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Prolonged QT interval

MedGen UID:
57494
Concept ID:
C0151878
Finding
Synonyms: Long Q-T syndrome; Long QT syndrome; Prolong qt interval on ekg
SNOMED CT: Prolonged QT interval (111975006); Increased QT interval (111975006)
 
HPO: HP:0001657

Definition

An electrocardiographic finding in which the QT interval not corrected for heart rate is prolonged. Thresholds for different age, gender, and patient populations exist. (CDISC) [from NCI]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVProlonged QT interval

Conditions with this feature

Jervell and Lange-Nielsen syndrome
MedGen UID:
5929
Concept ID:
C0022387
Disease or Syndrome
Jervell and Lange-Nielsen syndrome (JLNS) is characterized by congenital profound bilateral sensorineural hearing loss and long QTc, usually >500 msec. Prolongation of the QTc interval is associated with tachyarrhythmias, including ventricular tachycardia, episodes of torsade de pointes ventricular tachycardia, and ventricular fibrillation, which may culminate in syncope or sudden death. Iron-deficient anemia and elevated levels of gastrin are also frequent features of JLNS. The classic presentation of JLNS is a deaf child who experiences syncopal episodes during periods of stress, exercise, or fright. Fifty percent of individuals with JLNS had cardiac events before age three years. More than half of untreated children with JLNS die before age 15 years.
Long QT syndrome 1
MedGen UID:
19831
Concept ID:
C0035828
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Andersen Tawil syndrome
MedGen UID:
327586
Concept ID:
C1563715
Disease or Syndrome
Andersen-Tawil syndrome (ATS) is characterized by a triad of episodic flaccid muscle weakness (i.e., periodic paralysis), ventricular arrhythmias and prolonged QT interval, and anomalies including low-set ears, widely spaced eyes, small mandible, fifth-digit clinodactyly, syndactyly, short stature, and scoliosis. Affected individuals present in the first or second decade with either cardiac symptoms (palpitations and/or syncope) or weakness that occurs spontaneously following prolonged rest or following rest after exertion. Mild permanent weakness is common. Mild learning difficulties and a distinct neurocognitive phenotype (i.e., deficits in executive function and abstract reasoning) have been described.
Timothy syndrome
MedGen UID:
331395
Concept ID:
C1832916
Disease or Syndrome
Timothy syndrome is a multisystem disorder characterized by cardiac, hand/foot, facial, and neurodevelopmental features. Typical cardiac findings include a rate-corrected QT interval >480 ms, functional 2:1 AV block with bradycardia, tachyarrhythmias, and congenital heart defects (patent ductus arteriosus, patent foramen ovale, ventricular septal defect, tetralogy of Fallot, hypertrophic cardiomyopathy). The diagnosis of Timothy syndrome is generally made within the first few days of life although it may be suspected prenatally due to 2:1 AV block or bradycardia in the fetus. Hand/foot findings are unilateral or bilateral cutaneous syndactyly variably involving fingers two (index), three (middle), four (ring), and five (little) and bilateral cutaneous syndactyly of toes two and three. Facial findings include depressed nasal bridge, low-set ears, thin vermilion border of the upper lip, and round face. Neuropsychiatric involvement includes global developmental delays and autism spectrum disorders. Ventricular tachyarrhythmia is the leading cause of death, followed by infection and complications of intractable hypoglycemia. Average age of death is 2.5 years.
Long QT syndrome 4
MedGen UID:
331449
Concept ID:
C1833154
Disease or Syndrome
Sick sinus syndrome 1, autosomal recessive
MedGen UID:
325270
Concept ID:
C1837845
Disease or Syndrome
