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Secundum atrial septal defect

MedGen UID:
91034
Concept ID:
C0344724
Congenital Abnormality; Finding
Synonyms: ASD II; Atrial septal defect, ostium secundum type
SNOMED CT: Ostium secundum type atrial septal defect (204315000); ASD2 - Secundum atrial septal defect (204315000); Atrial septal defect within oval fossa (204315000); Ostium secundum defect (204315000); Secundum atrial septal defect (204315000); Atrial septal defect of fossa ovalis (204315000); ASD II - Secundum atrial septal defect (204315000); 2 ASD - Secundum atrial septal defect (204315000); Fossa ovalis defect (204315000)
 
HPO: HP:0001684
Monarch Initiative: MONDO:0020434
Orphanet: ORPHA99103

Definition

A kind of atrial septum defect arising from an enlarged foramen ovale, inadequate growth of the septum secundum, or excessive absorption of the septum primum. [from HPO]

Term Hierarchy

Conditions with this feature

Agnathia-otocephaly complex
MedGen UID:
78541
Concept ID:
C0265242
Congenital Abnormality
Agnathia-otocephaly is a rare condition characterized by mandibular hypoplasia or agnathia, ventromedial auricular malposition (melotia) and/or auricular fusion (synotia), and microstomia with oroglossal hypoplasia or aglossia. Holoprosencephaly is the most commonly identified association, but skeletal, genitourinary, and cardiovascular anomalies, and situs inversus have been reported. The disorder is almost always lethal (review by Faye-Petersen et al., 2006).
Holt-Oram syndrome
MedGen UID:
120524
Concept ID:
C0265264
Disease or Syndrome
Holt-Oram syndrome (HOS) is characterized by upper-limb defects, congenital heart malformation, and cardiac conduction disease. Upper-limb malformations may be unilateral, bilateral/symmetric, or bilateral/asymmetric and can range from triphalangeal or absent thumb(s) to phocomelia. Other upper-limb malformations can include unequal arm length caused by aplasia or hypoplasia of the radius, fusion or anomalous development of the carpal and thenar bones, abnormal forearm pronation and supination, abnormal opposition of the thumb, sloping shoulders, and restriction of shoulder joint movement. An abnormal carpal bone is present in all affected individuals and may be the only evidence of disease. A congenital heart malformation is present in 75% of individuals with HOS and most commonly involves the septum. Atrial septal defect and ventricular septal defect can vary in number, size, and location. Complex congenital heart malformations can also occur in individuals with HOS. Individuals with HOS with or without a congenital heart malformation are at risk for cardiac conduction disease. While individuals may present at birth with sinus bradycardia and first-degree atrioventricular (AV) block, AV block can progress unpredictably to a higher grade including complete heart block with and without atrial fibrillation.
CHARGE association
MedGen UID:
75567
Concept ID:
C0265354
Disease or Syndrome
CHD7 disorder encompasses the entire phenotypic spectrum of heterozygous CHD7 pathogenic variants that includes CHARGE syndrome as well as subsets of features that comprise the CHARGE syndrome phenotype. The mnemonic CHARGE syndrome, introduced in the premolecular era, stands for coloboma, heart defect, choanal atresia, retarded growth and development, genital hypoplasia, ear anomalies (including deafness). Following the identification of the genetic cause of CHD7 disorder, the phenotypic spectrum expanded to include cranial nerve anomalies, vestibular defects, cleft lip and/or palate, hypothyroidism, tracheoesophageal anomalies, brain anomalies, seizures, and renal anomalies. Life expectancy highly depends on the severity of manifestations; mortality can be high in the first few years when severe birth defects (particularly complex heart defects) are present and often complicated by airway and feeding issues. In childhood, adolescence, and adulthood, decreased life expectancy is likely related to a combination of residual heart defects, infections, aspiration or choking, respiratory issues including obstructive and central apnea, and possibly seizures. Despite these complications, the life expectancy for many individuals can be normal.
Neonatal pseudo-hydrocephalic progeroid syndrome
MedGen UID:
140806
Concept ID:
C0406586
Disease or Syndrome
