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{{Infobox disease |
This is a preview for the new '''MathML rendering mode''' (with SVG fallback), which is availble in production for registered users.
  Name          = Dilated cardiomyopathy |
  Image          = Myocardiopathy dilated2.JPG |
  Caption        = Mouse heart slice showing dilated cardiomyopathy
  DiseasesDB    = 3066 |
  ICD10          = {{ICD10|I|42|0|i|30}} |
  ICD9          = {{ICD9|425.4}} |
  ICDO          = |
  OMIM          = 212110 |
  MedlinePlus    = 000168 |
  eMedicineSubj  = med |
  eMedicineTopic = 289 |
  eMedicine_mult = {{eMedicine2|emerg|80}}  {{eMedicine2|ped|2502}} |
  MeshID        = D002311
| GeneReviewsNBK  = NBK1309
| GeneReviewsName = Dilated Cardiomyopathy Overview
| GeneReviewsNBK2  = NBK1119
| GeneReviewsName2 = Dystrophinopathies
}}
'''Dilated cardiomyopathy''' or '''DCM''' is a condition in which the [[heart]] becomes weakened and enlarged and cannot pump blood efficiently. The decreased heart function can affect the lungs, liver, and other body systems.


DCM is one of the [[cardiomyopathy|cardiomyopathies]], a group of diseases that affect primarily the [[myocardium]] (the [[muscle]] of the [[heart]]). Different cardiomyopathies have different causes and affect the heart in different ways. In DCM a portion of the myocardium is dilated, often without any obvious cause. Left or right ventricular [[Systole (medicine)|systolic]] pump function of the heart is impaired, leading to progressive cardiac enlargement and [[Organ hypertrophy|hypertrophy]], a process called ''remodeling''.<ref name=Harrisons>{{cite book |author=Jameson JN, Kasper DL, Harrison TR, Braunwald E, Fauci AS, Hauser SL, Longo DL. |title=Harrison's principles of internal medicine |publisher=McGraw-Hill Medical Publishing Division |location=New York |year=2005 |edition=16th |isbn=0-07-140235-7 |url=http://highered.mcgraw-hill.com/sites/0071402357/information_center_view0/}}</ref>
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Dilated cardiomyopathy is the most common form of non-[[Ischemia|ischemic]] cardiomyopathy. It occurs more frequently in men than in women, and is most common between the ages of 20 and 60 years.<ref>{{cite book |author=Robbins SL, Kumar V, Cotran RS |title=Robbins basic pathology |publisher=Saunders |location=Philadelphia |year=2003 |isbn=0-7216-9274-5 |edition=7th}}</ref> About one in three cases of [[congestive heart failure]] (CHF) is due to dilated cardiomyopathy.<ref name=Harrisons/> Dilated cardiomyopathy also occurs in children.
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==Causes==
'''MathML'''
Although in many cases no cause ([[etiology]]) is apparent, dilated cardiomyopathy is probably the result of damage to the [[myocardium]] produced by a variety of [[toxic]], [[metabolic]], or infectious agents. It may be due to fibrous change of the myocardium from a previous [[myocardial infarction]]. Or, it may be the late sequelae of acute viral [[myocarditis]], such as with [[Coxsackie B virus]] and other [[enterovirus]]es,<ref name=Robbins8th>{{cite book |author=Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson |title=Robbins Basic Pathology|publisher=Saunders |location=Philadelphia |isbn=1-4160-2973-7 |edition=8th}}</ref> possibly mediated through an immunologic mechanism.<ref>{{cite journal |author=Martino TA, Liu P, Sole MJ |title=Viral infection and the pathogenesis of dilated cardiomyopathy |journal=Circ Res. |volume=74 |issue=2 |pages=182–8 |date=February 1994 |pmid=8293557 }}</ref>
:<math forcemathmode="mathml">E=mc^2</math>


