- Mutation-specific genetic testing is recommended for family members and appropriate relatives following the identification of the CPVT-causative mutation in an index case. Those family members with identified mutations should be treated even in the absence of a positive exercise stress test.[26]
Treatment
- The therapeutic approach to CPVT includes changes in lifestyle, medical therapy, left ventricular sympathetic denervation, and the use of implantable cardioverter-defibrillators.
Medical therapy
Medications to treat CPVT include beta blockers, flecainide and verapamil.
Beta-blockers
- The first-line therapeutic option for patients with CPVT is exercise restriction combined with beta-blockers without intrinsic sympathomimetic activity.[27]
- Because of the adrenergic nature of arrhythmias in CPVT, non-selective beta-blockers, titrated at the maximum tolerated dose in the absence of contraindications (example, asthma) are considered the most effective pharmacological therapy.
- Indications:
- All patients with stress-induced ventricular arrhythmias.
- Silent carriers of a pathogenic mutation, even when they do not exhibit arrhythmias during exercise stress testing since cardiac arrest may occur in them.[28]
- Drugs used:
- Nadolol[8][29]
- Long-acting, non-selective beta-blocker.
- Preferred for prophylactic treatment of CPVT.
- It is considered the most clinically effective choice.
- Dosage: 1-2 mg/kg per day.
- Propranolol
- Long-acting, non-selective beta-blocker.
- It is also considered an effective medication when Nadolol is unavailable.
- Dosage: 3-5 mg/kg per day.
- Nadolol[8][29]
- Holter monitoring and exercise stress testing should be repeated periodically throughout beta blocker therapy, to ensure that the heart-rate is in control during exercise.
- Non-compliance and abrupt interruption of beta blockade may cause a rebound effect of catecholamines on the heart, leading to arrhythmic events while on therapy. Thus, it is important to educate and highlight to patients the need to be compliant with therapy.[1][26]
- Even with appropriate use, beta blockers cannot completely suppress the arrhythmias.
- Recurrent arrhythmias or persistence of complex arrhythmias at exercise stress test may occur in up to one-third of the CPVT patients, with the annual arrhythmic event rate ranging between 11% per year and 3% per year.[8][21][2]
Verampil
- Calcium channel blocker.
- Verapamil might be considered as adjunctive therapy for CPVT patients with ongoing ventricular arrhythmias despite therapy with beta blockers.[30][31]
- However, the long-term efficacy of verapamil is still controversial.
Flecainide
- Flecainide which is best known as a cardiac sodium channel blocker (a Class IC antiarrhythmic) is also found to inhibit the cardiac ryanodine receptor (RyR2. This dual-action makes it an effective medication for CPVT.[32]
- Indications:[32][33]
- Patients with persistent arrhythmias despite beta blocker therapy.
- Patients with an ICD who continue to have stress-induced ventricular arrhythmias despite beta-blocker therapy.
- Dosage: 100-300 mg/day (1.5-4.5 mg/kg/day).[26]
- Randomized clinical trials for the long-term efficacy of flecainide are still ongoing.[34]
Implantable cardioverter-defibrillator
- ICD should be used with pharmacologic therapy.[35]
- Indications:[26]
- Patients who are at high risk of cardiac arrest
- Patients who have survived a sudden cardiac arrest
- Patients who have experienced syncope or sustained VT despite optimal medical therapy and left cardiac sympathetic denervation. [].
- Implantable cardioverter-defibrillator may have harmful pro-arrhythmic effects in some patients, since painful shocks can increase catecholamine release and trigger further arrhythmias and triggering VT storm, leading to a malignant cycle of shocks that may even culminate in death.
- To reduce the risk of inappropriate shocks, it is important to program ICD with long delays before shock delivery and high cut-off rates for heart rate recognition; and always administer beta blockers concurrently.[36]
Sympathectomy
- Left cardiac sympathetic denervation, where a portion of the sympathetic chain is surgically or endoscopically resected, and bilateral thoracoscopic sympathectomy have reported to be useful therapeutic methods for suppressing ventricular arrhythmias in CPVT patients.[26][37][38][39]
- Indications:[26][40][41]
- Patients who experience recurrent symptoms and/or implantable cardioverter-defibrillator (ICD) shocks despite optimal medical therapy
- Patients who are intolerant or have contraindications to beta blockers
- Limitations:
- Complexity of the surgical procedure
- Requirement of a specialised surgical centre
- Complications, such as:[42]
- In spite of the side-effects and complications, the procedure was safe and satisfactory among the vast majority of patients.
