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Left ventricular hypertrophy

MedGen UID:
57442
Concept ID:
C0149721
Disease or Syndrome
Synonyms: Heart left ventricle hypertrophy; Left ventricular wall hypertrophy
SNOMED CT: LV hypertrophy (55827005); LV+ - Left ventricular hypertrophy (55827005); LVH - Left ventricular hypertrophy (55827005); Left ventricular hypertrophy (55827005)
 
HPO: HP:0001712

Definition

Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality. [from MeSH]

Conditions with this feature

Fabry disease
MedGen UID:
8083
Concept ID:
C0002986
Disease or Syndrome
Fabry disease results from deficient activity of the enzyme alpha-galactosidase A (a-Gal A) and progressive lysosomal deposition of globotriaosylceramide (GL-3) in cells throughout the body. The classic form, occurring in males with less than 1% a-Gal A enzyme activity, usually has its onset in childhood or adolescence with periodic crises of severe pain in the extremities (acroparesthesia), the appearance of vascular cutaneous lesions (angiokeratomas), sweating abnormalities (anhidrosis, hypohidrosis, and rarely hyperhidrosis), characteristic corneal and lenticular opacities, and proteinuria. Gradual deterioration of renal function to end-stage renal disease (ESRD) usually occurs in men in the third to fifth decade. In middle age, most males successfully treated for ESRD develop cardiac and/or cerebrovascular disease, a major cause of morbidity and mortality. Heterozygous females typically have milder symptoms at a later age of onset than males. Rarely, they may be relatively asymptomatic throughout a normal life span or may have symptoms as severe as those observed in males with the classic phenotype. In contrast, males with greater than 1% a-Gal A activity may have: (1) a cardiac variant phenotype that usually presents in the sixth to eighth decade with left ventricular hypertrophy, cardiomyopathy and arrhythmia, and proteinuria, but without ESRD; or (2) a renal variant phenotype, associated with ESRD but without the skin lesions or pain; or (3) cerebrovascular disease presenting as stroke or transient ischemic attack.
Tangier disease
MedGen UID:
52644
Concept ID:
C0039292
Disease or Syndrome
Tangier disease is an autosomal recessive disorder characterized by markedly reduced levels of plasma high density lipoproteins (HDL) resulting in tissue accumulation of cholesterol esters. Clinical features include very large, yellow-orange tonsils, enlarged liver, spleen and lymph nodes, hypocholesterolemia, and abnormal chylomicron remnants (Brooks-Wilson et al., 1999).
Juvenile myopathy, encephalopathy, lactic acidosis AND stroke
MedGen UID:
56485
Concept ID:
C0162671
Disease or Syndrome
MELAS syndrome, comprising mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes, is a genetically heterogeneous mitochondrial disorder with a variable clinical phenotype. The disorder is accompanied by features of central nervous system involvement, including seizures, hemiparesis, hemianopsia, cortical blindness, and episodic vomiting (Pavlakis et al., 1984; Montagna et al., 1988). Other mitochondrial encephalomyopathies include Leigh syndrome (LS; 256000), Kearns-Sayre syndrome (KSS; 530000), MERRF syndrome (545000), and Leber optic atrophy (535000).
Somatotroph adenoma
MedGen UID:
91097
Concept ID:
C0346302
Neoplastic Process
AIP-related isolated familial pituitary adenoma (AIP-related FIPA) is defined as the presence of an AIP germline pathogenic variant in an individual with a pituitary adenoma (regardless of family history). The most commonly occurring pituitary adenomas in this disorder are growth hormone-secreting adenomas (somatotropinoma), followed by prolactin-secreting adenomas (prolactinoma), growth hormone and prolactin co-secreting adenomas (somatomammotropinoma), and non-functioning pituitary adenomas (NFPA). Rarely TSH- or ACTH-secreting adenomas (thyrotropinoma and corticotropinoma) are observed. Clinical findings result from excess hormone secretion, lack of hormone secretion, and/or mass effects (e.g., headaches, visual field loss). Within the same family, pituitary adenomas can be of the same or different type. Age of onset in AIP-related FIPA is around 20-24 years (age range: 6-66 years).