Other causes include:
<!--'''PNG'''  (currently default in production)
* [[Chagas disease]], due to [[Trypanosoma cruzi]]. This is the most common infectious cause of dilated cardiomyopathy in Latin America<ref name="test">http://www.merckmanuals.com/professional/cardiovascular_disorders/cardiomyopathies/dilated_cardiomyopathy.html</ref>
:<math forcemathmode="png">E=mc^2</math>
* [[Pregnancy]]. Dilated cardiomyopathy occurs late in gestation or several weeks to months postpartum as a [[peripartum cardiomyopathy]].<ref name=Robbins8th/> It is reversible in half of cases.<ref name=Robbins8th/>
* [[Alcohol]] abuse ([[Alcoholic cardiomyopathy]]), although the cause-and-effect relationship with alcohol alone is debated.<ref name=Robbins8th/> Nonalcoholic toxic insults include administration of certain [[chemotherapeutic agent]]s, in particular [[doxorubicin]] (Adriamycin), and [[cobalt]].<ref name=Robbins8th/>
* [[Thyroid disease]], [[stimulant]] use, and chronic uncontrolled [[tachycardia]]. {{Citation needed|date=August 2013}}


[[Autoimmune]] mechanisms are also suggested as a cause for dilated cardiomyopathy.<ref>{{cite journal |author=San Martín MA, García A, Rodríguez FJ, Terol I |title=[Dilated cardiomyopathy and autoimmunity: an overview of current knowledge and perspectives] |language=Spanish; Castilian |journal=Rev Esp Cardiol. |volume=55 |issue=5 |pages=514–24 |date=May 2002 |pmid=12015932 |url=http://www.revespcardiol.org/cgi-bin/wdbcgi.exe/cardio/mrevista_cardio.pubmed_full?inctrl=05ZI0113&vol=55&num=5&pag=514}}</ref>
'''source'''
:<math forcemathmode="source">E=mc^2</math> -->


Recent studies have shown that those subjects with an extremely high occurrence (several thousands a day) of [[premature ventricular contractions]] (extrasystole) can develop dilated cardiomyopathy. In these cases, if the extrasystole are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses.<ref>{{cite journal |author=Belhassen B |title=Radiofrequency ablation of "benign" right ventricular outflow tract extrasystoles: a therapy that has found its disease? |journal=J. Am. Coll. Cardiol. |volume=45 |issue=8 |pages=1266–8 |date=April 2005 |pmid=15837260 |doi=10.1016/j.jacc.2005.01.028 |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(05)00234-2}}</ref><ref>{{cite journal |author=Shiraishi H, Ishibashi K, Urao N, ''et al.'' |title=A case of cardiomyopathy induced by premature ventricular complexes |journal=Circ. J. |volume=66 |issue=11 |pages=1065–7 |date=November 2002 |pmid=12419942 |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/circj/66.1065?from=PubMed}}</ref>
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Although the disease is more common in African-Americans than in Caucasians,<ref>{{cite journal |author=Coughlin SS, Labenberg JR, Tefft MC |title=Black-white differences in idiopathic dilated cardiomyopathy: the Washington DC dilated Cardiomyopathy Study |journal=Epidemiology |volume=4 |issue=2 |pages=165–72 |date=March 1993 |pmid=8452906 |doi=10.1097/00001648-199303000-00013 }}</ref> it may occur in any patient population.
==Demos==