The term 'sick sinus syndrome' encompasses a variety of conditions caused by sinus node dysfunction. The most common clinical manifestations are syncope, presyncope, dizziness, and fatigue. Electrocardiogram typically shows sinus bradycardia, sinus arrest, and/or sinoatrial block. Episodes of atrial tachycardias coexisting with sinus bradycardia ('tachycardia-bradycardia syndrome') are also common in this disorder. SSS occurs most often in the elderly associated with underlying heart disease or previous cardiac surgery, but can also occur in the fetus, infant, or child without heart disease or other contributing factors, in which case it is considered to be a congenital disorder (Benson et al., 2003). Genetic Heterogeneity of Sick Sinus Syndrome Sick sinus syndrome-2 (SSS2; 163800) is caused by mutation in the HCN4 gene (605206). Susceptibility to sick sinus syndrome (SSS3; 614090) is influenced by variation in the MYH6 gene (160710).
3-methylglutaconic aciduria type V
MedGen UID:
347542
Concept ID:
C1857776
Disease or Syndrome
3-Methylglutaconic aciduria type V is an autosomal recessive disorder characterized by the onset of dilated or noncompaction cardiomyopathy in infancy or early childhood. Many patients die of cardiac failure. Other features include microcytic anemia, growth retardation, mild ataxia, mild muscle weakness, genital anomalies in males, and increased urinary excretion of 3-methylglutaconic acid. Some patients may have optic atrophy or delayed psychomotor development (summary by Davey et al., 2006 and Ojala et al., 2012). For a discussion of genetic heterogeneity of 3-methylglutaconic aciduria, see MGCA type I (250950).
Long QT syndrome 3
MedGen UID:
349087
Concept ID:
C1859062
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Long QT syndrome 5
MedGen UID:
358092
Concept ID:
C1867904
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Cardiac arrhythmia, ankyrin B-related
MedGen UID:
370181
Concept ID:
C1970119
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Progressive familial heart block type 1B
MedGen UID:
370220
Concept ID:
C1970298
Disease or Syndrome
Progressive 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.Heart 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.Progressive 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.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.
Jervell and Lange-Nielsen syndrome 2
MedGen UID:
394108
Concept ID:
C2676723
Disease or Syndrome
Jervell and Lange-Nielsen syndrome (JLNS) is characterized by congenital profound bilateral sensorineural hearing loss and long QTc, usually >500 msec. Prolongation of the QTc interval is associated with tachyarrhythmias, including ventricular tachycardia, episodes of torsade de pointes ventricular tachycardia, and ventricular fibrillation, which may culminate in syncope or sudden death. Iron-deficient anemia and elevated levels of gastrin are also frequent features of JLNS. The classic presentation of JLNS is a deaf child who experiences syncopal episodes during periods of stress, exercise, or fright. Fifty percent of individuals with JLNS had cardiac events before age three years. More than half of untreated children with JLNS die before age 15 years.
Long QT syndrome 11
MedGen UID:
437218
Concept ID:
C2678483
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Long QT syndrome 10
MedGen UID:
394836
Concept ID:
C2678484
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Long QT syndrome 9
MedGen UID:
395635
Concept ID:
C2678485
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Lipodystrophy, congenital generalized, type 4
MedGen UID:
412871
Concept ID:
C2750069
Disease or Syndrome
Congenital generalized lipodystrophy type 4 combines the phenotype of classic Berardinelli-Seip lipodystrophy (608594) with muscular dystrophy and cardiac conduction anomalies (Hayashi et al., 2009). For a general description and a discussion of genetic heterogeneity of congenital generalized lipodystrophy, see CGL1 (608594).
Long QT syndrome 13
MedGen UID:
462083
Concept ID:
C3150733
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Long QT syndrome 2
MedGen UID:
462293
Concept ID:
C3150943
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Long QT syndrome 6
MedGen UID:
462303
Concept ID:
C3150953
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Long QT syndrome 14
MedGen UID:
864108
Concept ID:
C4015671
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Long QT syndrome 15
MedGen UID:
864132
Concept ID:
C4015695
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the ECG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7), hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8), and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.