Osteopathia striata with cranial sclerosis
MedGen UID:
96590
Concept ID:
C0432268
Disease or Syndrome
Osteopathia striata with cranial sclerosis is an X-linked dominant sclerosing bone dysplasia that presents in females with macrocephaly, cleft palate, mild learning disabilities, sclerosis of the long bones and skull, and longitudinal striations visible on radiographs of the long bones, pelvis, and scapulae (Jenkins et al., 2009). In males, the disorder is usually associated with fetal or neonatal lethality. Occasional surviving males have, in addition to hyperostosis, cardiac, intestinal, and genitourinary malformations. Osteosclerosis in the cranial and facial bones leads to disfigurement and to disability due to pressure on cranial nerves, e.g., deafness. Osteopathia striata is a frequent feature of focal dermal hypoplasia (FDH; 305600). Although early reports of familial cases of this disorder appeared to suggest autosomal dominant inheritance (see, e.g., Horan and Beighton, 1978 and Konig et al., 1996), reappraisal of the literature (Behninger and Rott, 2000; Rott et al., 2003) and the finding of a molecular basis for the disorder by Jenkins et al. (2009) confirms that the inheritance pattern is X-linked dominant. Affected males who survive have a more severe phenotype than affected females, and sporadic male cases may result from somatic mosaicism (Behninger and Rott, 2000).
Bardet-Biedl syndrome
MedGen UID:
156019
Concept ID:
C0752166
Disease or Syndrome
Bardet-Biedl syndrome (BBS) is characterized by rod-cone dystrophy, truncal obesity, postaxial polydactyly, cognitive impairment, male hypogonadotropic hypogonadism, complex female genitourinary malformations, and renal abnormalities. The visual prognosis for children with BBS is poor. Night blindness is usually evident by age seven to eight years; the mean age of legal blindness is 15.5 years. Birth weight is usually normal, but significant weight gain begins within the first year and becomes a lifelong issue for most individuals. A majority of individuals have significant learning difficulties; a minority have severe impairment on IQ testing. Renal disease is a major cause of morbidity and mortality.
Vici syndrome
MedGen UID:
340962
Concept ID:
C1855772
Disease or Syndrome
Vici syndrome is a rare congenital multisystem disorder characterized by agenesis of the corpus callosum (ACC), cataracts, pigmentary defects, progressive cardiomyopathy, and variable immunodeficiency. Affected individuals also have profound psychomotor retardation and hypotonia due to a myopathy (summary by Finocchi et al., 2012).
Left ventricular noncompaction 1
MedGen UID:
349005
Concept ID:
C1858725
Disease or Syndrome
Left ventricular noncompaction (LVNC) is characterized by numerous prominent trabeculations and deep intertrabecular recesses in hypertrophied and hypokinetic segments of the left ventricle (Sasse-Klaassen et al., 2004). The mechanistic basis is thought to be an intrauterine arrest of myocardial development with lack of compaction of the loose myocardial meshwork. LVNC may occur in isolation or in association with congenital heart disease. Distinctive morphologic features can be recognized on 2-dimensional echocardiography (Kurosaki et al., 1999). Noncompaction of the ventricular myocardium is sometimes referred to as spongy myocardium. Stollberger et al. (2002) commented that the term 'isolated LVNC,' meaning LVNC without coexisting cardiac abnormalities, is misleading, because additional cardiac abnormalities are found in nearly all patients with LVNC. Genetic Heterogeneity of Left Ventricular Noncompaction A locus for autosomal dominant left ventricular noncompaction has been identified on chromosome 11p15 (LVNC2; 609470). LVNC3 (see 605906) is caused by mutation in the LDB3 gene (605906) on chromosome 10q23. LVNC4 (see 613424) is caused by mutation in the ACTC1 gene (102540) on chromosome 15q14. LVNC5 (see 613426) is caused by mutation in the MYH7 gene (160760) on chromosome 14q12. LVNC6 (see 601494) is caused by mutation in the TNNT2 gene (191045) on chromosome 1q32. LVNC7 (615092) is caused by mutation in the MIB1 gene (608677) on chromosome 18q11. LVNC8 (615373) is caused by mutation in the PRDM16 gene (605557) on chromosome 1p36. LVNC9 (see 611878) is caused by mutation in the TPM1 gene (191010) on chromosome 15q22. LVNC10 (615396) is caused by mutation in the MYBPC3 gene (600958) on chromosome 11p11. LVNC can also occur as part of an X-linked disorder, Barth syndrome (302060), caused by mutation in the TAZ gene (300394) on chromosome Xq28.
