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| Image = 1151.jpg| | | Image = 1151.jpg| |
| Caption = Dilated Cardiomyopathy: Gross dilated left ventricle with marked endocardial sclerosis <br> <small> [http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] </small>| | | Caption = Dilated Cardiomyopathy: Gross dilated left ventricle with marked endocardial sclerosis <br> <small> [http://www.peir.net Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology] </small>| |
| DiseasesDB = 3066 |
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| ICD10 = {{ICD10|I|42|0|i|30}} |
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| ICD9 = {{ICD9|425.4}} |
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| ICDO = |
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| OMIM = 212110 |
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| MedlinePlus = 000168 |
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| eMedicineSubj = |
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| eMedicineTopic = |
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| eMedicine_mult = |
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| MeshID = D002311 |
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| }} | | }} |
| {{Dilated cardiomyopathy}} | | {{Dilated cardiomyopathy}} |
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| {{CMG}}; '''Associate Editor-in-Chief:''' Sachin Shah, M.D.
| | '''For patient information, click [[Dilated cardiomyopathy (patient information)|here]]''' |
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| {{SK}} DCM; congestive cardiomyopathy | | {{CMG}}; {{AE}}{{AIA}}; Sachin Shah, M.D. |
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| | {{SK}} Congestive cardiomyopathy; DCM |
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| ==[[Dilated cardiomyopathy overview|Overview]]== | | ==[[Dilated cardiomyopathy overview|Overview]]== |
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| ==Causes== | | ==[[Dilated cardiomyopathy historical perspective|Historical Perspective]]== |
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| ==Clinical Presentation== | | ==[[Dilated cardiomyopathy pathophysiology|Pathophysiology]]== |
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| ==Diagnosis== | | ==[[Dilated cardiomyopathy causes|Causes]]== |
| The diagnosis of dilated cardiomyopathy is based on clinical presentation and imaging findings. The most common imaging modality used to diagnose dilated cardiomyopathy is 2D-echocardiography. Echocardiographic findings of dilated cardiomyopathy include dilation of the left ventricle; however, may include dilation of all 4 cardiac chambers, LV (left ventricular) wall thickness usually is normal but given the dilation the LV mass is increased. In addition there is a global reduciton in systolic function. Occasionally there may also be focal wall motion abnormalities even in patients ''without'' flow limiting coronary artery disease.<ref> Mayo Clinic Cardiology. Concise Textbook. Murphy, Joseph G; Lloyd, Margaret A. Mayo Clinic Scientific Press. 2007.</ref>
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| | ==[[Dilated cardiomyopathy differential diagnosis|Differentiating Dilated cardiomyopathy from other Diseases]]== |
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| The diagnosis requires a dilated left ventricle and low ejection fraction.
| | ==[[Dilated cardiomyopathy epidemiology and demographics|Epidemiology and Demographics]]== |
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| In terms of determining the etiology a careful history is most instrumental. If the patient has CAD (coronary artery disease) risk factors, known CAD, or angina then a workup for CAD should be undertaken with coronary angiography. A viral prodrome such as viral URI or viral gastroenteritis may make viral myocarditis as a more likely cause. If the patient was exposed to chemotherapy such as anthracyclines then this would be the likely cause. Patients at risk for HIV should undergo testing as HIV can cause a dilated cardiomyopathy. Peripartum cardiomyopathy most often occurs 1 month prior to expected delivery or 5 months after delivery, so recent childbirth is important information. Often by 8 months gestational age pregnancy is physically apparent but it is important to rule out pregnancy in women of childbearing age with dilated cardiomyopathy. Screening questions regarding cocaine or alcohol abuse or other toxin exposure (such as cobalt) should be addressed.
| | ==[[Dilated cardiomyopathy risk factors|Risk Factors]]== |
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| A review of systems is also helpful in regards to connective tissue disease associated dilated cardiomyopathy (which can be related to SLE (systemic lupus erythematosis), rheumatoid arthritis, sarcoidosis, scleroderma, as well as other connective tissue diseases).