Wiedemann-Rautenstrauch syndrome (WDRTS) is a rare autosomal recessive neonatal progeroid disorder characterized by intrauterine growth retardation, failure to thrive, short stature, a progeroid appearance, hypotonia, and variable mental impairment (summary by Toriello, 1990). Average survival in WDRTS is 7 months, although survival into the third decade of life has been reported (Akawi et al., 2013).
Cardiac malformation, cleft lip/palate, microcephaly, and digital anomalies
MedGen UID:
318752
Concept ID:
C1832950
Disease or Syndrome
Microgastria-limb reduction defect syndrome
MedGen UID:
322532
Concept ID:
C1834929
Disease or Syndrome
A rare multiple congenital anomalies syndrome characterized by congenital microgastria and a uni- or bilateral limb reduction defect, that can include absent or hypoplastic thumbs, radius, ulna and/or amelia. Association with other variable abnormalities, including intestinal malrotation, asplenia, dysplastic kidneys, hypoplastic lungs, dysplastic corpus collosum, and abnormal genitalia, has been reported.
Permanent neonatal diabetes mellitus-pancreatic and cerebellar agenesis syndrome
MedGen UID:
332288
Concept ID:
C1836780
Disease or Syndrome
Permanent neonatal diabetes mellitus-pancreatic and cerebellar agenesis syndrome is characterized by neonatal diabetes mellitus associated with cerebellar and/or pancreatic agenesis.
Frank-Ter Haar syndrome
MedGen UID:
383652
Concept ID:
C1855305
Disease or Syndrome
The primary characteristics of the Frank-ter Haar syndrome are brachycephaly, wide fontanels, prominent forehead, hypertelorism, prominent eyes, macrocornea with or without glaucoma, full cheeks, small chin, bowing of the long bones, and flexion deformity of the fingers. Protruding, simple ears and prominent coccyx are also regarded as important diagnostic signs (summary by Maas et al., 2004). Borrone syndrome was described as a severe progressive multisystem disorder with features overlapping those of FTHS, including thick skin, acne conglobata, osteolysis, gingival hypertrophy, brachydactyly, camptodactyly, and mitral valve prolapse. Although it was initially thought to be a distinct phenotype, mutations in the FTHS-associated gene SH3PXD2B have been identified in patients diagnosed with Borrone syndrome. The earlier differential description was attributed to phenotypic variability as well as to differences in the ages at which patients were examined (Wilson et al., 2014).
Dohle bodies and leukemia
MedGen UID:
346548
Concept ID:
C1857225
Neoplastic Process
Cardiac septal defects with coarctation of the aorta
MedGen UID:
347855
Concept ID:
C1859331
Disease or Syndrome
Atrial septal defect 1
MedGen UID:
349495
Concept ID:
C1862389
Congenital Abnormality
Secundum atrial septal defect (ASD) is a common congenital heart malformation that occurs as an isolated anomaly in 10% of individuals with congenital heart disease. Uncorrected ASD can cause pulmonary overcirculation, right heart volume overload, and premature death (summary by Benson et al., 1998). Genetic Heterogeneity of Atrial Septal Defect The ASD1 locus has been mapped to chromosome 5p. Other forms of atrial septal defect that are associated with other congenital heart disease but no conduction defects or noncardiac abnormalities include ASD2 (607941), caused by mutation in the GATA4 gene (600576), and ASD4 (611363), caused by mutation in the TBX20 gene (606061). ASD3 (614089) and ASD5 (612794), in which atrial septal defect is not associated with other cardiac abnormalities, are caused by mutation in the MYH6 (160710) and ACTC1 (102540) genes, respectively. ASD6 (613087), in which atrial septal defect may be associated with aneurysm of the interatrial septum and cardiac arrhythmias, is caused by mutation in the TLL1 gene (606742). ASD7 (108900), in which ASD is often associated with atrioventricular conduction defects, is caused by mutation in the NKX2-5 gene (600584). ASD8 (614433), in which ASD may be associated with other cardiac anomalies, is caused by mutation in the CITED2 gene (602937). ASD9 (614475) is caused by mutation in the GATA6 gene (601656). Somatic mutations in the HAND1 gene (602406) have been identified in tissue samples from patients with ASDs.
Pulmonic stenosis, atrial septal defect, and unique electrocardiographic abnormalities
MedGen UID:
357274
Concept ID:
C1867407
Disease or Syndrome