Glycogen storage disease 0, muscle
MedGen UID:
409741
Concept ID:
C1969054
Disease or Syndrome
Glycogen storage disease type 0 (also known as GSD 0) is a condition caused by the body's inability to form a complex sugar called glycogen, which is a major source of stored energy in the body. GSD 0 has two types: in muscle GSD 0, glycogen formation in the muscles is impaired, and in liver GSD 0, glycogen formation in the liver is impaired.The signs and symptoms of muscle GSD 0 typically begin in early childhood. Affected individuals often experience muscle pain and weakness or episodes of fainting (syncope) following moderate physical activity, such as walking up stairs. The loss of consciousness that occurs with fainting typically lasts up to several hours. Some individuals with muscle GSD 0 have a disruption of the heart's normal rhythm (arrhythmia) known as long QT syndrome. In all affected individuals, muscle GSD 0 impairs the heart's ability to effectively pump blood and increases the risk of cardiac arrest and sudden death, particularly after physical activity. Sudden death from cardiac arrest can occur in childhood or adolescence in people with muscle GSD 0.Individuals with liver GSD 0 usually show signs and symptoms of the disorder in infancy. People with this disorder develop low blood sugar (hypoglycemia) after going long periods of time without food (fasting). Signs of hypoglycemia become apparent when affected infants begin sleeping through the night and stop late-night feedings; these infants exhibit extreme tiredness (lethargy), pale skin (pallor), and nausea. During episodes of fasting, ketone levels in the blood may increase (ketosis). Ketones are molecules produced during the breakdown of fats, which occurs when stored sugars (such as glycogen) are unavailable. These short-term signs and symptoms of liver GSD 0 often improve when food is eaten and sugar levels in the body return to normal. The features of liver GSD 0 vary; they can be mild and go unnoticed for years, or they can include developmental delay and growth failure.
Congenital muscular dystrophy-dystroglycanopathy with brain and eye anomalies type A5
MedGen UID:
461763
Concept ID:
C3150413
Disease or Syndrome
Congenital muscular dystrophy-dystroglycanopathy with brain and eye anomalies (type A), which includes both the more severe Walker-Warburg syndrome (WWS) and the slightly less severe muscle-eye-brain disease (MEB), is an autosomal recessive disorder with characteristic brain and eye malformations, profound mental retardation, congenital muscular dystrophy, and death usually in the first years of life. It represents the most severe end of a phenotypic spectrum of similar disorders resulting from defective glycosylation of DAG1 (128239), collectively known as 'dystroglycanopathies' (Beltran-Valero de Bernabe et al., 2004). For a general phenotypic description and a discussion of genetic heterogeneity of muscular dystrophy-dystroglycanopathy type A, see MDDGA1 (236670).
Loeys-Dietz syndrome 3
MedGen UID:
462437
Concept ID:
C3151087
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.
Familial hypertrophic cardiomyopathy 16
MedGen UID:
462554
Concept ID:
C3151204
Disease or Syndrome
Hypertrophic cardiomyopathy (HCM) is typically defined by the presence of unexplained left ventricular hypertrophy (LVH). Such LVH occurs in a non-dilated ventricle in the absence of other cardiac or systemic disease capable of producing the observed magnitude of increased LV wall thickness, such as pressure overload (e.g., long-standing hypertension, aortic stenosis) or storage/infiltrative disorders (e.g., Fabry disease, amyloidosis). The clinical manifestations of HCM range from asymptomatic LVH to progressive heart failure to sudden cardiac death (SCD), and vary from individual to individual even within the same family. Common symptoms include shortness of breath (particularly with exertion), chest pain, palpitations, orthostasis, presyncope, and syncope. Most often the LVH of HCM becomes apparent during adolescence or young adulthood, although it may also develop late in life, in infancy, or in childhood.