Catheter ablation
- The onset of CPVT may be initiated from purkinje cells and successful catheter ablation has been reported.[22]
- Catheter ablation of the bidirectional VPCs that trigger VF has been reported and this procedure could become an adjunctive therapy in patients with refractory CPVT.[43]
- Further evidence and experiences are required for its recommendation.
Prevention
- Limit or avoid competitive sports.
- Limit or avoid strenuous exercises.
- Limit exposure to stressful environments.
- The limits for allowed physical activity can be set on the basis of exercise stress testing done in the hospital.
- Holter monitor can be helpful in keeping the heart-rate within a safe range during physical activity.
- Follow-up visits with a cardiologist every six to twelve months to monitor the efficacy of therapy.
ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (DO NOT EDIT) [44]
| 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
- ↑ 1.0 1.1 1.2 1.3 1.4 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.
- ↑ 2.0 2.1 2.2 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.
- ↑ 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.
- ↑ 5.0 5.1 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.
- ↑ 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.
- ↑ 8.0 8.1 8.2 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.
- ↑ Neco, Patricia; Torrente, Angelo G.; Mesirca, Pietro; Zorio, Esther; Liu, Nian; Priori, Silvia G.; Napolitano, Carlo; Richard, Sylvain; Benitah, Jean-Pierre; Mangoni, Matteo E.; Gómez, Ana María (2012). "Paradoxical Effect of Increased Diastolic Ca
2+
Release and Decreased Sinoatrial Node Activity in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation. 126 (4): 392–401. doi:10.1161/CIRCULATIONAHA.111.075382. ISSN 0009-7322. line feed character in
|title=at position 45 (help) - ↑ Aizawa, Yoshiyasu; Komura, Satoru; Okada, Shinsuke; Chinushi, Masaomi; Aizawa, Yoshifusa; Morita, Hiroshi; Ohe, Tohru (2006). "Distinct U Wave Changes in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)". International Heart Journal. 47 (3): 381–389. doi:10.1536/ihj.47.381. ISSN 1349-2365.
- ↑ Sumitomo, Naokata; Sakurada, Harumizu; Taniguchi, Kazuo; Matsumura, Masaharu; Abe, Osamu; Miyashita, Michio; Kanamaru, Hiroshi; Karasawa, Kensuke; Ayusawa, Mamoru; Fukamizu, Seiji; Nagaoka, Iori; Horie, Minoru; Harada, Kensuke; Hiraoka, Masayasu (2007). "Association of Atrial Arrhythmia and Sinus Node Dysfunction in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation Journal. 71 (10): 1606–1609. doi:10.1253/circj.71.1606. ISSN 1346-9843.
- ↑ Lawrenz, Wolfgang; Krogmann, Otto N.; Wieczorek, Marcus (2013). "Complex atrial arrhythmias as first manifestation of catecholaminergic polymorphic ventricular tachycardia: an unusual course in a patient with a new mutation in ryanodine receptor type 2 gene". Cardiology in the Young. 24 (4): 741–744. doi:10.1017/S1047951113001091. ISSN 1047-9511.
- ↑ van der Werf, Christian; Nederend, Ineke; Hofman, Nynke; van Geloven, Nan; Ebink, Corné; Frohn-Mulder, Ingrid M.E.; Alings, A. Marco W.; Bosker, Hans A.; Bracke, Frank A.; van den Heuvel, Freek; Waalewijn, Reinier A.; Bikker, Hennie; van Tintelen, J. Peter; Bhuiyan, Zahurul A.; van den Berg, Maarten P.; Wilde, Arthur A.M. (2012). "Familial Evaluation in Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation: Arrhythmia and Electrophysiology. 5 (4): 748–756. doi:10.1161/CIRCEP.112.970517. ISSN 1941-3149.
- ↑ 15.0 15.1 Sy, Raymond W.; Gollob, Michael H.; Klein, George J.; Yee, Raymond; Skanes, Allan C.; Gula, Lorne J.; Leong-Sit, Peter; Gow, Robert M.; Green, Martin S.; Birnie, David H.; Krahn, Andrew D. (2011). "Arrhythmia characterization and long-term outcomes in catecholaminergic polymorphic ventricular tachycardia". Heart Rhythm. 8 (6): 864–871. doi:10.1016/j.hrthm.2011.01.048. ISSN 1547-5271.
- ↑ Sumitomo, Naokata; Nakamura, Takahiro; Fukuhara, Junji; Nakai, Toshiko; Watanabe, Ichiro; Mugishima, Hideo; Hiraoka, Masayasu (2010). "Clinical effectiveness of pulmonary vein isolation for arrhythmic events in a patient with catecholaminergic polymorphic ventricular tachycardia". Heart and Vessels. 25 (5): 448–452. doi:10.1007/s00380-009-1214-6. ISSN 0910-8327.
