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Right bundle branch block

MedGen UID:
88445
Concept ID:
C0085615
Disease or Syndrome
Synonyms: Block, Right Bundle-Branch; Blocks, Right Bundle-Branch; Bundle-Branch Block, Right; Bundle-Branch Blocks, Right; Right Bundle Branch Block; Right Bundle-Branch Block; Right Bundle-Branch Blocks
SNOMED CT: Right fascicular block (59118001); RBBB - Right bundle branch block (59118001); Right bundle branch block (59118001)
 
HPO: HP:0011712

Definition

A conduction block of the right branch of the bundle of His. This manifests as a prolongation of the QRS complex (greater than 0.12 s) with delayed activation of the right ventricle and terminal delay on the EKG. [from HPO]

Term Hierarchy

Conditions with this feature

Ebstein anomaly
MedGen UID:
4435
Concept ID:
C0013481
Congenital Abnormality
Ebstein anomaly is characterized by downward displacement of variable severity of the tricuspid valve into the right ventricle. The valve leaflets may be dysplastic, and a variable portion of the proximal part of the right ventricle is in continuity with the right atrium ('atrialized'), because of the abnormally positioned tricuspid valve. The severity of this defect includes a spectrum ranging from severe disturbance in fetal and neonatal life to virtually asymptomatic survival to adult life. Associated extracardiac anomalies in the setting of chromosomal or mendelian disorders occur in about 20% of patients with Ebstein anomaly. Nonsyndromic Ebstein anomaly can occur as a sporadic or a familial defect (summary by Digilio et al., 2011).
Familial ventricular tachycardia
MedGen UID:
83309
Concept ID:
C0340485
Disease or Syndrome
An instance of ventricular tachycardia that is caused by an inherited modification of the individual's genome.
Familial isolated complete right bundle branch block
MedGen UID:
83311
Concept ID:
C0340504
Disease or Syndrome
Naxos disease
MedGen UID:
321991
Concept ID:
C1832600
Disease or Syndrome
Naxos disease (NXD) is characterized by arrhythmogenic right ventricular cardiomyopathy associated with abnormalities of the skin, hair, and nails. The ectodermal features are evident from birth or early childhood, whereas the cardiac symptoms develop in young adulthood or later. Clinical variability of ectodermal features has been observed, with hair anomalies ranging from woolly hair to alopecia, and skin abnormalities ranging from mild focal palmoplantar keratoderma to generalized skin fragility or even lethal neonatal epidermolysis bullosa (Protonotarios et al., 1986; Cabral et al., 2010; Pigors et al., 2011; Erken et al., 2011; Sen-Chowdhry and McKenna, 2014). Another syndrome involving cardiomyopathy, woolly hair, and keratoderma (DCWHK; 605676) is caused by mutation in the desmoplakin gene (DSP; 125647). Also see 610476 for a similar disorder caused by homozygous mutation in the DSC2 gene (125645).
Dilated cardiomyopathy 1E
MedGen UID:
331341
Concept ID:
C1832680
Disease or Syndrome
Any familial isolated dilated cardiomyopathy in which the cause of the disease is a mutation in the SCN5A gene.
Myopathy, myosin storage, autosomal recessive
MedGen UID:
340603
Concept ID:
C1850709
Disease or Syndrome
Autosomal recessive myosin storage congenital myopathy-7B (CMYP7B) is a skeletal muscle disorder characterized by the onset of scapuloperoneal muscle weakness in early childhood or young adulthood. Affected individuals have difficulty walking, steppage gait, and scapular winging due to shoulder girdle involvement. The severity and progression of the disorder is highly variable, even within families. Most patients develop respiratory insufficiency, nocturnal hypoventilation, and restrictive lung disease; some develop hypertrophic cardiomyopathy. Additional features include myopathic facies, high-arched palate, scoliosis, and muscle wasting with thin body habitus. Serum creatine kinase may be normal or elevated. Skeletal muscle biopsy shows variable findings, including myosin storage disease, type 1 fiber predominance, centralized nuclei, and multiminicore disease (Onengut et al., 2004; Tajsharghi et al., 2007; Beecroft et al., 2019). For a discussion of genetic heterogeneity of congenital myopathy, see CMYP1A (117000).
Arrhythmogenic right ventricular dysplasia 10
MedGen UID:
347543
Concept ID:
C1857777
Disease or Syndrome