===Genetics===
Here are some [https://commons.wikimedia.org/w/index.php?title=Special:ListFiles/Frederic.wang demos]:
{{Collapse top|Genetic associations with dilated cardiomyopathy}}
{| class="wikitable" class="sortable wikitable"
|-
! Type
! [[OMIM]]
! [[Gene]]
! [[Locus (genetics)|Locus]]
|-
| CMD1A
| {{OMIM2|115200}}
| [[LMNA]]
| 1q21
|-
| CMD1B
| {{OMIM2|600884}}
| unknown ([[TMOD1]] candidate)
| 9q13
|-
| CMD1C
| {{OMIM2|601493}}
| [[LDB3]]
| 10q22-q23
|-
| CMD1D
| {{OMIM2|601494}}
| [[TNNT2]]
| 1q32
|-
| CMD1E
| {{OMIM2|601154}}
| [[SCN5A]]
| 3p
|-
| CMD1F
| {{OMIM2|602067}}
|
| 6q23
|-
| CMD1G
| {{OMIM2|604145}}
| [[Titin|TTN]]
| 2q31
|-
| CMD1H
| {{OMIM2|604288}}
|
| 2q14-q22
|-
| CMD1I
| {{OMIM2|604765}}
| [[Desmin|DES]]
| 2q35
|-
| CMD1J
| {{OMIM2|605362}}
| [[EYA4]]
| 6q23-q24
|-
| CMD1K
| {{OMIM2|605582}}
|
| 6q12-q16
|-
| CMD1L
| {{OMIM2|606685}}
| [[SGCD]]
| 5q33
|-
| CMD1M
| {{OMIM2|607482}}
| [[CSRP3]]
| 11p15.1
|-
| CMD1N
| {{OMIM2|607487}}
| [[TCAP (gene)|TCAP]]
| 17q12
|-
| CMD1O
| {{OMIM2|608569}}
| [[ABCC9]]
| 12p12.1
|-
| CMD1P
| {{OMIM2|609909}}
| [[Phospholamban|PLN]]
| 6q22.1
|-
| CMD1Q
| {{OMIM2|609915}}
|
| 7q22.3-q31.1
|-
| CMD1R
|
| [[ACTC1|ACTC]]
| 15q14
|-
| CMD1S
|
| [[MYH7]]
| 14q12
|-
| CMD1T
|
| [[TMPO]]
| 12q22
|-
| CMD1U
|
| [[PSEN1]]
| 14q24.3
|-
| CMD1V
|
| [[PSEN2]]
| 1q31-q42
|-
| CMD1W
| {{OMIM2|611407}}
| [[metavinculin|VCL]]
| 10q22-q23
|-
| CMD1X
|
| [[fukutin|FCMD]]
| 9q31
|-
| CMD1Y
| {{OMIM2|611878}}
| [[TPM1]]
| 15q22.1
|-
| CMD1Z
| {{OMIM2|611879}}
| [[TNNC1]]
| 3p21.3-p14.3
|-
| CMD1AA
| {{OMIM2|612158}}
| [[ACTN2]]
| 1q42-q43
|-
| CMD2A
| {{OMIM2|611880}}
| [[TNNI3]]
| 19q13.4
|-
| CMD3A
| {{OMIM2|300069}}
| [[Tafazzin|TAZ]]
| Xq28
|-
| CMD3B
| {{OMIM2|302045}}
| [[dystrophin|DMD]]
| Xp21.2
|}
{{Collapse bottom}}


About 25–35% of patients have familial forms of the disease,<ref name=Robbins8th/> with most [[mutation]]s affecting genes encoding [[cytoskeletal]] proteins,<ref name=Robbins8th/> while some affect other proteins involved in contraction.<ref>{{cite journal |author=Ross J |title=Dilated cardiomyopathy: concepts derived from gene deficient and transgenic animal models |journal=Circ J. |volume=66 |issue=3 |pages=219–24 |date=March 2002 |pmid=11922267 |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/circj/66.219?from=PubMed |doi=10.1253/circj.66.219 }}</ref> The disease is genetically heterogeneous, but the most common form of its transmission is an [[autosomal dominant]] pattern.<ref name=Robbins8th/>
[[Autosomal recessive]] (as found, for example, in [[Alström syndrome]]<ref name=Robbins8th/>), [[X-linked]] (as in [[Duchenne muscular dystrophy]]), and [[Mitochondrial disease|mitochondrial]] inheritance of the disease is also found.<ref>{{cite journal |author=Schönberger J, Seidman CE |title=Many roads lead to a broken heart: the genetics of dilated cardiomyopathy |journal=American Journal of Human Genetics |volume=69 |issue=2 |pages=249–60 |date=August 2001 |pmid=11443548 |pmc=1235300 |doi=10.1086/321978 }}</ref> Some relatives of patients with dilated cardiomyopathy have preclinical, asymptomatic heart-muscle changes.<ref>{{cite journal |author=Mahon NG, Murphy RT, MacRae CA, Caforio AL, Elliott PM, McKenna WJ |title=Echocardiographic evaluation in asymptomatic relatives of patients with dilated cardiomyopathy reveals preclinical disease |journal=Annals of Internal Medicine |volume=143 |issue=2 |pages=108–15 |date=July 2005 |pmid=16027452 }}</ref>


