Hypertrophic cardiomyopathy causes: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Hypertrophic cardiomyopathy}} | {{Hypertrophic cardiomyopathy}} | ||
{{CMG}} {{AE}} {{Ochuko}} | {{CMG}} {{AE}} {{Ochuko}} {{Soroush}} | ||
==Overview== | ==Overview== | ||
[[Hypertrophic cardiomyopathy]] is a condition that is most often passed down through families (inherited). It is thought to result from [[gene mutation]]s that control heart muscle growth. | [[Hypertrophic cardiomyopathy]] is a condition that is most often passed down through families (inherited). It is thought to result from [[gene mutation]]s that control heart muscle growth. Genes involved in the [[pathogenesis]] of [[hypertrophic cardiomyopathy]] include [[MYH7]], [[TNNT2]], [[TPM1]]. Nevertheless, a number of chronic medical conditions might be contributed to [[hypertrophic cardiomyopathy]] development, among them are thyroid disease, diabetes, and obesity, and hypertension. | ||
==Causes== | ==Causes== | ||
===Life Threatening Causes=== | ===Life Threatening Causes=== | ||
Life-threatening causes include conditions | Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated. | ||
===Common Causes=== | ===Common Causes=== | ||
| Line 14: | Line 14: | ||
*[[Gene mutation]] | *[[Gene mutation]] | ||
*[[Hypertension]] | *[[Hypertension]] | ||
*Thyroid disease | |||
*Diabetes | |||
*Obesity | |||
===Causes by Organ System=== | ===Causes by Organ System=== | ||
| Line 19: | Line 22: | ||
{|style="width:80%; height:100px" border="1" | {|style="width:80%; height:100px" border="1" | ||
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular''' | |style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular''' | ||
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | | |style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Atrial myxoma]], [[cardiofaciocutaneous syndrome]], [[congenital generalized lipodystrophy|congenital generalized lipodystrophy type 2]], [[Costello syndrome]], [[hypertension]], [[hypertrichotic osteochondrodysplasia]], [[hypertrophic obstructive cardiomyopathy]], [[Noonan syndrome]], subendocardial ischemia, [[very long-chain acyl-CoA dehydrogenase deficiency]], [[Yunis-Varon syndrome]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| Line 27: | Line 30: | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Dermatologic''' | | '''Dermatologic''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Cardiofaciocutaneous syndrome]], [[congenital generalized lipodystrophy|congenital generalized lipodystrophy type 2]], [[Yunis-Varon syndrome]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Drug Side Effect''' | | '''Drug Side Effect''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Prednisolone]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| Line 39: | Line 42: | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Endocrine''' | | '''Endocrine''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Diabetes mellitus]], [[glycogenosis type 2]], [[thyroid disease]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| Line 47: | Line 50: | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Gastroenterologic''' | | '''Gastroenterologic''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Glycogenosis type 2]], [[very long-chain acyl-CoA dehydrogenase deficiency]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Genetic''' | | '''Genetic''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Cardiofaciocutaneous syndrome]], [[congenital generalized lipodystrophy|congenital generalized lipodystrophy type 2]], [[Costello syndrome]], [[cytochrome c oxidase deficiency]], [[Fabry's disease]], [[familial]], [[Friedreich's ataxia]], [[gene mutation]], [[glycogenosis type 2]], [[long-chain acyl-CoA dehydrogenase deficiency]], [[malonyl-CoA decarboxylase deficiency]], [[MELAS]], [[multiple lentigines syndrome]], [[myotonic dystrophy]], [[Noonan syndrome]], sarcomeric protein mutations | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Hematologic''' | | '''Hematologic''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Hereditary spherocytosis]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| Line 67: | Line 70: | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Musculoskeletal / Ortho''' | | '''Musculoskeletal / Ortho''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Hypertrichotic osteochondrodysplasia]], [[myotonic dystrophy]], [[Yunis-Varon syndrome]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Neurologic''' | | '''Neurologic''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Friedreich's ataxia]], [[MELAS]], [[myotonic dystrophy]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Nutritional / Metabolic''' | | '''Nutritional / Metabolic''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Cytochrome c oxidase deficiency]], dihydrolipoamide dehydrogenase deficiency, [[Fabry's disease]], [[long-chain acyl-CoA dehydrogenase deficiency]], [[malonyl-CoA decarboxylase deficiency]], [[MELAS]], [[glycogen synthase|muscle glycogen synthase deficiency]], [[very long-chain acyl-CoA dehydrogenase deficiency]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| Line 95: | Line 98: | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Psychiatric''' | | '''Psychiatric''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Costello syndrome]], [[hypertrichotic osteochondrodysplasia]] | ||
|- | |- | ||
|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
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|-bgcolor="LightSteelBlue" | |-bgcolor="LightSteelBlue" | ||
| '''Miscellaneous''' | | '''Miscellaneous''' | ||
|bgcolor="Beige"| | |bgcolor="Beige"| [[Aging]], [[idiopathic]] | ||
|- | |- | ||
|} | |} | ||
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===Causes in Alphabetical Order=== | ===Causes in Alphabetical Order=== | ||
*[[Aging]] | *[[Aging]] | ||
*[[Atrial myxoma]] | *[[Atrial myxoma]]<ref name="pmid24082380">{{cite journal| author=Abdou M, Hayek S, Williams BR| title=Atrial myxoma in a patient with hypertrophic cardiomyopathy. | journal=Tex Heart Inst J | year= 2013 | volume= 40 | issue= 4 | pages= 462-4 | pmid=24082380 | doi= | pmc=PMC3783132 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24082380 }} </ref> | ||
*[[Cardiofaciocutaneous syndrome]] | *[[Cardiofaciocutaneous syndrome]] | ||
*[[congenital generalized lipodystrophy|Congenital generalized lipodystrophy type 2]] | *[[congenital generalized lipodystrophy|Congenital generalized lipodystrophy type 2]] | ||
*[[Costello syndrome]] | *[[Costello syndrome]] <ref name="pmid9001809">{{cite journal| author=Fukao T, Sakai S, Shimozawa N, Kuwahara T, Kano M, Goto E et al.| title=Life-threatening cardiac involvement throughout life in a case of Costello syndrome. | journal=Clin Genet | year= 1996 | volume= 50 | issue= 4 | pages= 244-7 | pmid=9001809 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9001809 }} </ref> | ||
*[[Cytochrome c oxidase deficiency]] | *[[Cytochrome c oxidase deficiency]] | ||
*[[Diabetes mellitus]] | *[[Diabetes mellitus]] | ||
*Dihydrolipoamide dehydrogenase deficiency | *Dihydrolipoamide dehydrogenase deficiency | ||
*[[Fabry's disease]] | *[[Fabry's disease]]<ref name="pmid18386622">{{cite journal| author=Adam T, Alexandrescu L, Voinea F, Toringhibel M, Hâncu A| title=Fabry's disease. | journal=Rom J Intern Med | year= 2006 | volume= 44 | issue= 4 | pages= 455-64 | pmid=18386622 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18386622 }} </ref> | ||
*[[Familial]] | *[[Familial]] | ||
*[[Friedreich's ataxia]] | *[[Friedreich's ataxia]]<ref name="pmid12417527">{{cite journal| author=Jauslin ML, Wirth T, Meier T, Schoumacher F| title=A cellular model for Friedreich Ataxia reveals small-molecule glutathione peroxidase mimetics as novel treatment strategy. | journal=Hum Mol Genet | year= 2002 | volume= 11 | issue= 24 | pages= 3055-63 | pmid=12417527 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12417527 }} </ref> | ||
*[[Gene mutation]] | *[[Gene mutation]] | ||
*[[Glycogenosis type 2]] | *[[Glycogenosis type 2]] | ||
| Line 148: | Line 151: | ||
*[[Hypertension]] | *[[Hypertension]] | ||
*[[Hypertrichotic osteochondrodysplasia]] | *[[Hypertrichotic osteochondrodysplasia]] | ||
*[[Hypertrophic obstructive cardiomyopathy]] | |||
*[[Idiopathic]] | *[[Idiopathic]] | ||