Diamond-Blackfan anemia 7
MedGen UID:
436451
Concept ID:
C2675512
Disease or Syndrome
Diamond-Blackfan anemia (DBA) is characterized by a profound normochromic and usually macrocytic anemia with normal leukocytes and platelets, congenital malformations in up to 50%, and growth deficiency in 30% of affected individuals. The hematologic complications occur in 90% of affected individuals during the first year of life. The phenotypic spectrum ranges from a mild form (e.g., mild anemia or no anemia with only subtle erythroid abnormalities, physical malformations without anemia) to a severe form of fetal anemia resulting in nonimmune hydrops fetalis. DBA is associated with an increased risk for acute myelogenous leukemia (AML), myelodysplastic syndrome (MDS), and solid tumors including osteogenic sarcoma.
Autosomal recessive severe congenital neutropenia due to G6PC3 deficiency
MedGen UID:
414066
Concept ID:
C2751630
Disease or Syndrome
G6PC3 deficiency is characterized by severe congenital neutropenia which occurs in a phenotypic continuum that includes the following: Isolated severe congenital neutropenia (nonsyndromic). Classic G6PC3 deficiency (severe congenital neutropenia plus cardiovascular and/or urogenital abnormalities). Severe G6PC3 deficiency (classic G6PC3 deficiency plus involvement of non-myeloid hematopoietic cell lines, additional extra-hematologic features, and pulmonary hypertension; known as Dursun syndrome). Neutropenia usually presents with recurrent bacterial infections in the first few months of life. Intrauterine growth restriction (IUGR), failure to thrive (FTT), and poor postnatal growth are common. Other findings in classic and severe G6PC3 deficiency can include inflammatory bowel disease (IBD) resembling Crohn's disease, and endocrine disorders (growth hormone deficiency, hypogonadotropic hypogonadism, and delayed puberty).
Neurofibromatosis-Noonan syndrome
MedGen UID:
419089
Concept ID:
C2931482
Disease or Syndrome
A variant of neurofibromatosis type 1 characterized by the combination of features of neurofibromatosis type 1, such as café-au-lait spots, iris Lisch nodules, axillary and inguinal freckling, optic nerve glioma and multiple neurofibromas; and Noonan syndrome, with features such as short stature, typical facial features, congenital heart defects and unusual pectus deformity.
Lung fibrosis-immunodeficiency-46,XX gonadal dysgenesis syndrome
MedGen UID:
461506
Concept ID:
C3150156
Disease or Syndrome
Lung fibrosis-immunodeficiency-46,XX gonadal dysgenesis syndrome is characterised by immune deficiency, gonadal dysgenesis and fatal lung fibrosis. So far, it has been described in two sisters born to consanguineous parents. Both karyotypes were normal female (46,XX). No genetic anomalies could be identified by comparative genome hybridization analysis of their genomes or by analysis of genes known to be associated with these types of anomalies.
Congenital heart defects, multiple types, 6
MedGen UID:
462571
Concept ID:
C3151221
Congenital Abnormality
Multiple types of congenital heart defects are associated with mutation in the GDF1 gene, including tetralogy of fallot (TOF), transposition of the great arteries (TGA), double-outlet right ventricle (DORV), total anomalous pulmonary venous return (TAPVR), pulmonary stenosis or atresia, atrioventricular canal, ventricular septal defect (VSD), and hypoplastic left or right ventricle (Jin et al., 2017). For a discussion of genetic heterogeneity of multiple types of congenital heart defects, see 306955.
Ogden syndrome
MedGen UID:
477078
Concept ID:
C3275447
Disease or Syndrome
Ogden syndrome (OGDNS) is an X-linked neurodevelopmental disorder characterized by postnatal growth failure, severely delayed psychomotor development, variable dysmorphic features, and hypotonia. Many patients also have cardiac malformations or arrhythmias (summary by Popp et al., 2015).
Atrial septal defect 7
MedGen UID:
477726
Concept ID:
C3276096
Disease or Syndrome
An extremely rare genetic congenital heart disease characterized by the presence of atrial septal defect, mostly of the ostium secundum type, associated with conduction anomalies like atrioventricular block, atrial fibrillation or right bundle branch block.
Atrial septal defect 3
MedGen UID:
481420
Concept ID:
C3279790
Disease or Syndrome
