(Circulation. 1996;93:841-842.)
© 1996 American Heart Association, Inc.
Articles |
Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies
Correspondence to W.J. McKenna, MD, Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, England.
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Introduction |
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 Top Introduction Definition and Classification Specific Cardiomyopathies References |
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A classification serves to bridge the gap between ignorance and knowledge.1 Previously the cardiomyopathies were defined as "heart muscle diseases of unknown cause" and were differentiated from specific heart muscle disease (of known cause).2 With increasing understanding of etiology and pathogenesis, the difference between cardiomyopathy and specific heart muscle disease has become indistinct. The original classification described three types, which have become established clinical entities, and this terminology has been preserved. The cardiomyopathies are now classified by the dominant pathophysiology or, if possible, by etiological/pathogenetic factors.
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Definition and Classification |
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TopIntroductionDefinition and Classification Specific Cardiomyopathies References |
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Cardiomyopathies are defined as diseases of the myocardium associated with cardiac dysfunction. They are classified as dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy.
Dilated Cardiomyopathy
Dilated cardiomyopathy is
characterized by
dilatation and impaired contraction of the left ventricle or both
ventricles. It may be idiopathic, familial/genetic,
viral3 4 5 and/or
immune,6 7 alcoholic/toxic,
or associated with recognized cardiovascular disease in
which the degree of myocardial dysfunction is not explained by the
abnormal loading conditions or the extent of ischemic damage
(see below). Histology is nonspecific. Presentation is
usually with heart failure, which is often progressive.
Arrhythmias, thromboembolism, and sudden death are common and
may occur at any stage.
Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy is
characterized
by left and/or right ventricular hypertrophy,
which is usually asymmetric and involves the
interventricular septum.8 Typically, the
left ventricular volume is normal or reduced.
Systolic gradients are common. Familial disease with autosomal
dominant inheritance predominates. Mutations in sarcomeric contractile
protein genes cause disease.9 Typical morphological
changes include myocyte hypertrophy and disarray
surrounding areas of increased loose connective tissue.
Arrhythmias and premature sudden death are
common.10
Restrictive Cardiomyopathy
Restrictive cardiomyopathy is
characterized by
restrictive filling and reduced diastolic volume of either
or both ventricles with normal or near-normal systolic
function and wall thickness. Increased interstitial
fibrosis may be present. It may be idiopathic or associated with
other disease (eg, amyloidosis; endomyocardial
disease with or without hypereosinophilia).
Arrhythmogenic Right Ventricular
Cardiomyopathy
Arrhythmogenic right ventricular
cardiomyopathy is characterized by progressive
fibrofatty replacement of right ventricular
myocardium, initially with typical regional and later
global right and some left ventricular involvement, with
relative sparing of the septum.11 Familial disease is
common, with autosomal dominant inheritance and incomplete penetrance;
a recessive form is described. Presentation with
arrhythmias and sudden death is common, particularly in the
young.12
Unclassified Cardiomyopathies
Unclassified cardiomyopathies
include a few
cases that do not fit readily into any group (eg, fibroelastosis,
noncompacted myocardium, systolic dysfunction with
minimal dilatation, mitochondrial involvement).
Some diseases may present with features of more than one type of cardiomyopathy (ie, amyloidosis, systemic hypertension). It is recognized that arrhythmias and conduction disease may be primary myocardial disorders. At this time, however, it was elected not to include them as cardiomyopathies.
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Specific Cardiomyopathies |
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TopIntroductionDefinition and Classification Specific Cardiomyopathies References |
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The term specific cardiomyopathies is now used to describe heart muscle diseases that are associated with specific cardiac or systemic disorders. These were previously defined as specific heart muscle diseases.
Ischemic cardiomyopathy presents as a dilated cardiomyopathy with impaired contractile performance not explained by the extent of coronary artery disease or ischemic damage.
Valvular cardiomyopathy presents with ventricular dysfunction that is out of proportion to the abnormal loading conditions.
Hypertensive cardiomyopathy often presents with left ventricular hypertrophy in association with features of dilated or restrictive cardiomyopathy with cardiac failure.