*[[Long-chain acyl-CoA dehydrogenase deficiency]] | *[[Long-chain acyl-CoA dehydrogenase deficiency]] | ||
| Line 154: | Line 158: | ||
*[[Multiple lentigines syndrome]] | *[[Multiple lentigines syndrome]] | ||
*[[glycogen synthase|Muscle glycogen synthase deficiency]] | *[[glycogen synthase|Muscle glycogen synthase deficiency]] | ||
*[[Myotonic dystrophy]] | *[[Myotonic dystrophy]]<ref name="pmid17603429">{{cite journal| author=Halawa A, Iskandar SB, Brahmbhatt V, Fahrig SA| title=Atrial flutter and myotonic dystrophy in a male adolescent treated with radiofrequency catheter ablation. | journal=Rev Cardiovasc Med | year= 2007 | volume= 8 | issue= 2 | pages= 118-22 | pmid=17603429 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17603429 }} </ref> | ||
*[[Noonan syndrome]] | *[[Noonan syndrome]]<ref name="pmid24534818">{{cite journal| author=Prendiville TW, Gauvreau K, Tworog-Dube E, Patkin L, Kucherlapati RS, Roberts AE et al.| title=Cardiovascular disease in Noonan syndrome. | journal=Arch Dis Child | year= 2014 | volume= 99 | issue= 7 | pages= 629-34 | pmid=24534818 | doi=10.1136/archdischild-2013-305047 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24534818 }} </ref> | ||
*Sarcomeric protein mutations | *Sarcomeric protein mutations | ||
*Subendocardial ischemia | *Subendocardial ischemia | ||
*[[Thyroid disease]] | *[[Thyroid disease]] | ||
*[[Very long-chain acyl-CoA dehydrogenase deficiency]] | *[[Very long-chain acyl-CoA dehydrogenase deficiency]]<ref name="pmid24530811">{{cite journal| author=Tucci S, Flögel U, Hermann S, Sturm M, Schäfers M, Spiekerkoetter U| title=Development and pathomechanisms of cardiomyopathy in very long-chain acyl-CoA dehydrogenase deficient (VLCAD(-/-)) mice. | journal=Biochim Biophys Acta | year= 2014 | volume= 1842 | issue= 5 | pages= 677-85 | pmid=24530811 | doi=10.1016/j.bbadis.2014.02.001 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24530811 }} </ref> | ||
*[[Yunis-Varon syndrome]] | *[[Yunis-Varon syndrome]] | ||
==Genetics== | |||
Hypertrophic cardiomyopathy is transmitted in an [[Dominance relationship|autosomal dominant]] pattern. | |||
Genes involved in the [[pathogenesis]] of [[hypertrophic cardiomyopathy]] include: | |||
* [[MYH7]] | |||
* [[TNNT2]] | |||
* [[TPM1]] | |||
The development of Hypertrophic cardiomyopathy is the result of multiple genetic mutations such as: | |||
* [[Myosin|Beta-myosin heavy chain]] | |||
* [[Myosin]] binding protein C | |||
* [[Cardiac troponin|Cardiac troponin T]] | |||
HCM is the most common [[Genetics|geneticall]]<nowiki/>y transmitted cardiovascular disease. Hypertrophic cardiomyopathy is inherited as an [[autosomal dominant]] trait and is attributed to mutations in one of a number of genes that encode for one of the [[sarcomere]] [[Protein|proteins]]. [[Penetrance]] of HCM is incomplete, variable and time or age-related. The disease may be sporadic but affected family members are discovered in 13% of cases. More than 200 mutations involving at least 10 [[chromosome]]<nowiki/>s encoding structural proteins of the myocyte have been discovered. These mutations have varying degrees of penetrance and even the same mutation may have variable expression, implying the superimposed effects of other genes or environmental influences. Children of a patient with HCM have a 50% chance of inheriting the trait. | |||
<br /> | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Latest revision as of 19:15, 10 December 2019
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Differentiating Hypertrophic Cardiomyopathy from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2] Soroush Seifirad, M.D.[3]
Overview
Hypertrophic cardiomyopathy is a condition that is most often passed down through families (inherited). It is thought to result from gene mutations that control heart muscle growth. Genes involved in the pathogenesis of hypertrophic cardiomyopathy include MYH7, TNNT2, TPM1. Nevertheless, a number of chronic medical conditions might be contributed to hypertrophic cardiomyopathy development, among them are thyroid disease, diabetes, and obesity, and hypertension.
Causes
Life Threatening Causes
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.