Any atrial heart septal defect in which the cause of the disease is a mutation in the MYH6 gene.
Atrial septal defect 9
MedGen UID:
482573
Concept ID:
C3280943
Disease or Syndrome
Any atrial heart septal defect in which the cause of the disease is a mutation in the GATA6 gene.
Intellectual disability, autosomal recessive 42
MedGen UID:
862780
Concept ID:
C4014343
Disease or Syndrome
Neurodevelopmental disorder with dysmorphic features, spasticity, and brain abnormalities (NEDDSBA) is an autosomal recessive neurodevelopmental disorder characterized by severely delayed global development, with hypotonia, impaired intellectual development, and poor or absent speech. Most patients have spasticity with limb hypertonia and brisk tendon reflexes. Additional features include nonspecific dysmorphic facial features, structural brain abnormalities, and cortical visual impairment (summary by Bosch et al., 2015). Novarino et al. (2014) labeled the disorder 'spastic paraplegia-67' (SPG67). The disorder is caused by a defect in glycosylphosphatidylinositol (GPI) biosynthesis. For a discussion of genetic heterogeneity of GPI biosynthesis defects, see GPIBD1 (610293).
Spinal muscular atrophy with congenital bone fractures 1
MedGen UID:
896011
Concept ID:
C4225177
Disease or Syndrome
Spinal muscular atrophy with congenital bone fractures is an autosomal recessive severe neuromuscular disorder characterized by onset of severe hypotonia with fetal hypokinesia in utero. This results in congenital contractures, consistent with arthrogryposis multiplex congenita, and increased incidence of prenatal fracture of the long bones. Affected infants have difficulty breathing and feeding and often die in the first days or months of life (summary by Knierim et al., 2016). Genetic Heterogeneity of Spinal Muscular Atrophy With Congenital Bone Fractures See also SMABF2 (616867), caused by mutation in the ASCC1 gene (614215) on chromosome 10q22.
Autosomal dominant intellectual disability-craniofacial anomalies-cardiac defects syndrome
MedGen UID:
903767
Concept ID:
C4225396
Disease or Syndrome
Arboleda-Tham syndrome (ARTHS) is an autosomal dominant disorder with the core features of impaired intellectual development, speech delay, microcephaly, cardiac anomalies, and gastrointestinal complications (summary by Kennedy et al., 2019).
Pseudo-TORCH syndrome 2
MedGen UID:
1373355
Concept ID:
C4479376
Disease or Syndrome
Pseudo-TORCH syndrome-2 (PTORCH2) is an autosomal recessive multisystem disorder characterized by antenatal onset of intracranial hemorrhage, calcification, brain malformations, liver dysfunction, and often thrombocytopenia. Affected individuals tend to have respiratory insufficiency and seizures, and die in infancy. The phenotype resembles the sequelae of intrauterine infection, but there is no evidence of an infectious agent. The disorder results from inappropriate activation of the interferon (IFN) immunologic pathway (summary by Meuwissen et al., 2016). For a discussion of genetic heterogeneity of PTORCH, see PTORCH1 (251290).
Adenosine kinase deficiency
MedGen UID:
1632232
Concept ID:
C4706555
Disease or Syndrome
Hypermethioninemia due to adenosine kinase deficiency is an autosomal recessive inborn error of metabolism characterized by global developmental delay, early-onset seizures, mild dysmorphic features, and characteristic biochemical anomalies, including persistent hypermethioninemia with increased levels of S-adenosylmethionine (AdoMet) and S-adenosylhomocysteine (AdoHcy); homocysteine is typically normal (summary by Bjursell et al., 2011).
Intellectual disability, autosomal recessive 65
MedGen UID:
1648401
Concept ID:
C4748219
Mental or Behavioral Dysfunction
Intellectual developmental disorder, autosomal recessive 72
MedGen UID:
1684805
Concept ID:
C5231452
Disease or Syndrome
46,xx sex reversal 5
MedGen UID:
1713956
Concept ID:
C5394441
Disease or Syndrome
SRXX5 is characterized by genital virilization in 46,XX individuals, associated with congenital heart disease and variable somatic anomalies including blepharophimosis-ptosis-epicanthus inversus syndrome (BPES) and congenital diaphragmatic hernia (Bashamboo et al., 2018).
Neurodevelopmental disorder with cardiomyopathy, spasticity, and brain abnormalities
MedGen UID:
1750805
Concept ID:
C5436848
Disease or Syndrome