| | ==[[Dilated cardiomyopathy screening|Screening]]== |
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| A family history also has a great importance in the diagnosis of dilated cardiomyopathy. It has been suggested that a portion of those patients labeled as "idiopathic" may have a familial form of the disease. The prevalence of this in the population of patients with dilated cardiomyopathy has been estimated as high as 25%.<ref>Ross J Jr. Dilated cardiomyopathy: concepts derived from gene deficient and transgenic animal models. Circ J. 2002;66:219-24. PMID 11922267</ref> The majority of these are thought to be related to autosomal dominant transmission, the remaining are thought to be transimtted in an autosomal recessive and X-linked fashion.<ref>Mestroni L; Rocco C; et al. Familial dilated cardiomyopathy: evidence for genetic and phenotypic heterogeneity. Heart Muscle Disease Study Group. J Am Coll Cardiol 1999 Jul;34(1):181-90.</ref> Mitochondrial inheritance of the disease has also been identified.<ref>Schonberger J, Seidman CE. Many roads lead to a broken heart: the genetics of dilated cardiomyopathy. Am J Hum Genet. 2001;69:249-60. Epub 2001 Jul 6. PMID 11443548</ref>
| | ==[[Dilated cardiomyopathy natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| Pericardial effusion may accompany myocarditis but this finding is not specific. Cardiac MRI as discussed above may be helpful in diagnosing myocarditis. Endomyocardial biopsy as discussed above has low sensitivy and the findings are also notoriously non-specific. The findings on biopsy usually involve findings of inflammation and specific pathogens are unlikely to be identified. There may be an increased yield to using MRI to target endomyocardial biopsy as described above. Viral titiers (serologies) are often unhelpful and not routinely ordered in clinical practice.
| | ==Diagnosis== |
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| ==Prognosis==
| | [[Dilated cardiomyopathy history and symptoms|History and Symptoms]] | [[Dilated cardiomyopathy physical examination|Physical Examination]] | [[Dilated cardiomyopathy laboratory findings|Laboratory Findings]] | [[Dilated cardiomyopathy electrocardiogram|Electrocardiogram]] | [[Dilated cardiomyopathy chest x ray|Chest X-Ray]] | [[Dilated cardiomyopathy CT|CT]] | [[Dilated cardiomyopathy MRI|MRI]] | [[Dilated cardiomyopathy echocardiography|Echocardiography]] | [[Dilated cardiomyopathy other imaging findings|Other Imaging Findings]] | [[Dilated cardiomyopathy genetic testing|Genetic testing]] | [[Dilated cardiomyopathy other diagnostic studies|Other Diagnostic Studies]] |
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| ==Treatment== | | ==Treatment== |
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| | [[Dilated cardiomyopathy medical therapy|Medical Therapy]] | [[Dilated cardiomyopathy surgery|Surgery]] | [[Dilated cardiomyopathy primary prevention|Primary Prevention]] | [[Dilated cardiomyopathy secondary prevention|Secondary Prevention]] | [[Dilated cardiomyopathy cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Dilated cardiomyopathy future or investigational therapies|Future or Investigational Therapies]] |
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| In patients who have severe heart failure and are refractory to medical therapy cardiac transplantation may be an option (based upon patient characteristics such as age and comorbidities as well as disease characterisitics such as the etiology of dilated cardiomyopathy). As a bridge to cardiac transplantation multiple mechanical devices have been used. The most durable device is the LVAD (left ventricular assist device), certain patient populations not suitable for cardiac transplantation may also undergo LVAD placement by a cardiac surgeon as a "destination LVAD." This may be considered a palliative measure for end-stage heart failure patients. Other devices which may be more limited in the duration of use include the aortic balloon pump, Impella, and the PVAD (peripheral ventricular assist device) one of which is the Tandem Heart.
