Catecholaminergic polymorphic ventricular tachycardia: Difference between revisions
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***[[Pneumothorax]] | ***[[Pneumothorax]] | ||
*In spite of the side-effects and complications, the procedure was safe and satisfactory among the vast majority of patients. | *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.<ref name="PrioriWilde2013">{{cite journal|last1=Priori|first1=Silvia G.|last2=Wilde|first2=Arthur A.|last3=Horie|first3=Minoru|last4=Cho|first4=Yongkeun|last5=Behr|first5=Elijah R.|last6=Berul|first6=Charles|last7=Blom|first7=Nico|last8=Brugada|first8=Josep|last9=Chiang|first9=Chern-En|last10=Huikuri|first10=Heikki|last11=Kannankeril|first11=Prince|last12=Krahn|first12=Andrew|last13=Leenhardt|first13=Antoine|last14=Moss|first14=Arthur|last15=Schwartz|first15=Peter J.|last16=Shimizu|first16=Wataru|last17=Tomaselli|first17=Gordon|last18=Tracy|first18=Cynthia|last19=Ackerman|first19=Michael|last20=Belhassen|first20=Bernard|last21=Estes|first21=N. A. Mark|last22=Fatkin|first22=Diane|last23=Kalman|first23=Jonathan|last24=Kaufman|first24=Elizabeth|last25=Kirchhof|first25=Paulus|last26=Schulze-Bahr|first26=Eric|last27=Wolpert|first27=Christian|last28=Vohra|first28=Jitendra|last29=Refaat|first29=Marwan|last30=Etheridge|first30=Susan P.|last31=Campbell|first31=Robert M.|last32=Martin|first32=Edward T.|last33=Quek|first33=Swee Chye|title=Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes|journal=EP Europace|volume=15|issue=10|year=2013|pages=1389–1406|issn=1532-2092|doi=10.1093/europace/eut272}}</ref> | |||
*Catheter ablation of the bidirectional [[VPC]]s that trigger [[VF]] has been reported and this procedure could become an adjunctive therapy in patients with refractory CPVT.<ref name="KaneshiroNaruse2012">{{cite journal|last1=Kaneshiro|first1=Takashi|last2=Naruse|first2=Yoshihisa|last3=Nogami|first3=Akihiko|last4=Tada|first4=Hiroshi|last5=Yoshida|first5=Kentaro|last6=Sekiguchi|first6=Yukio|last7=Murakoshi|first7=Nobuyuki|last8=Kato|first8=Yoshiaki|last9=Horigome|first9=Hitoshi|last10=Kawamura|first10=Mihoko|last11=Horie|first11=Minoru|last12=Aonuma|first12=Kazutaka|title= | |||
Successful Catheter Ablation of Bidirectional Ventricular Premature Contractions Triggering Ventricular Fibrillation in Catecholaminergic Polymorphic Ventricular Tachycardia With | |||
RyR2 | |||
Mutation | |||
|journal=Circulation: Arrhythmia and Electrophysiology|volume=5|issue=1|year=2012|issn=1941-3149|doi=10.1161/CIRCEP.111.966549}}</ref> | |||
*Further evidence and experiences are required for its recommendation. | |||
===Prevention=== | ===Prevention=== |
Revision as of 08:44, 22 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
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 (RyR2) mutations were first identified 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]
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
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
- Screening of all the first-degree relatives is indicated when a likely pathogenetic mutation is identified in clinically affected index cases.
- Clinical and genetic evaluation, including exercise stress testing is recommended for both first- and second-degree relatives.
- Exercise stress testing has a specificity of 97% and a sensitivity of 50% for predicting the presence of the familial CPVT-associated mutation in asymptomatic relatives of CPVT patients.[23][24][25]
- Genetic testing for RyR2 and CASQ2 mutations should also be considered in first-degree relatives, even with a negative clinical phenotype.
- Screening by repeat exercise testing is also recommended in first-degree relatives of mutation-negative patients with CPVT, depending on the age of the relative.[7]
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] [26]
- However, molecular analysis showed that there is a small group of patients who remain asymptomatic, even after exercise tests suggesting them to be having normal phenotype CPVT (mutation carriers). Some of these phenotypically normal patients with CVPT do experience syncope and sudden death.[23]
- If left untreated, CPVT 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 CPVT is made when at least one of the following four diagnostic criteria are met:[27][28]
- CPVT is diagnosed in the presence of a structurally normal heart, normal ECG, and unexplained exercise or catecholamine-induced bidirectional VT, polymorphic ventricular premature beats or VT in individuals <40 years of age.
- CPVT is diagnosed in patients (index case or family member) who have a pathogenic mutation.
- CPVT is diagnosed in family members of a CPVT index case with a normal heart who manifest exercise-induced premature ventricular contractions or bidirectional/ polymorphic VT.
- CPVT can be diagnosed in the presence of a structurally normal heart and coronary arteries, normal ECG, and unexplained exercise or catecholamine-induced bidirectional VT, polymorphic ventricular premature beats or VT in individuals >40 years of age.
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.[31][32]
Electrocardiogram
- Resting ECG:
- CPVT patients usually have a normal resting 12-lead-ECG, and the QT interval is usually not prolonged.[3][23][22]
- 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.[26][33]
- 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.[34]
- 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.[3][35][36][24][37][38][39]
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.[3]
- 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.[40]
- 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.[12][41][42]
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.[27]
- 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.[43]
- Epinephrine test appears to be highly specific (98%), but not as sensitive as the exercise test for provoking arrhythmia in CPVT patients.[43]
- 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.[37]
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:[7][44]
- 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.[28]
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.[45]
- 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.[25]
- Drugs used:
- Nadolol[23][46]
- 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[23][46]
- 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.[3][28]
- 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.[23][42][4]
Verampil
- Calcium channel blocker.
- Verapamil might be considered as adjunctive therapy for CPVT patients with ongoing ventricular arrhythmias despite therapy with beta blockers.[47][48]
- 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.[49]
- Indications:[49][50]
- 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).[28]
- Randomized clinical trials for the long-term efficacy of flecainide are still ongoing.[51]
Implantable cardioverter-defibrillator
- ICD should be used with pharmacologic therapy.[52]
- Indications:[28]
- 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.[53]
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.[28][54][55]
- Indications:[28][56]
- 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:[57]
- 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.[27]
- 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.[58]
- Further evidence and experiences are required for its recommendation.
Prevention
ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (DO NOT EDIT) [59]
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 3.5 3.6 3.7 3.8 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 4.8 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 7.2 7.3 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.
- ↑ 12.0 12.1 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 22.4 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 23.2 23.3 23.4 23.5 23.6 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.
- ↑ 24.0 24.1 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.
- ↑ 25.0 25.1 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.
- ↑ 26.0 26.1 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.
- ↑ 27.0 27.1 27.2 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.
- ↑ 28.0 28.1 28.2 28.3 28.4 28.5 28.6 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.
- ↑ 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.
- ↑ 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.
- ↑ 37.0 37.1 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.
- ↑ 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.
- ↑ 42.0 42.1 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.
- ↑ 43.0 43.1 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.
- ↑ 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.
- ↑ 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) - ↑ 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.
- ↑ 49.0 49.1 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) - ↑ 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.
- ↑ 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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