Neurodevelopmental disorder with cardiomyopathy, spasticity, and brain abnormalities (NEDCASB) is an autosomal recessive multisystemic disorder characterized by global neurodevelopmental delay, severely impaired intellectual development, poor overall growth, and spasticity of the lower limbs resulting in gait difficulties. Most affected individuals also develop progressive hypertrophic cardiomyopathy in childhood or have cardiac developmental anomalies. Additional more variable features include dysmorphic facies and axonal sensory peripheral neuropathy. Brain imaging tends to show thin corpus callosum and polymicrogyria (summary by Garcia-Cazorla et al., 2020).
Biliary, renal, neurologic, and skeletal syndrome
MedGen UID:
1794200
Concept ID:
C5561990
Disease or Syndrome
Biliary, renal, neurologic, and skeletal syndrome (BRENS) is an autosomal recessive complex ciliopathy with multisystemic manifestations. The most common presentation is severe neonatal cholestasis that progresses to liver fibrosis and cirrhosis. Most patients have additional clinical features suggestive of a ciliopathy, including postaxial polydactyly, hydrocephalus, retinal abnormalities, and situs inversus. Additional features of the syndrome may include congenital cardiac defects, echogenic kidneys with renal failure, ocular abnormalities, joint hyperextensibility, and dysmorphic facial features. Some patients have global developmental delay. Brain imaging typically shows dilated ventricles, hypomyelination, and white matter abnormalities, although some patients have been described with abnormal pituitary development (summary by Shaheen et al., 2020 and David et al., 2020).
Tessadori-van Haaften neurodevelopmental syndrome 1
MedGen UID:
1810348
Concept ID:
C5676922
Disease or Syndrome
Tessadori-Bicknell-van Haaften neurodevelopmental syndrome-1 (TEBIVANED1) is characterized by poor overall growth with short stature, microcephaly, hypotonia, profound global developmental delay often with poor or absent speech, and characteristic dysmorphic facial features, including hypertelorism and abnormal nose. Other variable neurologic and systemic features may also occur (Tessadori et al., 2017). Genetic Heterogeneity of Tessadori-van Haaften Neurodevelopmental Syndrome See also TEBIVANED2 (619759), caused by mutation in the H4C11 gene (602826); TEBIVANED3 (619950), caused by mutation in the H4C5 gene (602830); and TEBIVANED4 (619951), caused by mutation in the H4C9 gene (602833).
Pontocerebellar hypoplasia, IIA 17
MedGen UID:
1809583
Concept ID:
C5676999
Disease or Syndrome
Pontocerebellar hypoplasia type 17 (PCH17) is a severe autosomal recessive developmental disorder characterized by neonatal hypotonia, severe feeding difficulties, and respiratory insufficiency. Brain imaging shows cerebellar and brainstem hypoplasia. Most affected individuals die in infancy. Those who survive show variable developmental delay. Other features of the disorder include distal hypertonia, poor overall growth, visual defects, autonomic problems, dysmorphic features, and seizures (Coolen et al., 2022). For a phenotypic description and a discussion of genetic heterogeneity of PCH, see PCH1A (607596).
Intellectual developmental disorder, autosomal dominant 66
MedGen UID:
1812470
Concept ID:
C5677000
Mental or Behavioral Dysfunction
Autosomal dominant intellectual developmental disorder-66 (MRD66) is characterized by global developmental delay with mildly to moderately impaired intellectual development and mild speech delay. The phenotype and severity are highly variable. Some patients have behavioral problems or autism spectrum disorder, and about 50% have variable types of seizures. Additional features may include nonspecific dysmorphic facial features, tall or short stature, and mild skeletal anomalies (Rahimi et al., 2022).
Tessadori-Van Haaften neurodevelopmental syndrome 4
MedGen UID:
1804234
Concept ID:
C5677016
Disease or Syndrome
Tessadori-Bicknell-van Haaften neurodevelopmental syndrome-4 (TEBIVANED4) is characterized by global developmental delay with poor overall growth, variably impaired intellectual development, learning difficulties, distal skeletal anomalies, and dysmorphic facies. Some patients have visual or hearing deficits. The severity and manifestations of the disorder are highly variable (Tessadori et al., 2022). For a discussion of genetic heterogeneity of TEBIVANED, see TEBIVANED1 (619758).