Inflammatory cardiomyopathy is defined by myocarditis in association with cardiac dysfunction. Myocarditis is an inflammatory disease of the myocardium and is diagnosed by established histological, immunological, and immunohistochemical criteria. Idiopathic, autoimmune, and infectious forms of inflammatory cardiomyopathy are recognized. Inflammatory myocardial disease is involved in the pathogenesis of dilated cardiomyopathy and other cardiomyopathies, eg, Chagas' disease, HIV, enterovirus, adenovirus, and cytomegalovirus.13
Metabolic cardiomyopathy includes the following categories: Endocrine, eg, thyrotoxicosis, hypothyroidism, adrenal cortical insufficiency, pheochromocytoma, acromegaly, and diabetes mellitus; familial storage disease and infiltrations, eg, hemochromatosis, glycogen storage disease, Hurler's syndrome, Refsum's syndrome, Niemann-Pick disease, Hand-Schüller-Christian disease, Fabry-Anderson disease, and Morquio-Ullrich disease; deficiency, eg, disturbances of potassium metabolism, magnesium deficiency, and nutritional disorders such as kwashiorkor, anemia, beri-beri, and selenium deficiency; amyloid, eg, primary, secondary, familial, and hereditary cardiac amyloidoses, familial Mediterranean fever, and senile amyloidosis.
General system disease includes connective tissue disorders, eg, systemic lupus erythematosus, polyarteritis nodosa, rheumatoid arthritis, scleroderma, and dermatomyositis. Infiltrations and granulomas include sarcoidosis and leukemia.
Muscular dystrophies include Duchenne, Becker-type, and myotonic dystrophies.
Neuromuscular disorders include Friedreich's ataxia, Noonan's syndrome, and lentiginosis.
Sensitivity and toxic reactions include reactions to alcohol, catecholamines, anthracyclines, irradiation, and miscellaneous. Alcoholic cardiomyopathy may be associated with a heavy alcohol intake. At present we cannot define a causal versus a conditioning role of alcohol or apply precise diagnostic criteria.
Peripartal cardiomyopathy may first manifest in the peripartum period. This is probably a heterogeneous group.
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Footnotes |
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P.Nordet,MD \
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References |
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TopIntroductionDefinition and Classification Specific Cardiomyopathies References |
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1. Goodwin JF. The frontiers of cardiomyopathy. Br Heart J. 1982;48:11-18.
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Why HJ, Meany BT, Richardson PJ, Olsen EG, Bowles NE,
Cunningham L, Freeke CA, Archard LC. Clinical and prognostic
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myocardium of patients with myocarditis or dilated
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9. Seidman CE, McKenna WJ, Watkins HC, Seidman JG. Molecular genetic approaches to diagnosis and management of hypertrophic cardiomyopathy. In: Braunwald E, ed. Heart Disease. A Textbook of Cardiovascular Medicine. New York, NY: WB Saunders Co, 1992:77-83.