Familial hypertrophic cardiomyopathy 17
MedGen UID:
462614
Concept ID:
C3151264
Disease or Syndrome
Familial hypertrophic cardiomyopathy 18
MedGen UID:
462615
Concept ID:
C3151265
Disease or Syndrome
Hypertrophic cardiomyopathy (HCM) is typically defined by the presence of unexplained left ventricular hypertrophy (LVH). Such LVH occurs in a non-dilated ventricle in the absence of other cardiac or systemic disease capable of producing the observed magnitude of increased LV wall thickness, such as pressure overload (e.g., long-standing hypertension, aortic stenosis) or storage/infiltrative disorders (e.g., Fabry disease, amyloidosis). The clinical manifestations of HCM range from asymptomatic LVH to progressive heart failure to sudden cardiac death (SCD), and vary from individual to individual even within the same family. Common symptoms include shortness of breath (particularly with exertion), chest pain, palpitations, orthostasis, presyncope, and syncope. Most often the LVH of HCM becomes apparent during adolescence or young adulthood, although it may also develop late in life, in infancy, or in childhood.
Familial hypertrophic cardiomyopathy 20
MedGen UID:
462617
Concept ID:
C3151267
Disease or Syndrome
Hypertrophic cardiomyopathy (HCM) is typically defined by the presence of unexplained left ventricular hypertrophy (LVH). Such LVH occurs in a non-dilated ventricle in the absence of other cardiac or systemic disease capable of producing the observed magnitude of increased LV wall thickness, such as pressure overload (e.g., long-standing hypertension, aortic stenosis) or storage/infiltrative disorders (e.g., Fabry disease, amyloidosis). The clinical manifestations of HCM range from asymptomatic LVH to progressive heart failure to sudden cardiac death (SCD), and vary from individual to individual even within the same family. Common symptoms include shortness of breath (particularly with exertion), chest pain, palpitations, orthostasis, presyncope, and syncope. Most often the LVH of HCM becomes apparent during adolescence or young adulthood, although it may also develop late in life, in infancy, or in childhood.
Coenzyme Q10 deficiency, primary, 5
MedGen UID:
766288
Concept ID:
C3553374
Disease or Syndrome
Primary coenzyme Q10 (CoQ10) deficiency is usually associated with multisystem involvement, including neurologic manifestations such as fatal neonatal encephalopathy with hypotonia; a late-onset slowly progressive multiple-system atrophy-like phenotype (neurodegeneration with autonomic failure and various combinations of parkinsonism and cerebellar ataxia, and pyramidal dysfunction); and dystonia, spasticity, seizures, and intellectual disability. Steroid-resistant nephrotic syndrome (SRNS), the hallmark renal manifestation, is often the initial manifestation either as isolated renal involvement that progresses to end-stage renal disease (ESRD), or associated with encephalopathy (seizures, stroke-like episodes, severe neurologic impairment) resulting in early death. Hypertrophic cardiomyopathy (HCM), retinopathy or optic atrophy, and sensorineural hearing loss can also be seen.
Familial hypertrophic cardiomyopathy 21
MedGen UID:
766356
Concept ID:
C3553442
Disease or Syndrome
Hypertrophic cardiomyopathy (CMH) is characterized by unexplained cardiac hypertrophy: thickening of the myocardial wall in the absence of any other identifiable cause for left ventricular hypertrophy such as systemic hypertension or valvular heart disease. Myocyte hypertrophy, disarray, and fibrosis are the histopathologic hallmarks of this disorder. Clinical features are diverse and include arrhythmias, sudden cardiac death, and heart failure. With an estimated prevalence of 1 in 500, CMH is the most common cardiovascular genetic disease and the most common cause of sudden death in competitive athletes in the United States (summary by Song et al., 2006). For a discussion of genetic heterogeneity of familial hypertrophic cardiomyopathy, see CMH1 (192600).
Primary aldosteronism, seizures, and neurologic abnormalities
MedGen UID:
815939
Concept ID:
C3809609
Disease or Syndrome