- ↑ Faggioni, Michela; van der Werf, Christian; Knollmann, Bjorn C. (2014). "Sinus node dysfunction in catecholaminergic polymorphic ventricular tachycardia: Risk factor and potential therapeutic target?". Trends in Cardiovascular Medicine. 24 (7): 273–278. doi:10.1016/j.tcm.2014.07.001. ISSN 1050-1738.
- ↑ Faggioni, Michela; Hwang, Hyun Seok; van der Werf, Christian; Nederend, Ineke; Kannankeril, Prince J.; Wilde, Arthur A.M.; Knollmann, Björn C. (2013). "Accelerated Sinus Rhythm Prevents Catecholaminergic Polymorphic Ventricular Tachycardia in Mice and in Patients". Circulation Research. 112 (4): 689–697. doi:10.1161/CIRCRESAHA.111.300076. ISSN 0009-7330.
- ↑ 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.
- ↑ Herron, Todd J.; Milstein, Michelle L.; Anumonwo, Justus; Priori, Silvia G.; Jalife, José (2010). "Purkinje cell calcium dysregulation is the cellular mechanism that underlies catecholaminergic polymorphic ventricular tachycardia". Heart Rhythm. 7 (8): 1122–1128. doi:10.1016/j.hrthm.2010.06.010. ISSN 1547-5271.
- ↑ 21.0 21.1 Cerrone, Marina; Colombi, Barbara; Santoro, Massimo; di Barletta, Marina Raffaele; Scelsi, Mario; Villani, Laura; Napolitano, Carlo; Priori, Silvia G (2005). "Bidirectional Ventricular Tachycardia and Fibrillation Elicited in a Knock-In Mouse Model Carrier of a Mutation in the Cardiac Ryanodine Receptor". Circulation Research. 96 (10). doi:10.1161/01.RES.0000169067.51055.72. ISSN 0009-7330.
- ↑ 22.0 22.1 Priori, Silvia G.; Wilde, Arthur A.; Horie, Minoru; Cho, Yongkeun; Behr, Elijah R.; Berul, Charles; Blom, Nico; Brugada, Josep; Chiang, Chern-En; Huikuri, Heikki; Kannankeril, Prince; Krahn, Andrew; Leenhardt, Antoine; Moss, Arthur; Schwartz, Peter J.; Shimizu, Wataru; Tomaselli, Gordon; Tracy, Cynthia; Ackerman, Michael; Belhassen, Bernard; Estes, N. A. Mark; Fatkin, Diane; Kalman, Jonathan; Kaufman, Elizabeth; Kirchhof, Paulus; Schulze-Bahr, Eric; Wolpert, Christian; Vohra, Jitendra; Refaat, Marwan; Etheridge, Susan P.; Campbell, Robert M.; Martin, Edward T.; Quek, Swee Chye (2013). "Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes". EP Europace. 15 (10): 1389–1406. doi:10.1093/europace/eut272. ISSN 1532-2092.
- ↑ 23.0 23.1 Marjamaa, Annukka; Hiippala, Anita; Arrhenius, Bianca; Lahtinen, Annukka M.; Kontula, Kimmo; Toivonen, Lauri; Happonen, Juha-Matti; Swan, Heikki (2012). "Intravenous Epinephrine Infusion Test in Diagnosis of Catecholaminergic Polymorphic Ventricular Tachycardia". Journal of Cardiovascular Electrophysiology. 23 (2): 194–199. doi:10.1111/j.1540-8167.2011.02188.x. ISSN 1045-3873.
- ↑ 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.
- ↑ Hofman, Nynke; Tan, Hanno L.; Alders, Mariëlle; Kolder, Iris; de Haij, Simone; Mannens, Marcel M.A.M.; Lombardi, Maria Paola; Lekanne dit Deprez, Ronald H.; van Langen, Irene; Wilde, Arthur A.M. (2013). "Yield of Molecular and Clinical Testing for Arrhythmia Syndromes". Circulation. 128 (14): 1513–1521. doi:10.1161/CIRCULATIONAHA.112.000091. ISSN 0009-7322.