Recent clinical studies

Etiology

Abdulwahab H, Husain MR, Khalid KA
J Interv Cardiol 2022;2022:2764296. Epub 2022 Apr 4 doi: 10.1155/2022/2764296. PMID: 35463208Free PMC Article
Hong H, Wu L, Shang XK, Su W, Dong NG
Curr Med Sci 2021 Dec;41(6):1225-1230. Epub 2021 Nov 28 doi: 10.1007/s11596-021-2466-3. PMID: 34839434
Dolgner SJ, Steinberg ZL, Jones TK, Reisman M, Buber J
Heart 2021 Dec;107(23):1875-1880. Epub 2021 Aug 11 doi: 10.1136/heartjnl-2021-319050. PMID: 34380660
O'Neill L, Floyd CN, Sim I, Whitaker J, Mukherjee R, O'Hare D, Gatzoulis M, Frigiola A, O'Neill MD, Williams SE
Int J Cardiol 2020 Dec 15;321:104-112. Epub 2020 Jul 15 doi: 10.1016/j.ijcard.2020.07.014. PMID: 32679141
de Beco G, Mambour N, Vô C, Vanhoutte L, Moniotte S, Poncelet A, Sluysmans T
Pediatr Cardiol 2018 Oct;39(7):1440-1444. Epub 2018 May 22 doi: 10.1007/s00246-018-1914-8. PMID: 29789918

Diagnosis

Dolgner SJ, Steinberg ZL, Jones TK, Reisman M, Buber J
Heart 2021 Dec;107(23):1875-1880. Epub 2021 Aug 11 doi: 10.1136/heartjnl-2021-319050. PMID: 34380660
O'Neill L, Floyd CN, Sim I, Whitaker J, Mukherjee R, O'Hare D, Gatzoulis M, Frigiola A, O'Neill MD, Williams SE
Int J Cardiol 2020 Dec 15;321:104-112. Epub 2020 Jul 15 doi: 10.1016/j.ijcard.2020.07.014. PMID: 32679141
Ordoñez MV, Moharem-Elgamal S, Bedair R
Cardiol Young 2019 Sep;29(9):1202-1205. Epub 2019 Aug 5 doi: 10.1017/S1047951119001677. PMID: 31379319
Asada D, Tomita H, Fujii T
Cardiol Young 2018 Oct;28(10):1162-1164. Epub 2018 Jul 11 doi: 10.1017/S1047951118000896. PMID: 29991370
Shen L, Liu J, Li JK, Xu M, Yuan L, Zhang GQ, Wang JY, Huang YJ
Pediatr Cardiol 2018 Jun;39(5):1031-1035. Epub 2018 Mar 22 doi: 10.1007/s00246-018-1857-0. PMID: 29564520