Other cytoskeletal proteins involved in DCM include [[α-cardiac actin]], [[desmin]], and the nuclear [[lamins]] A and C.<ref name=Robbins8th/> Mitochondrial deletions and mutations presumably cause DCM by altering myocardial [[ATP generation]].<ref name=Robbins8th/>
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==Signs and symptoms==
==Test pages ==
{{Main|Heart failure#Signs and symptoms}}
Dilated cardiomyopathy may not cause symptoms significant enough to impact on [[quality of life]]. {{Citation needed|date=August 2013}} A minority of patients can experience significant symptoms. These might include: {{Citation needed|date=August 2013}}
* [[Dyspnea|breathlessness]]
* [[Syncope (medicine)|Syncope]]
* [[Angina pectoris|angina]], but only in the presence of [[ischemic heart disease]]


A patient suffering from dilated cardiomyopathy may have an [[cardiomegaly|enlarged heart]], with [[pulmonary edema]] and an elevated [[jugular venous pressure]] and a low [[pulse pressure]]. Signs of [[mitral regurgitation|mitral]] and [[tricuspid regurgitation]] may be present. A [[tachycardia]] with no change during the respiratory cycle may also be found {{Citation needed|date=August 2013}}
To test the '''MathML''', '''PNG''', and '''source''' rendering modes, please go to one of the following test pages:
*[[Displaystyle]]
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*[[Styling]]
*[[Linebreaking]]
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==Pathophysiology==
*[[Inputtypes|Inputtypes (private Wikis only)]]
The progression of heart failure is associated with left ventricular remodeling, which manifests as gradual increases in left ventricular end-diastolic and end-systolic volumes, wall thinning, and a change in chamber geometry to a more spherical, less elongated shape. This process is usually associated with a continuous decline in [[ejection fraction]]. The concept of cardiac remodeling was initially developed to describe changes that occur in the days and months following myocardial infarction.<ref name=PIESKE2004>{{cite journal |author=Pieske B |title=Reverse remodeling in heart failure – fact or fiction? |journal=Eur Heart J Suppl. |volume=6 |pages=D66–78 |year=2004 |url=http://eurheartjsupp.oxfordjournals.org/cgi/content/abstract/6/suppl_D/D66 |doi=10.1016/j.ehjsup.2004.05.019}}</ref>
*[[Url2Image|Url2Image (private Wikis only)]]
 
==Bug reporting==
Death is due to either [[congestive heart failure]] or ventricular [[tachyarrhythmia|tachy-]] or [[bradyarrhythmia]]s. {{Citation needed|date=August 2013}}
If you find any bugs, please report them at [https://bugzilla.wikimedia.org/enter_bug.cgi?product=MediaWiki%20extensions&component=Math&version=master&short_desc=Math-preview%20rendering%20problem Bugzilla], or write an email to math_bugs (at) ckurs (dot) de .
 