Arrhythmogenic right ventricular cardiomyopathy (ARVC) – previously referred to as arrhythmogenic right ventricular dysplasia (ARVD) – is characterized by progressive fibrofatty replacement of the myocardium that predisposes to ventricular tachycardia and sudden death in young individuals and athletes. It primarily affects the right ventricle, and it may also involve the left ventricle. The presentation of disease is highly variable even within families, and some affected individuals may not meet established clinical criteria. The mean age at diagnosis is 31 years (±13; range: 4-64 years).
Hypertrophic cardiomyopathy 4
MedGen UID:
350526
Concept ID:
C1861862
Disease or Syndrome
While most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nNonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nHypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. 
Hypertrophic cardiomyopathy 2
MedGen UID:
349383
Concept ID:
C1861864
Disease or Syndrome
Hypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. \n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nNonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nWhile most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.
Progressive familial heart block, type 1A
MedGen UID:
406301
Concept ID:
C1879286
Disease or Syndrome
Progressive familial heart block type I (PFHBI, PFHB1) is an autosomal dominant cardiac bundle branch disorder that may progress to complete heart block (Brink and Torrington, 1977; van der Merwe et al., 1986; van der Merwe et al., 1988). It is defined on electrocardiogram by evidence of bundle branch disease, i.e., right bundle branch block, left anterior or posterior hemiblock, or complete heart block, with broad QRS complexes. Progression has been shown from a normal electrocardiogram to right bundle branch block and from the latter to complete heart block. These electrocardiographic features differentiate PFHB type I from progressive familial heart block type II (PFHBII, PFHB2; 140400), in which the onset of complete heart block is associated with narrow complexes. Electrocardiographically the changes represent, respectively, bundle branch disease (PFHB1) and atrioventricular nodal disease with an atrioventricular block and an idionodal escape rhythm (PFHB2). PFHBI is manifested symptomatically when complete heart block supervenes, either with dyspnea, syncopal episodes, or sudden death. Treatment, which is best managed by regular electrocardiographic follow-up, is by the timely implantation of a pacemaker (Brink et al., 1995). Genetic Heterogeneity of Progressive Familial Heart Block Type I Progressive familial heart block type IB (PFHB1B; 604559) is caused by mutation in the TRPM4 gene (606936) on chromosome 19q13.32.
Progressive familial heart block type IB
MedGen UID:
370220
Concept ID:
C1970298
Disease or Syndrome
Most cases of heart block are not genetic and are not considered progressive familial heart block. The most common cause of heart block is fibrosis of the heart, which occurs as a normal process of aging. Other causes of heart block can include the use of certain medications or an infection of the heart tissue.\n\nProgressive familial heart block can be divided into type I and type II, with type I being further divided into types IA and IB. These types differ in where in the heart signaling is interrupted and the genetic cause. In types IA and IB, the heart block originates in the bundle branch, and in type II, the heart block originates in the atrioventricular node. The different types of progressive familial heart block have similar signs and symptoms.\n\nHeart block occurs when the electrical signaling is obstructed anywhere from the atria to the ventricles. In people with progressive familial heart block, the condition worsens over time: early in the disorder, the electrical signals are partially blocked, but the block eventually becomes complete, preventing any signals from passing through the heart. Partial heart block causes a slow or irregular heartbeat (bradycardia or arrhythmia, respectively), and can lead to the buildup of scar tissue (fibrosis) in the cells that carry electrical impulses. Fibrosis contributes to the development of complete heart block, resulting in uncoordinated electrical signaling between the atria and the ventricles and inefficient pumping of blood in the heart. Complete heart block can cause a sensation of fluttering or pounding in the chest (palpitations), shortness of breath, fainting (syncope), or sudden cardiac arrest and death.\n\nProgressive familial heart block is a genetic condition that alters the normal beating of the heart. A normal heartbeat is controlled by electrical signals that move through the heart in a highly coordinated way. These signals begin in a specialized cluster of cells called the sinoatrial node (the heart's natural pacemaker) located in the heart's upper chambers (the atria). From there, a group of cells called the atrioventricular node carries the electrical signals to another cluster of cells called the bundle of His. This bundle separates into multiple thin spindles called bundle branches, which carry electrical signals into the heart's lower chambers (the ventricles). Electrical impulses move from the sinoatrial node down to the bundle branches, stimulating a normal heartbeat in which the ventricles contract slightly later than the atria.