- ↑ 26.0 26.1 26.2 26.3 26.4 26.5 Priori, Silvia G.; Blomström-Lundqvist, Carina; Mazzanti, Andrea; Blom, Nico; Borggrefe, Martin; Camm, John; Elliott, Perry Mark; Fitzsimons, Donna; Hatala, Robert; Hindricks, Gerhard; Kirchhof, Paulus; Kjeldsen, Keld; Kuck, Karl-Heinz; Hernandez-Madrid, Antonio; Nikolaou, Nikolaos; Norekvål, Tone M.; Spaulding, Christian; Van Veldhuisen, Dirk J. (2015). "2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death". European Heart Journal. 36 (41): 2793–2867. doi:10.1093/eurheartj/ehv316. ISSN 0195-668X.
- ↑ 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) - ↑ Hayashi, Miyuki; Denjoy, Isabelle; Hayashi, Meiso; Extramiana, Fabrice; Maltret, Alice; Roux-Buisson, Nathalie; Lupoglazoff, Jean-Marc; Klug, Didier; Maury, Philippe; Messali, Anne; Guicheney, Pascale; Leenhardt, Antoine (2012). "The role of stress test for predicting genetic mutations and future cardiac events in asymptomatic relatives of catecholaminergic polymorphic ventricular tachycardia probands". EP Europace. 14 (9): 1344–1351. doi:10.1093/europace/eus031. ISSN 1532-2092.
- ↑ Leren, Ida S.; Saberniak, Jørg; Majid, Eman; Haland, Trine F.; Edvardsen, Thor; Haugaa, Kristina H. (2016). "Nadolol decreases the incidence and severity of ventricular arrhythmias during exercise stress testing compared with β1-selective β-blockers in patients with catecholaminergic polymorphic ventricular tachycardia". Heart Rhythm. 13 (2): 433–440. doi:10.1016/j.hrthm.2015.09.029. ISSN 1547-5271.
- ↑ Swan, Heikki; Laitinen, Paivi; Kontula, Kimmo; Toivonen, Lauri (2005). "Calcium Channel Antagonism Reduces Exercise-Induced Ventricular Arrhythmias in Catecholaminergic Polymorphic Ventricular Tachycardia Patients with RyR2 Mutations". Journal of Cardiovascular Electrophysiology. 16 (2): 162–166. doi:10.1046/j.1540-8167.2005.40516.x. ISSN 1045-3873.
- ↑ Rosso, Rafael; Kalman, Jonathan M.; Rogowski, Ori; Diamant, Shmuel; Birger, Amir; Biner, Simon; Belhassen, Bernard; Viskin, Sami (2007). "Calcium channel blockers and beta-blockers versus beta-blockers alone for preventing exercise-induced arrhythmias in catecholaminergic polymorphic ventricular tachycardia". Heart Rhythm. 4 (9): 1149–1154. doi:10.1016/j.hrthm.2007.05.017. ISSN 1547-5271.
- ↑ 32.0 32.1 Watanabe, Hiroshi; Chopra, Nagesh; Laver, Derek; Hwang, Hyun Seok; Davies, Sean S; Roach, Daniel E; Duff, Henry J; Roden, Dan M; Wilde, Arthur A M; Knollmann, Björn C (2009). "Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans". Nature Medicine. 15 (4): 380–383. doi:10.1038/nm.1942. ISSN 1078-8956.
- ↑ van der Werf, Christian; Kannankeril, Prince J.; Sacher, Frederic; Krahn, Andrew D.; Viskin, Sami; Leenhardt, Antoine; Shimizu, Wataru; Sumitomo, Naokata; Fish, Frank A.; Bhuiyan, Zahurul A.; Willems, Albert R.; van der Veen, Maurits J.; Watanabe, Hiroshi; Laborderie, Julien; Haïssaguerre, Michel; Knollmann, Björn C.; Wilde, Arthur A.M. (2011). "Flecainide Therapy Reduces Exercise-Induced Ventricular Arrhythmias in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia". Journal of the American College of Cardiology. 57 (22): 2244–2254. doi:10.1016/j.jacc.2011.01.026. ISSN 0735-1097.
- ↑ "Flecainide for Catecholaminergic Polymorphic Ventricular Tachycardia - Full Text View - ClinicalTrials.gov".
- ↑ Roston, Thomas M.; Jones, Karolina; Hawkins, Nathaniel M.; Bos, J. Martijn; Schwartz, Peter J.; Perry, Frances; Ackerman, Michael J.; Laksman, Zachary W.M.; Kaul, Padma; Lieve, Krystien V.V.; Atallah, Joseph; Krahn, Andrew D.; Sanatani, Shubhayan (2018). "Implantable cardioverter-defibrillator use in catecholaminergic polymorphic ventricular tachycardia: A systematic review". Heart Rhythm. 15 (12): 1791–1799. doi:10.1016/j.hrthm.2018.06.046. ISSN 1547-5271.