===Computational models of eccentric cardiac growth===
Cardiac dilation is a transversely [[isotropic]], irreversible process resulting from excess strains on the [[myocardium]].<ref>{{cite journal |doi=10.1016/j.jmps.2010.07.003 |title=Generic approach towards finite growth with examples of athlete's heart, cardiac dilation, and cardiac wall thickening |year=2010 |last1=Goektepe |first1=Serdar |last2=Abilez |first2=Oscar John |last3=Kuhl |first3=Ellen |journal=Mechanics and Physics of Solids}}</ref> A computation model of volumetric, isotropic, and cardiac wall growth predicts the relationship between cardiac strains (e.g. volume overload after myocardial infarction) and dilation using the following governing equations:
 
<math>F = F^e \cdot F^g\,</math>
 
where <math>F^e</math> is elastic volume stretch that is reversible and <math>F^g</math> is irreversible, isotropic volume growth described by:
 
<math>F^g = \mathbb{I}+[\lambda^{g}-1]f_{0}\otimes f_{0} \,</math>
 
where <math>f_{0}</math> is a vector, which points along a [[cardiomyocyte]]'s long axis and <math> \lambda^g </math> is the cardiomyocyte stretch due to growth. The total cardiomyocyte growth is given by:
 
<math>\lambda = \lambda^e \cdot F\lambda^g\,</math>
 
The above model reveals a gradual dilation of the [[myocardium]], especially the ventricular myocardium, to support the blood volume overload in the chambers. Dilation manifests itself in an increase in total cardiac mass and cardiac diameter. Cardiomyocytes reach their maximum length of 150 <math>\mu</math>m in the endocardium and 130 <math>\mu</math>m in the epicardium by the addition of sarcomeres.<ref>{{cite journal |doi=10.1016/j.jmps.2010.07.003 |title=A multiscale model for eccentric and concentric cardiac growth through sarcomerogenesis. |year=2010 |last1=Goektepe |first1=Serdar |last2=Abilez |first2=Oscar John |last3=Parker |first3=K |last4=Kuhl |first4=Ellen |journal=Theoretical Biology}}</ref>  Due to the increase in diameter, the dilated heart appears spherical in shape, as opposed the elliptical shape of a healthy human heart. In addition, the ventricular walls maintain the same thickness, characteristic of pathophysiological cardiac dilation.
 
==Diagnosis==
Generalized enlargement of the heart is seen upon normal [[chest X-ray]]. [[Pleural effusion]] may also be noticed, which is due to pulmonary venous hypertension.
 
[[File:LBBB+RADandTransplant.png|thumb|300px|Serial 12-lead ECGs from a 49-year-old black man with cardiomyopathy. (TOP): [[Sinus tachycardia]] (rate about 101/min) with [[LBBB]] accompanied by [[Right axis deviation|RAD]] (here about 108°). Frequent multifocal [[Premature ventricular contraction|PVCs]] (both singly and in pairs) and [[left atrial enlargement]]. (BOTTOM): Same patient about 5 months later status-post orthotopic [[heart transplant]].]]
 
The [[electrocardiogram]] often shows [[sinus tachycardia]] or [[atrial fibrillation]], [[Cardiac arrhythmia#List of common cardiac dysrhythmias|ventricular arrhythmia]]s, [[left atrial enlargement]], and sometimes intraventricular conduction defects and low voltage. When [[left bundle-branch block]] (LBBB) is accompanied by [[right axis deviation]] (RAD), the rare combination is considered to be highly suggestive of dilated or congestive cardiomyopathy.<ref>{{cite journal |author=Nikolic G, Marriott HJ|title=Left bundle branch block with right axis deviation: a marker of congestive cardiomyopathy|journal=J Electrocardiol |volume=18 |issue=4 |pages=395–404|date=Oct 1985 |pmid=3906012 }}</ref><ref>{{cite journal |author=Childers R, Lupovich S, Sochanski M, Konarzewska H.|title=Left bundle branch block and right axis deviation: a report of 36 cases|journal=J Electrocardiol |volume=33 |issue=Suppl |pages=93–102|year=2000 |pmid=11265743 }}</ref> [[Echocardiogram]] shows left ventricular dilatation with normal or thinned walls and reduced [[ejection fraction]]. Cardiac [[catheterization]] and [[coronary angiography]] are often performed to exclude ischemic heart disease.
 