Brugada syndrome 2
MedGen UID:
382031
Concept ID:
C2673193
Disease or Syndrome
Brugada syndrome is characterized by cardiac conduction abnormalities (ST segment abnormalities in leads V1-V3 on EKG and a high risk for ventricular arrhythmias) that can result in sudden death. Brugada syndrome presents primarily during adulthood, although age at diagnosis may range from infancy to late adulthood. The mean age of sudden death is approximately 40 years. Clinical presentations may also include sudden infant death syndrome (SIDS; death of a child during the first year of life without an identifiable cause) and sudden unexpected nocturnal death syndrome (SUNDS), a typical presentation in individuals from Southeast Asia. Other conduction defects can include first-degree AV block, intraventricular conduction delay, right bundle branch block, and sick sinus syndrome.
Hypertrophic cardiomyopathy 11
MedGen UID:
436962
Concept ID:
C2677506
Disease or Syndrome
An autosomal dominant subtype of familial hypertrophic cardiomyopathy caused by mutation(s) in the ACTC1 gene, encoding actin, alpha cardiac muscle 1.
X-linked scapuloperoneal muscular dystrophy
MedGen UID:
395530
Concept ID:
C2678061
Disease or Syndrome
A rare, genetic, muscular dystrophy disease characterized by the co-occurrence of late onset scapular and peroneal muscle weakness, principally manifesting with distal lower limb and proximal upper limb weakness and scapular winging.
Hypertrophic cardiomyopathy 14
MedGen UID:
442484
Concept ID:
C2750467
Disease or Syndrome
An autosomal dominant subtype of familial hypertrophic cardiomyopathy caused by mutation(s) in the MYH6 gene, encoding myosin-6.
Hypertrophic cardiomyopathy 13
MedGen UID:
442487
Concept ID:
C2750472
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the TNNC1 gene.
Brugada syndrome 8
MedGen UID:
413928
Concept ID:
C2751083
Disease or Syndrome
Brugada syndrome is characterized by cardiac conduction abnormalities (ST segment abnormalities in leads V1-V3 on EKG and a high risk for ventricular arrhythmias) that can result in sudden death. Brugada syndrome presents primarily during adulthood, although age at diagnosis may range from infancy to late adulthood. The mean age of sudden death is approximately 40 years. Clinical presentations may also include sudden infant death syndrome (SIDS; death of a child during the first year of life without an identifiable cause) and sudden unexpected nocturnal death syndrome (SUNDS), a typical presentation in individuals from Southeast Asia. Other conduction defects can include first-degree AV block, intraventricular conduction delay, right bundle branch block, and sick sinus syndrome.
Myotonic dystrophy type 2
MedGen UID:
419137
Concept ID:
C2931689
Disease or Syndrome
Myotonic dystrophy type 2 (DM2) is characterized by myotonia and muscle dysfunction (proximal and axial weakness, myalgia, and stiffness), and less commonly by posterior subcapsular cataracts, cardiac conduction defects, insulin-insensitive type 2 diabetes mellitus, and other endocrine abnormalities. While myotonia (involuntary muscle contraction with delayed relaxation) has been reported during the first decade, onset is typically in the third to fourth decade, most commonly with fluctuating or episodic muscle pain that can be debilitating and proximal and axial weakness of the neck flexors and the hip flexors. Subsequently, weakness occurs in the elbow extensors and finger flexors. Facial weakness and weakness of the ankle dorsiflexors are less common. Myotonia rarely causes severe symptoms. In a subset of individuals, calf hypertrophy in combination with brisk reflexes is notable.
Autosomal recessive limb-girdle muscular dystrophy type 2N
MedGen UID:
461768
Concept ID:
C3150418
Disease or Syndrome