Recent clinical studies

Etiology

Weissler-Snir A, Gollob MH, Chauhan V, Care M, Spears DA
Pacing Clin Electrophysiol 2017 Apr;40(4):417-424. Epub 2017 Mar 16 doi: 10.1111/pace.13040. PMID: 28155223
Kuo HL, Liu YL, Liang CC, Chang CT, Wang SM, Liu JH, Lin HH, Wang IK, Yang YF, Chou CY, Huang CC
Nephrology (Carlton) 2017 Jun;22(6):436-440. doi: 10.1111/nep.12808. PMID: 27149688
Ninkovic VM, Ninkovic SM, Miloradovic V, Stanojevic D, Babic M, Giga V, Dobric M, Trenell MI, Lalic N, Seferovic PM, Jakovljevic DG
Acta Diabetol 2016 Oct;53(5):737-44. Epub 2016 Apr 23 doi: 10.1007/s00592-016-0864-y. PMID: 27107571Free PMC Article
Rivera-Fernández R, Arias-Verdú MD, García-Paredes T, Delgado-Rodríguez M, Arboleda-Sánchez JA, Aguilar-Alonso E, Quesada-García G, Vera-Almazán A
J Cardiovasc Med (Hagerstown) 2016 Jan;17(1):11-9. doi: 10.2459/JCM.0000000000000015. PMID: 24922196
Chen TY, Yeh YW, Kuo SC, Chen CY, Lin TP, Chang CC
J Clin Pharm Ther 2014 Jun;39(3):325-7. Epub 2014 Mar 5 doi: 10.1111/jcpt.12142. PMID: 24597640

Diagnosis

Weissler-Snir A, Gollob MH, Chauhan V, Care M, Spears DA
Pacing Clin Electrophysiol 2017 Apr;40(4):417-424. Epub 2017 Mar 16 doi: 10.1111/pace.13040. PMID: 28155223
Wentlandt M, Morris SC, Mitchell SH
Am J Emerg Med 2017 May;35(5):804.e5-804.e6. Epub 2016 Nov 22 doi: 10.1016/j.ajem.2016.11.051. PMID: 27914889
Kuo HL, Liu YL, Liang CC, Chang CT, Wang SM, Liu JH, Lin HH, Wang IK, Yang YF, Chou CY, Huang CC
Nephrology (Carlton) 2017 Jun;22(6):436-440. doi: 10.1111/nep.12808. PMID: 27149688
Ninkovic VM, Ninkovic SM, Miloradovic V, Stanojevic D, Babic M, Giga V, Dobric M, Trenell MI, Lalic N, Seferovic PM, Jakovljevic DG
Acta Diabetol 2016 Oct;53(5):737-44. Epub 2016 Apr 23 doi: 10.1007/s00592-016-0864-y. PMID: 27107571Free PMC Article
Rivera-Fernández R, Arias-Verdú MD, García-Paredes T, Delgado-Rodríguez M, Arboleda-Sánchez JA, Aguilar-Alonso E, Quesada-García G, Vera-Almazán A
J Cardiovasc Med (Hagerstown) 2016 Jan;17(1):11-9. doi: 10.2459/JCM.0000000000000015. PMID: 24922196

Therapy

Wentlandt M, Morris SC, Mitchell SH
Am J Emerg Med 2017 May;35(5):804.e5-804.e6. Epub 2016 Nov 22 doi: 10.1016/j.ajem.2016.11.051. PMID: 27914889
Rivera-Fernández R, Arias-Verdú MD, García-Paredes T, Delgado-Rodríguez M, Arboleda-Sánchez JA, Aguilar-Alonso E, Quesada-García G, Vera-Almazán A
J Cardiovasc Med (Hagerstown) 2016 Jan;17(1):11-9. doi: 10.2459/JCM.0000000000000015. PMID: 24922196
Gupta A, Mody P, Pandey A
JAMA Intern Med 2015 Nov;175(11):1748-9. doi: 10.1001/jamainternmed.2015.5047. PMID: 26389523
Ries R, Sayadipour A
J Psychiatr Pract 2014 Sep;20(5):338-44. doi: 10.1097/01.pra.0000454778.29433.7c. PMID: 25226194
Chen TY, Yeh YW, Kuo SC, Chen CY, Lin TP, Chang CC
J Clin Pharm Ther 2014 Jun;39(3):325-7. Epub 2014 Mar 5 doi: 10.1111/jcpt.12142. PMID: 24597640