Common Causes
- Familial
- Gene mutation
- Hypertension
- Thyroid disease
- Diabetes
- Obesity
Causes by Organ System
Causes in Alphabetical Order
- Aging
- Atrial myxoma[1]
- Cardiofaciocutaneous syndrome
- Congenital generalized lipodystrophy type 2
- Costello syndrome [2]
- Cytochrome c oxidase deficiency
- Diabetes mellitus
- Dihydrolipoamide dehydrogenase deficiency
- Fabry's disease[3]
- Familial
- Friedreich's ataxia[4]
- Gene mutation
- Glycogenosis type 2
- Hereditary spherocytosis
- Hypertension
- Hypertrichotic osteochondrodysplasia
- Hypertrophic obstructive cardiomyopathy
- Idiopathic
- Long-chain acyl-CoA dehydrogenase deficiency
- Malonyl-CoA decarboxylase deficiency
- MELAS
- Multiple lentigines syndrome
- Muscle glycogen synthase deficiency
- Myotonic dystrophy[5]
- Noonan syndrome[6]
- Sarcomeric protein mutations
- Subendocardial ischemia
- Thyroid disease
- Very long-chain acyl-CoA dehydrogenase deficiency[7]
- Yunis-Varon syndrome
Genetics
Hypertrophic cardiomyopathy is transmitted in an autosomal dominant pattern.
Genes involved in the pathogenesis of hypertrophic cardiomyopathy include:
The development of Hypertrophic cardiomyopathy is the result of multiple genetic mutations such as:
- Beta-myosin heavy chain
- Myosin binding protein C
- Cardiac troponin T
HCM is the most common genetically transmitted cardiovascular disease. Hypertrophic cardiomyopathy is inherited as an autosomal dominant trait and is attributed to mutations in one of a number of genes that encode for one of the sarcomere proteins. Penetrance of HCM is incomplete, variable and time or age-related. The disease may be sporadic but affected family members are discovered in 13% of cases. More than 200 mutations involving at least 10 chromosomes encoding structural proteins of the myocyte have been discovered. These mutations have varying degrees of penetrance and even the same mutation may have variable expression, implying the superimposed effects of other genes or environmental influences. Children of a patient with HCM have a 50% chance of inheriting the trait.
References
- ↑ Abdou M, Hayek S, Williams BR (2013). "Atrial myxoma in a patient with hypertrophic cardiomyopathy". Tex Heart Inst J. 40 (4): 462–4. PMC 3783132. PMID 24082380.
- ↑ Fukao T, Sakai S, Shimozawa N, Kuwahara T, Kano M, Goto E; et al. (1996). "Life-threatening cardiac involvement throughout life in a case of Costello syndrome". Clin Genet. 50 (4): 244–7. PMID 9001809.
- ↑ Adam T, Alexandrescu L, Voinea F, Toringhibel M, Hâncu A (2006). "Fabry's disease". Rom J Intern Med. 44 (4): 455–64. PMID 18386622.
- ↑ Jauslin ML, Wirth T, Meier T, Schoumacher F (2002). "A cellular model for Friedreich Ataxia reveals small-molecule glutathione peroxidase mimetics as novel treatment strategy". Hum Mol Genet. 11 (24): 3055–63. PMID 12417527.
- ↑ Halawa A, Iskandar SB, Brahmbhatt V, Fahrig SA (2007). "Atrial flutter and myotonic dystrophy in a male adolescent treated with radiofrequency catheter ablation". Rev Cardiovasc Med. 8 (2): 118–22. PMID 17603429.
- ↑ Prendiville TW, Gauvreau K, Tworog-Dube E, Patkin L, Kucherlapati RS, Roberts AE; et al. (2014). "Cardiovascular disease in Noonan syndrome". Arch Dis Child. 99 (7): 629–34. doi:10.1136/archdischild-2013-305047. PMID 24534818.
- ↑ Tucci S, Flögel U, Hermann S, Sturm M, Schäfers M, Spiekerkoetter U (2014). "Development and pathomechanisms of cardiomyopathy in very long-chain acyl-CoA dehydrogenase deficient (VLCAD(-/-)) mice". Biochim Biophys Acta. 1842 (5): 677–85. doi:10.1016/j.bbadis.2014.02.001. PMID 24530811.