MDDGC2 is an autosomal recessive muscular dystrophy with onset after ambulation is achieved. Cognition is normal (Biancheri et al., 2007). It is part of a group of similar disorders resulting from defective glycosylation of alpha-dystroglycan (DAG1; 128239), collectively known as 'dystroglycanopathies' (Godfrey et al., 2007). For a discussion of genetic heterogeneity of muscular dystrophy-dystroglycanopathy type C, see MDDGC1 (609308).
Glycogen storage disease XV
MedGen UID:
462104
Concept ID:
C3150754
Disease or Syndrome
Glycogen storage disease type 15 is an extremely rare genetic glycogen storage disease reported in one patient to date. Clinical signs included muscle weakness, cardiac arrhythmia associated with accumulation of abnormal storage material in the heart and glycogen depletion in skeletal muscle.
Nestor-Guillermo progeria syndrome
MedGen UID:
462796
Concept ID:
C3151446
Disease or Syndrome
Nestor-Guillermo progeria syndrome (NGPS) is an autosomal recessive disorder characterized by lipoatrophy, osteoporosis, and very severe osteolysis. Patients have no cardiovascular impairment, diabetes mellitus, or hypertriglyceridemia, but suffer profound skeletal abnormalities that affect their quality of life. Onset is after 2 years of age, and lifespan is relatively long (summary by Cabanillas et al., 2011).
Congenital heart defects, multiple types, 3
MedGen UID:
767108
Concept ID:
C3554194
Disease or Syndrome
Multiple types of congenital heart defects-3 (CHTD3) is an autosomal dominant condition characterized by various types of congenital heart defects and low atrial rhythm (van de Meerakker et al., 2011). For a general phenotypic description and a discussion of genetic heterogeneity of multiple types of congenital heart defects, see 306955.
Pulmonary hypertension, primary, 4
MedGen UID:
815528
Concept ID:
C3809198
Disease or Syndrome
Primary pulmonary hypertension is a rare progressive disease characterized by increased pulmonary artery pressure in the absence of common causes of pulmonary hypertension, such as chronic heart, lung, or thromboembolic disease. There is often vascular remodeling. The clinical presentation can be nonspecific, and patients often receive a diagnosis late in their clinical course (summary by Ma et al., 2013). For a general phenotypic description and a discussion of genetic heterogeneity of primary pulmonary hypertension, see PPH1 (178600).
Atrial conduction disease
MedGen UID:
863722
Concept ID:
C4015285
Disease or Syndrome
A rare genetic cardiac disease characterized by variably expressed atrial tachyarrhythmia (such as atrial flutter, paroxysmal or chronic atrial fibrillation, ectopic atrial tachycardia, or multifocal atrial tachycardia), infra-Hisian conduction system disease, and vulnerability to dilated cardiomyopathy. Age of onset ranges between childhood and adulthood.
Progressive external ophthalmoplegia with mitochondrial DNA deletions, autosomal recessive 2
MedGen UID:
901897
Concept ID:
C4225312
Disease or Syndrome
Autosomal recessive progressive external ophthalmoplegia with mitochondrial DNA deletions-2 (PEOB2) is a mitochondrial disorder characterized by adult onset of progressive external ophthalmoplegia, exercise intolerance, muscle weakness, and signs and symptoms of spinocerebellar ataxia, such as impaired gait and dysarthria. Some patients may have respiratory insufficiency. Laboratory studies are consistent with a defect in mtDNA replication (summary by Reyes et al., 2015). For a discussion of genetic heterogeneity of autosomal recessive PEO, see PEOB1 (258450).
Autosomal recessive cutis laxa type 2C
MedGen UID:
1385755
Concept ID:
C4479387
Disease or Syndrome
Autosomal recessive cutis laxa type IIC (ARCL2C) is characterized by generalized skin wrinkling with sparse subcutaneous fat and dysmorphic progeroid facial features. Most patients also exhibit severe hypotonia as well as cardiovascular involvement (summary by Van Damme et al., 2017). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal recessive cutis laxa, see ARCL1A (219100).
Autosomal recessive cutis laxa type 2D
MedGen UID:
1376619
Concept ID:
C4479409
Disease or Syndrome
Autosomal recessive cutis laxa type IID (ARCL2D) is characterized by generalized skin wrinkling with sparse subcutaneous fat and dysmorphic progeroid facial features. Most patients also exhibit severe hypotonia as well as cardiovascular and neurologic involvement (summary by Van Damme et al., 2017). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal recessive cutis laxa, see ARCL1A (219100).
Noonan syndrome-like disorder with loose anagen hair 2
MedGen UID:
1376945
Concept ID:
C4479577
Disease or Syndrome
An inherited condition caused by autosomal dominant mutation(s) in the PPP1CB gene, encoding serine/threonine-protein phosphatase PP1-beta catalytic subunit. The condition is characterized by facial features similar to those seen in Noonan syndrome but may also include short stature, cognitive deficits, relative macrocephaly, small posterior fossa resulting in Chiari I malformation, hypernasal voice, cardiac defects, and ectodermal abnormalities, which typically presents as slow-growing, sparse, and/or unruly hair.
Brugada syndrome 1
MedGen UID:
1646402
Concept ID:
C4551804
Disease or Syndrome
Brugada syndrome is characterized by cardiac conduction abnormalities (ST segment abnormalities in leads V1-V3 on EKG and a high risk for ventricular arrhythmias) that can result in sudden death. Brugada syndrome presents primarily during adulthood, although age at diagnosis may range from infancy to late adulthood. The mean age of sudden death is approximately 40 years. Clinical presentations may also include sudden infant death syndrome (SIDS; death of a child during the first year of life without an identifiable cause) and sudden unexpected nocturnal death syndrome (SUNDS), a typical presentation in individuals from Southeast Asia. Other conduction defects can include first-degree AV block, intraventricular conduction delay, right bundle branch block, and sick sinus syndrome.
Glycosylphosphatidylinositol biosynthesis defect 21
MedGen UID:
1684749
Concept ID:
C5231419
Disease or Syndrome
Neurodevelopmental disorder with brain anomalies, seizures, and scoliosis (NEDBSS) is an autosomal recessive disorder characterized by severely impaired psychomotor development, hypotonia, seizures, and structural brain anomalies, including thin corpus callosum and cerebellar atrophy. Other features include scoliosis, dysmorphic facies, and visual impairment. Affected individuals are usually unable to walk or speak and may require tube feeding in severe cases. The disorder is caused by a defect in glycosylphosphatidylinositol (GPI) biosynthesis (summary by Knaus et al., 2019). For a discussion of genetic heterogeneity of GPI biosynthesis defects, see GPIBD1 (610293).
Marbach-Rustad progeroid syndrome
MedGen UID:
1784907
Concept ID:
C5543388
Disease or Syndrome
Marbach-Rustad progeroid syndrome (MARUPS) is characterized by progeroid appearance with little subcutaneous fat and triangular facies, growth retardation with short stature, hypoplastic mandible crowded with unerupted supernumerary teeth, and cerebellar intention tremor. Psychomotor development is normal. Although features are reminiscent of Hutchinson-Gilford progeria syndrome (HGPS; 176670), MARUPS is less severe, with a relatively good prognosis. Two patients have been reported (Marbach et al., 2019).
Cerebellar ataxia, brain abnormalities, and cardiac conduction defects
MedGen UID:
1794215
Concept ID:
C5562005
Disease or Syndrome
Cerebellar ataxia, brain abnormalities, and cardiac conduction defects (CABAC) is an autosomal recessive primarily neurologic disorder with variable manifestations. Common features included infantile-onset hypotonia, poor motor development, poor feeding and overall growth, and ataxic gait due to cerebellar ataxia. Other features include dysarthria, nystagmus, variable ocular anomalies, spasticity, hyperreflexia, and nonspecific dysmorphic features. Most, but not all, patients have global developmental delay with impaired intellectual development and speech delay. Brain imaging shows cerebellar hypoplasia, often with brainstem hypoplasia, enlarged ventricles, delayed myelination, and thin corpus callosum. A significant number of patients develop cardiac conduction defects in childhood or adolescence, often requiring pacemaker placement (summary by Slavotinek et al., 2020).
Cardiomyopathy, dilated, 2G
MedGen UID:
1801983
Concept ID:
C5676995
Disease or Syndrome
Dilated cardiomyopathy-2G (CMD2G) is characterized by early-onset severe dilated cardiomyopathy that progresses rapidly to heart failure in the neonatal period without evidence of intervening hypertrophy. Cardiac tissue exhibits markedly shortened thin filaments, disorganized myofibrils, and reduced contractile force generation, resulting in the severe ventricular dysfunction observed. There is no evidence of skeletal muscle hypertrophy (Ahrens-Nicklas et al., 2019). For a general phenotypic description and a discussion of genetic heterogeneity of dilated cardiomyopathy, see 115200.