Recent clinical studies

Etiology

Brown AJM, Lang C, McCrimmon R, Struthers A
BMC Cardiovasc Disord 2017 Aug 23;17(1):229. doi: 10.1186/s12872-017-0663-6. PMID: 28835229Free PMC Article
Samesima N, Azevedo LF, De Matos LDNJ, Echenique LS, Negrao CE, Pastore CA
Clinics (Sao Paulo) 2017 Jun;72(6):343-350. doi: 10.6061/clinics/2017(06)03. PMID: 28658433Free PMC Article
Abdalla M, Caughey MC, Tanner RM, Booth JN 3rd, Diaz KM, Anstey DE, Sims M, Ravenell J, Muntner P, Viera AJ, Shimbo D
J Am Heart Assoc 2017 Apr 5;6(4) doi: 10.1161/JAHA.116.004847. PMID: 28381465Free PMC Article
Zhang N, Chen Y, Guo X, Sun G, Dai D, Sun Y
Heart Lung Circ 2017 Mar;26(3):251-257. Epub 2016 Aug 4 doi: 10.1016/j.hlc.2016.06.1212. PMID: 27555052
Hiremath P, Lawler PR, Ho JE, Correia AW, Abbasi SA, Kwong RY, Jerosch-Herold M, Ho CY, Cheng S
Circ Heart Fail 2016 Sep;9(9) doi: 10.1161/CIRCHEARTFAILURE.116.003026. PMID: 27623770Free PMC Article

Diagnosis

Brown AJM, Lang C, McCrimmon R, Struthers A
BMC Cardiovasc Disord 2017 Aug 23;17(1):229. doi: 10.1186/s12872-017-0663-6. PMID: 28835229Free PMC Article
Samesima N, Azevedo LF, De Matos LDNJ, Echenique LS, Negrao CE, Pastore CA
Clinics (Sao Paulo) 2017 Jun;72(6):343-350. doi: 10.6061/clinics/2017(06)03. PMID: 28658433Free PMC Article
Hiremath P, Lawler PR, Ho JE, Correia AW, Abbasi SA, Kwong RY, Jerosch-Herold M, Ho CY, Cheng S
Circ Heart Fail 2016 Sep;9(9) doi: 10.1161/CIRCHEARTFAILURE.116.003026. PMID: 27623770Free PMC Article
Zimarino M, Montebello E, Radico F, Gallina S, Perfetti M, Iachini Bellisarii F, Severi S, Limbruno U, Emdin M, De Caterina R
Eur J Prev Cardiol 2016 Oct;23(15):1632-9. Epub 2016 Jun 27 doi: 10.1177/2047487316655259. PMID: 27353130
Svehlikova J, Zelinka J, Bacharova L, Tysler M
J Electrocardiol 2016 Sep-Oct;49(5):755-62. Epub 2016 May 16 doi: 10.1016/j.jelectrocard.2016.05.007. PMID: 27241185

Therapy

Brown AJM, Lang C, McCrimmon R, Struthers A
BMC Cardiovasc Disord 2017 Aug 23;17(1):229. doi: 10.1186/s12872-017-0663-6. PMID: 28835229Free PMC Article
Nam D, Reineke EL
Methodist Debakey Cardiovasc J 2017 Jan-Mar;13(1):9-14. doi: 10.14797/mdcj-13-1-9. PMID: 28413576Free PMC Article
Abdalla M, Caughey MC, Tanner RM, Booth JN 3rd, Diaz KM, Anstey DE, Sims M, Ravenell J, Muntner P, Viera AJ, Shimbo D
J Am Heart Assoc 2017 Apr 5;6(4) doi: 10.1161/JAHA.116.004847. PMID: 28381465Free PMC Article
Zhang N, Chen Y, Guo X, Sun G, Dai D, Sun Y
Heart Lung Circ 2017 Mar;26(3):251-257. Epub 2016 Aug 4 doi: 10.1016/j.hlc.2016.06.1212. PMID: 27555052
Hassan K, Hassan F, Hassan D, Anwar S, Shadi H
Clin Exp Nephrol 2016 Oct;20(5):770-777. Epub 2015 Nov 22 doi: 10.1007/s10157-015-1198-8. PMID: 26593247