- ↑ Al-Khatib, Sana M.; Stevenson, William G.; Ackerman, Michael J.; Bryant, William J.; Callans, David J.; Curtis, Anne B.; Deal, Barbara J.; Dickfeld, Timm; Field, Michael E.; Fonarow, Gregg C.; Gillis, Anne M.; Granger, Christopher B.; Hammill, Stephen C.; Hlatky, Mark A.; Joglar, José A.; Kay, G. Neal; Matlock, Daniel D.; Myerburg, Robert J.; Page, Richard L. (2018). "2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". Journal of the American College of Cardiology. 72 (14): e91–e220. doi:10.1016/j.jacc.2017.10.054. ISSN 0735-1097.
- ↑ Schneider, Heike E.; Steinmetz, Michael; Krause, Ulrich; Kriebel, Thomas; Ruschewski, Wolfgang; Paul, Thomas (2012). "Left cardiac sympathetic denervation for the management of life-threatening ventricular tachyarrhythmias in young patients with catecholaminergic polymorphic ventricular tachycardia and long QT syndrome". Clinical Research in Cardiology. 102 (1): 33–42. doi:10.1007/s00392-012-0492-7. ISSN 1861-0684.
- ↑ 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) - ↑ Collura, Christopher A.; Johnson, Jonathan N.; Moir, Christopher; Ackerman, Michael J. (2009). "Left cardiac sympathetic denervation for the treatment of long QT syndrome and catecholaminergic polymorphic ventricular tachycardia using video-assisted thoracic surgery". Heart Rhythm. 6 (6): 752–759. doi:10.1016/j.hrthm.2009.03.024. ISSN 1547-5271.
- ↑ De Ferrari, Gaetano M.; Dusi, Veronica; Spazzolini, Carla; Bos, J. Martijn; Abrams, Dominic J.; Berul, Charles I.; Crotti, Lia; Davis, Andrew M.; Eldar, Michael; Kharlap, Maria; Khoury, Asaad; Krahn, Andrew D.; Leenhardt, Antoine; Moir, Christopher R.; Odero, Attilio; Olde Nordkamp, Louise; Paul, Thomas; Rosés i Noguer, Ferran; Shkolnikova, Maria; Till, Jan; Wilde, Arthur A.M.; Ackerman, Michael J.; Schwartz, Peter J. (2015). "Clinical Management of Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation. 131 (25): 2185–2193. doi:10.1161/CIRCULATIONAHA.115.015731. ISSN 0009-7322.
- ↑ Wilde, Arthur A.M.; Bhuiyan, Zahurul A.; Crotti, Lia; Facchini, Mario; De Ferrari, Gaetano M.; Paul, Thomas; Ferrandi, Chiara; Koolbergen, Dave R.; Odero, Attilio; Schwartz, Peter J. (2008). "Left Cardiac Sympathetic Denervation for Catecholaminergic Polymorphic Ventricular Tachycardia". New England Journal of Medicine. 358 (19): 2024–2029. doi:10.1056/NEJMoa0708006. ISSN 0028-4793.
- ↑ Waddell-Smith, Kathryn E.; Ertresvaag, Kjetil N.; Li, Jian; Chaudhuri, Krish; Crawford, Jackie R.; Hamill, James K.; Haydock, David; Skinner, Jonathan R. (2015). "Physical and Psychological Consequences of Left Cardiac Sympathetic Denervation in Long-QT Syndrome and Catecholaminergic Polymorphic Ventricular Tachycardia". Circulation: Arrhythmia and Electrophysiology. 8 (5): 1151–1158. doi:10.1161/CIRCEP.115.003159. ISSN 1941-3149.
- ↑ Kaneshiro, Takashi; Naruse, Yoshihisa; Nogami, Akihiko; Tada, Hiroshi; Yoshida, Kentaro; Sekiguchi, Yukio; Murakoshi, Nobuyuki; Kato, Yoshiaki; Horigome, Hitoshi; Kawamura, Mihoko; Horie, Minoru; Aonuma, Kazutaka (2012). "Successful Catheter Ablation of Bidirectional Ventricular Premature Contractions Triggering Ventricular Fibrillation in Catecholaminergic Polymorphic Ventricular Tachycardia With
RyR2
Mutation". Circulation: Arrhythmia and Electrophysiology. 5 (1). doi:10.1161/CIRCEP.111.966549. ISSN 1941-3149. line feed character in
|title=at position 179 (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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