Professional guidelines

PubMed

Wu S, Chen X, Wang S, Xu L, Xiao F, Huang Z, Zheng R, Jiang L, Vijayaraman P, Sharma PS, Su L, Huang W
JACC Clin Electrophysiol 2021 Sep;7(9):1166-1177. Epub 2021 Apr 28 doi: 10.1016/j.jacep.2021.02.018. PMID: 33933414
Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD
Circulation 2019 Aug 20;140(8):e382-e482. Epub 2018 Nov 6 doi: 10.1161/CIR.0000000000000628. PMID: 30586772
Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD
J Am Coll Cardiol 2019 Aug 20;74(7):e51-e156. Epub 2018 Nov 6 doi: 10.1016/j.jacc.2018.10.044. PMID: 30412709

Recent clinical studies

Etiology

Gilge JL, Padanilam BJ
Cardiol Clin 2023 Aug;41(3):393-397. doi: 10.1016/j.ccl.2023.03.011. PMID: 37321689
Zhang FT, Liu XJ, Zhao DQ, Wu JT, Zhang LM, Hu J, Fan XW, Yang HT, Yan LJ, Liu JJ, Wang SL
Ann Noninvasive Electrocardiol 2022 Jul;27(4):e12966. Epub 2022 May 14 doi: 10.1111/anec.12966. PMID: 35567783Free PMC Article
Gilge JL, Padanilam BJ
Card Electrophysiol Clin 2021 Dec;13(4):685-689. Epub 2021 Sep 23 doi: 10.1016/j.ccep.2021.06.008. PMID: 34689895
Benito B, Brugada R, Brugada J, Brugada P
Prog Cardiovasc Dis 2008 Jul-Aug;51(1):1-22. doi: 10.1016/j.pcad.2008.05.002. PMID: 18634914
Brugada P, Brugada J
J Am Coll Cardiol 1992 Nov 15;20(6):1391-6. doi: 10.1016/0735-1097(92)90253-j. PMID: 1309182

Diagnosis

Gilge JL, Padanilam BJ
Cardiol Clin 2023 Aug;41(3):393-397. doi: 10.1016/j.ccl.2023.03.011. PMID: 37321689
Ikeda T
Curr Cardiol Rev 2021;17(1):24-30. doi: 10.2174/1573403X16666200708111553. PMID: 32640959Free PMC Article
Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ, Lee R, Marine JE, McLeod CJ, Oken KR, Patton KK, Pellegrini CN, Selzman KA, Thompson A, Varosy PD
J Am Coll Cardiol 2019 Aug 20;74(7):e51-e156. Epub 2018 Nov 6 doi: 10.1016/j.jacc.2018.10.044. PMID: 30412709
Strauss DG, Selvester RH, Wagner GS
Am J Cardiol 2011 Mar 15;107(6):927-34. doi: 10.1016/j.amjcard.2010.11.010. PMID: 21376930
Brugada P, Brugada J
J Am Coll Cardiol 1992 Nov 15;20(6):1391-6. doi: 10.1016/0735-1097(92)90253-j. PMID: 1309182