Prognosis

Samesima N, Azevedo LF, De Matos LDNJ, Echenique LS, Negrao CE, Pastore CA
Clinics (Sao Paulo) 2017 Jun;72(6):343-350. doi: 10.6061/clinics/2017(06)03. PMID: 28658433Free PMC Article
Zhang N, Chen Y, Guo X, Sun G, Dai D, Sun Y
Heart Lung Circ 2017 Mar;26(3):251-257. Epub 2016 Aug 4 doi: 10.1016/j.hlc.2016.06.1212. PMID: 27555052
Hiremath P, Lawler PR, Ho JE, Correia AW, Abbasi SA, Kwong RY, Jerosch-Herold M, Ho CY, Cheng S
Circ Heart Fail 2016 Sep;9(9) doi: 10.1161/CIRCHEARTFAILURE.116.003026. PMID: 27623770Free PMC Article
Zimarino M, Montebello E, Radico F, Gallina S, Perfetti M, Iachini Bellisarii F, Severi S, Limbruno U, Emdin M, De Caterina R
Eur J Prev Cardiol 2016 Oct;23(15):1632-9. Epub 2016 Jun 27 doi: 10.1177/2047487316655259. PMID: 27353130
Hassan K, Hassan F, Hassan D, Anwar S, Shadi H
Clin Exp Nephrol 2016 Oct;20(5):770-777. Epub 2015 Nov 22 doi: 10.1007/s10157-015-1198-8. PMID: 26593247

Clinical prediction guides

Brown AJM, Lang C, McCrimmon R, Struthers A
BMC Cardiovasc Disord 2017 Aug 23;17(1):229. doi: 10.1186/s12872-017-0663-6. PMID: 28835229Free PMC Article
Samesima N, Azevedo LF, De Matos LDNJ, Echenique LS, Negrao CE, Pastore CA
Clinics (Sao Paulo) 2017 Jun;72(6):343-350. doi: 10.6061/clinics/2017(06)03. PMID: 28658433Free PMC Article
Zhang N, Chen Y, Guo X, Sun G, Dai D, Sun Y
Heart Lung Circ 2017 Mar;26(3):251-257. Epub 2016 Aug 4 doi: 10.1016/j.hlc.2016.06.1212. PMID: 27555052
Hiremath P, Lawler PR, Ho JE, Correia AW, Abbasi SA, Kwong RY, Jerosch-Herold M, Ho CY, Cheng S
Circ Heart Fail 2016 Sep;9(9) doi: 10.1161/CIRCHEARTFAILURE.116.003026. PMID: 27623770Free PMC Article
Svehlikova J, Zelinka J, Bacharova L, Tysler M
J Electrocardiol 2016 Sep-Oct;49(5):755-62. Epub 2016 May 16 doi: 10.1016/j.jelectrocard.2016.05.007. PMID: 27241185

Recent systematic reviews

Cuspidi C, Dell'Oro R, Sala C, Tadic M, Gherbesi E, Grassi G, Mancia G
J Hypertens 2017 Dec;35(12):2339-2345. doi: 10.1097/HJH.0000000000001500. PMID: 28786861
D'Andrea A, Radmilovic J, Ballo P, Mele D, Agricola E, Cameli M, Rossi A, Esposito R, Novo G, Mondillo S, Montisci R, Gallina S, Bossone E, Galderisi M; Working Group on Echocardiography of the Italian Society of Cardiology.
Echocardiography 2017 May;34(5):746-759. Epub 2017 Mar 19 doi: 10.1111/echo.13506. PMID: 28317158
Smid BE, van der Tol L, Cecchi F, Elliott PM, Hughes DA, Linthorst GE, Timmermans J, Weidemann F, West ML, Biegstraaten M, Lekanne Deprez RH, Florquin S, Postema PG, Tomberli B, van der Wal AC, van den Bergh Weerman MA, Hollak CE
Int J Cardiol 2014 Dec 15;177(2):400-8. Epub 2014 Sep 20 doi: 10.1016/j.ijcard.2014.09.001. PMID: 25442977
Parry HM, Donnelly LA, Van Zuydam N, Doney AS, Elder DH, Morris AD, Struthers AD, Palmer CN, Lang CC; Wellcome Trust Case Control Consortium 2.
Cardiovasc Diabetol 2013 Jul 23;12:109. doi: 10.1186/1475-2840-12-109. PMID: 23879873Free PMC Article
Costanzo P, Savarese G, Rosano G, Musella F, Casaretti L, Vassallo E, Paolillo S, Marsico F, Rengo G, Leosco D, Perrone-Filardi P
Int J Cardiol 2013 Sep 10;167(6):2757-64. Epub 2012 Jul 13 doi: 10.1016/j.ijcard.2012.06.084. PMID: 22795718

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