[[Genetic testing]] can be important, since one study has shown that gene mutations in the TTN gene (which codes for a protein called [[titin]]) are responsible for "approximately 25% of familial cases of idiopathic dilated cardiomyopathy and 18% of sporadic cases."<ref>{{cite journal |author=Herman DS, Lam L, Taylor MR, Wang L, Teekakirikul P, Christodoulou D, Conner L, DePalma SR, McDonough B, Sparks E, Teodorescu DL, Cirino AL, Banner NR, Pennell DJ, Graw S, Merlo M, Di Lenarda A, Sinagra G, Bos JM, Ackerman MJ, Mitchell RN, Murry CE, Lakdawala NK, Ho CY, Barton PJ, Cook SA, Mestroni L, Seidman JG, Seidman CE |title=Truncations of Titin causing dilated cardiomyopathy |journal=N Engl J Med |volume=366 |issue=7 |pages=619–628 |date=Feb 16, 2012 |pmid=22335739 |doi=10.1056/NEJMoa1110186}}</ref> The results of the genetic testing can help the doctors and patients understand the underlying cause of the dilated cardiomyopathy. Genetic test results can also help guide decisions on whether a patient's relatives should undergo genetic testing (to see if they have the same genetic mutation) and cardiac testing to screen for early findings of dilated cardiomyopathy.
 
[[Cardiac magnetic resonance imaging]] (cardiac MRI) may also provide helpful diagnostic information in patients with dilated cardiomyopathy.<ref>{{cite journal |author=Pennell DJ, Sechtem UP, Higgins CB, Manning WJ, Pohost GM, Rademakers FE, van Rossum AC, Shaw LJ, Yucel EK.|title=Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report|journal=Eur Heart J |volume=25 |issue=21 |pages=1940–1965|year=2004 Nov |pmid=15522474 |doi=10.1016/j.ehj.2004.06.040}}</ref>
 
==Treatment==
Management and treatment of dilated cardiomyopathy has improved significantly in the last decade. {{Citation needed|date=February 2010}} Drug therapy can slow down progression and in some cases even improve the heart condition. Standard therapy may include salt restriction, [[angiotensin-converting enzyme|ACE inhibitors]], [[diuretic]]s, and [[digitalis]]. [[Anticoagulation|Anticoagulants]] may also be used. Alcohol should be avoided. {{Citation needed|date=August 2013}}
 
There is some evidence for the benefits of [[Coenzyme Q10]] in treating heart failure.<ref>{{cite journal |author=Langsjoen PH, Langsjoen PH, Folkers K |title=A six-year clinical study of therapy of cardiomyopathy with coenzyme Q10 |journal=Int J Tissue React. |volume=12 |issue=3 |pages=169–71 |year=1990 |pmid=2276895 }}</ref><ref>{{cite journal |author=Folkers K, Langsjoen P, Langsjoen PH |title=Therapy with coenzyme Q10 of patients in heart failure who are eligible or ineligible for a transplant |journal=Biochem Biophys Res Commun. |volume=182 |issue=1 |pages=247–53 |date=January 1992 |pmid=1731784 |url=http://linkinghub.elsevier.com/retrieve/pii/S0006-291X(05)80137-8 |doi=10.1016/S0006-291X(05)80137-8}}</ref><ref>{{cite journal |author=Baggio E, Gandini R, Plancher AC, Passeri M, Carmosino G |title=Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. CoQ10 Drug Surveillance Investigators |journal=Mol Aspects Med. |volume=15 |issue=Suppl |pages=s287–94 |year=1994 |pmid=7752841 |doi=10.1016/0098-2997(94)90040-X }}</ref> Other supplements provided may include [[L-Carnitine]], [[Taurine]] and D-Ribose. {{Citation needed|date=August 2013}}
 