Therapy

Ali H, Lupo P, Foresti S, De Ambroggi G, Anderson RH, De Lucia C, Turturiello D, Paganini EM, Bessi R, Contrafatto I, Farghaly AAA, Cristiano E, Cappato R
J Cardiovasc Electrophysiol 2023 Nov;34(11):2316-2329. Epub 2023 Sep 1 doi: 10.1111/jce.16050. PMID: 37655997
Chen Y, Lou L, Zhang X, Jin L, Chen Y, Chen L, Li Z, Zhang F, Fu T, Hu S, Yang J
Front Immunol 2023;14:1041591. Epub 2023 Apr 5 doi: 10.3389/fimmu.2023.1041591. PMID: 37090734Free PMC Article
Friedman DJ, Al-Khatib SM, Dalgaard F, Fudim M, Abraham WT, Cleland JGF, Curtis AB, Gold MR, Kutyifa V, Linde C, Tang AS, Ali-Ahmed F, Olivas-Martinez A, Inoue LYT, Sanders GD
Circulation 2023 Mar 7;147(10):812-823. Epub 2023 Jan 26 doi: 10.1161/CIRCULATIONAHA.122.062124. PMID: 36700426Free PMC Article
Zhou M, Ta S, Hahn RT, Hsi DH, Leon MB, Hu R, Zhang J, Zuo L, Li J, Wang J, Wang B, Zhu X, Liu J, Han Y, Li X, Xu B, Zhang L, Hou L, Han C, Liu J, Liu L
JAMA Cardiol 2022 May 1;7(5):529-538. doi: 10.1001/jamacardio.2022.0259. PMID: 35353129Free PMC Article
Strauss DG, Selvester RH, Wagner GS
Am J Cardiol 2011 Mar 15;107(6):927-34. doi: 10.1016/j.amjcard.2010.11.010. PMID: 21376930

Prognosis

Sammour Y, Krishnaswamy A, Kumar A, Puri R, Tarakji KG, Bazarbashi N, Harb S, Griffin B, Svensson L, Wazni O, Kapadia SR
JACC Cardiovasc Interv 2021 Jan 25;14(2):115-134. doi: 10.1016/j.jcin.2020.09.063. PMID: 33478630
Ikeda T
Curr Cardiol Rev 2021;17(1):24-30. doi: 10.2174/1573403X16666200708111553. PMID: 32640959Free PMC Article
Lévy S
J Interv Card Electrophysiol 2018 Aug;52(3):287-292. Epub 2018 Aug 22 doi: 10.1007/s10840-018-0430-3. PMID: 30136134
Calò L, Martino A, Goanta E, Okumura Y, de Ruvo E
J Interv Card Electrophysiol 2018 Aug;52(3):307-313. Epub 2018 May 26 doi: 10.1007/s10840-018-0386-3. PMID: 29804172
Zhang Y, Zhang J, Butler J, Yang X, Xie P, Guo D, Wei T, Yu J, Wu Z, Gao Y, Han X, Zhang X, Wen S, Anker SD, Filippatos G, Fonarow GC, Gan T, Zhang R; China-HF Investigators
J Card Fail 2017 Dec;23(12):868-875. Epub 2017 Oct 10 doi: 10.1016/j.cardfail.2017.09.014. PMID: 29029965

Clinical prediction guides

Ali H, Lupo P, Foresti S, De Ambroggi G, Anderson RH, De Lucia C, Turturiello D, Paganini EM, Bessi R, Contrafatto I, Farghaly AAA, Cristiano E, Cappato R
J Cardiovasc Electrophysiol 2023 Nov;34(11):2316-2329. Epub 2023 Sep 1 doi: 10.1111/jce.16050. PMID: 37655997
Chen Y, Lou L, Zhang X, Jin L, Chen Y, Chen L, Li Z, Zhang F, Fu T, Hu S, Yang J
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Recent systematic reviews

Aguiló O, Castells X, Miró Ò, Mueller C, Chioncel O, Trullàs JC
Clin Res Cardiol 2023 Aug;112(8):1020-1043. Epub 2022 Sep 18 doi: 10.1007/s00392-022-02105-z. PMID: 36116092
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