Therapy

Bashir F, Hameed M, Hanif B, Aijaz S
J Pak Med Assoc 2022 Feb;72(2):385-389. doi: 10.47391/JPMA.106. PMID: 35320204
Dolgner SJ, Steinberg ZL, Jones TK, Reisman M, Buber J
Heart 2021 Dec;107(23):1875-1880. Epub 2021 Aug 11 doi: 10.1136/heartjnl-2021-319050. PMID: 34380660
Celik M, Yilmaz Y, Kup A, Karagoz A, Kahyaoglu M, Cakmak EO, Celik FB, Sengor BG, Guner A, Izci S, Kilicgedik A, Candan O, Kahveci G, Gecmen C, Kaymaz C
J Electrocardiol 2021 Jul-Aug;67:158-165. Epub 2021 Jul 3 doi: 10.1016/j.jelectrocard.2021.06.010. PMID: 34246066
Yan C, Li S, Song H, Jin J, Zheng H, Wang C, Zhao S
J Thorac Cardiovasc Surg 2019 Apr;157(4):1603-1608. Epub 2018 Dec 12 doi: 10.1016/j.jtcvs.2018.11.093. PMID: 30712912
de Beco G, Mambour N, Vô C, Vanhoutte L, Moniotte S, Poncelet A, Sluysmans T
Pediatr Cardiol 2018 Oct;39(7):1440-1444. Epub 2018 May 22 doi: 10.1007/s00246-018-1914-8. PMID: 29789918

Prognosis

Bashir F, Hameed M, Hanif B, Aijaz S
J Pak Med Assoc 2022 Feb;72(2):385-389. doi: 10.47391/JPMA.106. PMID: 35320204
Dolgner SJ, Steinberg ZL, Jones TK, Reisman M, Buber J
Heart 2021 Dec;107(23):1875-1880. Epub 2021 Aug 11 doi: 10.1136/heartjnl-2021-319050. PMID: 34380660
Zieliński P, Kowalski M, Kuśmierczyk M, Hoffman P, Michałowska I
J Card Surg 2020 Nov;35(11):3153-3154. Epub 2020 Sep 16 doi: 10.1111/jocs.14990. PMID: 32939864
Murphy CE, Kenny CM, Wulfestieg TS, Fentanes E, Murphy CE
J Cardiovasc Comput Tomogr 2020 Nov - Dec;14(6):e165-e166. Epub 2020 Apr 21 doi: 10.1016/j.jcct.2020.03.006. PMID: 32446844
de Beco G, Mambour N, Vô C, Vanhoutte L, Moniotte S, Poncelet A, Sluysmans T
Pediatr Cardiol 2018 Oct;39(7):1440-1444. Epub 2018 May 22 doi: 10.1007/s00246-018-1914-8. PMID: 29789918

Clinical prediction guides

Bashir F, Hameed M, Hanif B, Aijaz S
J Pak Med Assoc 2022 Feb;72(2):385-389. doi: 10.47391/JPMA.106. PMID: 35320204
S A, N S, G RS, Majella J CM
J Assoc Physicians India 2022 Jan;70(1):11-12. PMID: 35062807
Dolgner SJ, Steinberg ZL, Jones TK, Reisman M, Buber J
Heart 2021 Dec;107(23):1875-1880. Epub 2021 Aug 11 doi: 10.1136/heartjnl-2021-319050. PMID: 34380660
Murphy CE, Kenny CM, Wulfestieg TS, Fentanes E, Murphy CE
J Cardiovasc Comput Tomogr 2020 Nov - Dec;14(6):e165-e166. Epub 2020 Apr 21 doi: 10.1016/j.jcct.2020.03.006. PMID: 32446844
Shen L, Liu J, Li JK, Xu M, Yuan L, Zhang GQ, Wang JY, Huang YJ
Pediatr Cardiol 2018 Jun;39(5):1031-1035. Epub 2018 Mar 22 doi: 10.1007/s00246-018-1857-0. PMID: 29564520

Recent systematic reviews

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