===Procedures and Surgery===
 
[[Artificial pacemaker]]s may be used in patients with intraventricular conduction delay, and [[implantable cardioverter-defibrillator]]s in those at risk of arrhythmia. These forms of treatment have been shown to improve symptoms and reduce hospitalization. {{Citation needed|date=August 2013}}
 
In patients with advanced disease who are refractory to medical therapy, [[heart transplantation]] may be considered. {{Citation needed|date=August 2013}}
 
=== Reverse remodeling ===
This refers to reversing the remodelling that has occurred. Therapies that support reverse remodeling have been investigated, and this may suggests a new approach to the prognosis of  cardiomyopathies.<ref name = PIESKE2004 />
 
== Dilated cardiomyopathy in animals ==<!-- This section is linked from [[Irish Wolfhound]] -->
 
Dilated cardiomyopathy is a heritable disease in some dog breeds, including the [[Boxer (dog)|Boxer]], [[Dobermann]], [[Great Dane]], [[Irish Wolfhound]], and [[St. Bernard (dog)|St Bernard]].<ref>{{cite journal |author=Oyama MA, Chittur S |title=Genomic expression patterns of cardiac tissues from dogs with dilated cardiomyopathy |journal=Am J Vet Res. |volume=66 |issue=7 |pages=1140–55 |date=July 2005 |pmid=16111151 |doi=10.2460/ajvr.2005.66.1140 }}</ref> Treatment is based on medication, including ACE inhibitors, loop diuretics and phosphodiesterase inhibitors.
 
Dilated cardiomyopathy is also a disease affecting some cat breeds, including the [[Oriental Shorthair]], [[Burmese (cat)|Burmese]], [[Persian (cat)|Persian]], and [[Abyssinian (cat)|Abyssinian]]. As opposed to these hereditary forms, non-hereditary DCM used to be common in the overall cat population before the addition of taurine to commercial cat food.
 
There is also a high incidence of heritable dilated cardiomyopathy in captive [[Golden Hamster]]s (''Mesocricetus auratus''), due in no small part to their being highly [[Inbreeding|inbred]]. The incidence is high enough that several strains of Golden Hamster have been developed to serve as animal models in clinical testing for human forms of the disease.<ref>{{cite journal |author=Nigro V, Okazaki Y, Belsito A, ''et al.'' |title=Identification of the Syrian hamster cardiomyopathy gene |journal=Hum. Mol. Genet. |volume=6 |issue=4 |pages=601–7 |date=April 1997 |pmid=9097966 |doi=10.1093/hmg/6.4.601 |url=http://hmg.oxfordjournals.org/content/6/4/601.full}}</ref>
 
==References==
{{reflist|2}}
 
==External links==
* [http://www.cardiomyopathy.org/html/which_card_dcm.htm Cardiomyopathy Association: Dilated cardiomyopathy]
* [http://www.childrenscardiomyopathy.org Children's Cardiomyopathy Foundation]
* [http://www.ncbi.nlm.nih.gov/books/NBK1309/ GeneReview/NIH/UW entry on Dilated Cardiomyopathy Overview]
* [http://www.ncbi.nlm.nih.gov/books/NBK1119/ GeneReviews/NCBI/NIH/UW entry on Dystrophinopathies]
*[http://www.gosh.nhs.uk/medical-conditions/search-for-medical-conditions/cardiomyopathy/ Dilated cardiomyopathy] information for parents.
 
{{Circulatory system pathology}}
{{Cytoskeletal defects}}
{{ABC transporter disorders}}
 
[[Category:Cardiomyopathy]]
[[Category:Cytoskeletal defects]]
[[Category:Cardiogenetic disorders]]

Latest revision as of 22:52, 15 September 2019

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