Prognosis

Weissler-Snir A, Gollob MH, Chauhan V, Care M, Spears DA
Pacing Clin Electrophysiol 2017 Apr;40(4):417-424. Epub 2017 Mar 16 doi: 10.1111/pace.13040. PMID: 28155223
Kuo HL, Liu YL, Liang CC, Chang CT, Wang SM, Liu JH, Lin HH, Wang IK, Yang YF, Chou CY, Huang CC
Nephrology (Carlton) 2017 Jun;22(6):436-440. doi: 10.1111/nep.12808. PMID: 27149688
Ninkovic VM, Ninkovic SM, Miloradovic V, Stanojevic D, Babic M, Giga V, Dobric M, Trenell MI, Lalic N, Seferovic PM, Jakovljevic DG
Acta Diabetol 2016 Oct;53(5):737-44. Epub 2016 Apr 23 doi: 10.1007/s00592-016-0864-y. PMID: 27107571Free PMC Article
Galluzzo A, Gallo C, Battaglia A, Frea S, Canavosio FG, Botta M, Bergerone S, Gaita F
J Cardiovasc Med (Hagerstown) 2016 Jun;17(6):440-5. doi: 10.2459/JCM.0000000000000317. PMID: 26556440
Rivera-Fernández R, Arias-Verdú MD, García-Paredes T, Delgado-Rodríguez M, Arboleda-Sánchez JA, Aguilar-Alonso E, Quesada-García G, Vera-Almazán A
J Cardiovasc Med (Hagerstown) 2016 Jan;17(1):11-9. doi: 10.2459/JCM.0000000000000015. PMID: 24922196

Clinical prediction guides

Ninkovic VM, Ninkovic SM, Miloradovic V, Stanojevic D, Babic M, Giga V, Dobric M, Trenell MI, Lalic N, Seferovic PM, Jakovljevic DG
Acta Diabetol 2016 Oct;53(5):737-44. Epub 2016 Apr 23 doi: 10.1007/s00592-016-0864-y. PMID: 27107571Free PMC Article
Galluzzo A, Gallo C, Battaglia A, Frea S, Canavosio FG, Botta M, Bergerone S, Gaita F
J Cardiovasc Med (Hagerstown) 2016 Jun;17(6):440-5. doi: 10.2459/JCM.0000000000000317. PMID: 26556440
Rivera-Fernández R, Arias-Verdú MD, García-Paredes T, Delgado-Rodríguez M, Arboleda-Sánchez JA, Aguilar-Alonso E, Quesada-García G, Vera-Almazán A
J Cardiovasc Med (Hagerstown) 2016 Jan;17(1):11-9. doi: 10.2459/JCM.0000000000000015. PMID: 24922196
Mozos I, Costea C, Serban C, Susan L
J Electrocardiol 2011 Mar-Apr;44(2):105-8. Epub 2010 Dec 13 doi: 10.1016/j.jelectrocard.2010.10.034. PMID: 21146831
Di Micoli A, Zambruni A, Bracci E, Benazzi B, Zappoli P, Berzigotti A, Zoli M, Bernardi M, Trevisani F
Dig Liver Dis 2009 Jul;41(7):535-8. Epub 2008 Feb 21 doi: 10.1016/j.dld.2007.11.017. PMID: 18294935

Recent systematic reviews

Srivastava A, Kahan M, Nader M
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