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| ===Implantable cardiac defibrillators in dilated cardiomyopathy===
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| Implantable cardiac defibrillators (ICDs) have also been extensively studied in systolic heart failure. A survival benefit has also been shown in select patient populations. ICDs are implanted in patients with systolic heart failure for primary prevention of sudden cardiac death. The AHA/ACC (American Heart Association/American College of Cardiology) class I indications for ICDs for primary prevention are: 1. EF < 35% due to prior MI, 40 days post MI, NYHA class II or III. 2. EF < 35% NYHA class II or III non ischemic dilated cardiomyopathy. 3. EF < 30%, prior MI, 40 days post MI, NYHA I. 4. EF < 40%, prior MI, NSVT and inducible VT/VF at EP study.
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| There are four major studies that have helped shape these indication for an ICD. The MADIT I evaluated NYHA class I to III heart failure patients with an EF < or = to 35%, with NSVT and inducible VT or VF on EP study and randomized 196 patients to ICD versus conventional medical therapy. The patients who received ICDs had improved survival at 5 years. 60% of patients received shocks by 2 years.<ref>N Engl J Med. 1996. Dec 355(26)</ref> The findings from this study are encompassed in the remaining three studies.
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| Madit II randomized 1232 patients who had a prior MI > 1 month prior to enrollment, an EF < or = to 30% to ICD or medical therapy and after a follow up of an average of 20 months there was a survival advantage in the ICD group. The number needed to treat was 18 patients. <ref>N Engl J Med. 2002. Mar 346(12)</ref>
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| MUSTT randomized 704 patients with an EF < or = to 40%, NSVT and inducible VT/VF at EP study to arrhythmia therapy (medications and ICDs) or no antiarrhythmia. At 5 years there was a 27 risk reduction in mortality in the antiarrhythmia group. The relative risk of mortality when comparing ICD vs. no ICD was 0.24. There was no difference in mortality in the antiarrhythmic medication vs. no antiarrthymic medication subgroups.<ref>N Engl J Med. 1999 Dec 341:1882-1890.</ref>
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| SCD-HeFT randomized 2521 patients with class II or III CHF and EF < or = to 35% (ischemic or non ischemic) to three arms: 1. conventional therapy, 2. conventional therapy plus amiodarone, and 3. conventional therapy plus an ICD. After a median follow up of 46 months there was a relative risk of death of 0.77 in the ICD arm. Findings were similar in the ischemic and non-ischemic subgroups.<ref>N Engl J Med. 2005. Jan 352(3).</ref>
| | ==Case Studies== |
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| NYHA class IV heart failure is a contraindication to ICD placement.
| | [[Dilated cardiomyopathy case study one|Case #1]] |
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| ==Related chapters== | | ==Related Chapters== |
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| * [[Cardiomyopathy]] | | * [[Cardiomyopathy]] |
| * [[Hypertrophic cardiomyopathy]] | | * [[Hypertrophic cardiomyopathy]] |
| | * [[Stress cardiomyopathy]] |
| | * [[Anticoagulation in patients with dilated cardiomyopathy]] |
| | * [[First degree AV block]] |
| | * [[Second degree AV block]] |
| | * [[Beriberi heart disease]] |
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| ==Resources==
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| * [http://www.cardiomyopathy.org/html/which_card_dcm.htm Cardiomyopathy Association: Dilated cardiomyopathy]
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| * [http://www.childrenscardiomyopathy.org Children's Cardiomyopathy Foundation]
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| ==References==
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| {{Reflist|2}}
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| {{clr}}
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| {{Circulatory system pathology}} | | {{Circulatory system pathology}} |
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| [[Category:Cardiomyopathy]] | | [[Category:Cardiomyopathy]] |
| [[Category:Cardiology]] | | [[Category:Cardiology]] |
| | | [[Category:Up-To-Date cardiology]] |
| | [[Category:Up-To-Date]] |
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