10. Maron BJ, Bonow RO, Cannon RO, Leon MB, Epstein SE. Hypertrophic cardiomyopathy: interrelations of clinical manifestations, pathophysiology, and therapy: parts 1 and 2. N Engl J Med. 1987;316:780-789, 844-852. [Medline] [Order article via Infotrieve]
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J. B. Geske, P. Sorajja, R. A. Nishimura, and S. R. Ommen Evaluation of Left Ventricular Filling Pressures by Doppler Echocardiography in Patients With Hypertrophic Cardiomyopathy: Correlation With Direct Left Atrial Pressure Measurement at Cardiac Catheterization Circulation, December 4, 2007; 116(23): 2702 - 2708. [Abstract] [Full Text] [PDF]
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F. Tona, A. L.P. Caforio, and S. Iliceto Microvascular dysfunction in left apical ballooning syndrome: Primary cause or secondary phenomenon? Eur J Echocardiogr, December 1, 2007; 8(6): 411 - 412. [Full Text] [PDF]
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M. W. Hansen and N. Merchant MRI of Hypertrophic Cardiomyopathy: Part I, MRI Appearances Am. J. Roentgenol., December 1, 2007; 189(6): 1335 - 1343. [Abstract] [Full Text] [PDF]
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S. Sen-Chowdhry, P. Syrris, and W. J. McKenna Role of Genetic Analysis in the Management of Patients With Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy J. Am. Coll. Cardiol., November 6, 2007; 50(19): 1813 - 1821. [Abstract] [Full Text] [PDF]
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J. D. Dodd, G. Holmvang, U. Hoffmann, M. Ferencik, S. Abbara, T. J. Brady, and R. C. Cury Quantification of Left Ventricular Noncompaction and Trabecular Delayed Hyperenhancement with Cardiac MRI: Correlation with Clinical Severity Am. J. Roentgenol., October 1, 2007; 189(4): 974 - 980. [Abstract] [Full Text] [PDF]
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N. H. Robin, P. B. Tabereaux, R. Benza, and B. R. Korf Genetic Testing in Cardiovascular Disease J. Am. Coll. Cardiol., August 21, 2007; 50(8): 727 - 737. [Abstract] [Full Text] [PDF]
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M. Iacoviello, C. Forleo, P. Guida, R. Romito, A. Sorgente, S. Sorrentino, S. Catucci, F. Mastropasqua, and M. Pitzalis Ventricular Repolarization Dynamicity Provides Independent Prognostic Information Toward Major Arrhythmic Events in Patients With Idiopathic Dilated Cardiomyopathy J. Am. Coll. Cardiol., July 17, 2007; 50(3): 225 - 231. [Abstract] [Full Text] [PDF]
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T. Kubo, J. R. Gimeno, A. Bahl, U. Steffensen, M. Steffensen, E. Osman, R. Thaman, J. Mogensen, P. M. Elliott, Y. Doi, et al. Prevalence, Clinical Significance, and Genetic Basis of Hypertrophic Cardiomyopathy With Restrictive Phenotype J. Am. Coll. Cardiol., June 26, 2007; 49(25): 2419 - 2426. [Abstract] [Full Text] [PDF]
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A. L.P. Caforio, F. Calabrese, A. Angelini, F. Tona, A. Vinci, S. Bottaro, A. Ramondo, E. Carturan, S. Iliceto, G. Thiene, et al. A prospective study of biopsy-proven myocarditis: prognostic relevance of clinical and aetiopathogenetic features at diagnosis Eur. Heart J., June 1, 2007; 28(11): 1326 - 1333. [Abstract] [Full Text] [PDF]
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A. Nasermoaddeli, K. Miura, A. Matsumori, Y. Soyama, Y. Morikawa, A. Kitabatake, Y. Inaba, and H. Nakagawa Prognosis and prognostic factors in patients with hypertrophic cardiomyopathy in Japan: results from a nationwide study Heart, June 1, 2007; 93(6): 711 - 715. [Abstract] [Full Text] [PDF]
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C. J McMahon, R. H Pignatelli, S. F Nagueh, V.-V. Lee, W. Vaughn, S. O Valdes, J. P Kovalchin, J Lynn Jefferies, W. J Dreyer, S. W Denfield, et al. Left ventricular non-compaction cardiomyopathy in children: characterisation of clinical status using tissue Doppler-derived indices of left ventricular diastolic relaxation Heart, June 1, 2007; 93(6): 676 - 681. [Abstract] [Full Text] [PDF]
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J. Davis, H. Wen, T. Edwards, and J. M. Metzger Thin Filament Disinhibition by Restrictive Cardiomyopathy Mutant R193H Troponin I Induces Ca2+-Independent Mechanical Tone and Acute Myocyte Remodeling Circ. Res., May 25, 2007; 100(10): 1494 - 1502. [Abstract] [Full Text] [PDF]
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S. E. Petersen, M. Jerosch-Herold, L. E. Hudsmith, M. D. Robson, J. M. Francis, H. A. Doll, J. B. Selvanayagam, S. Neubauer, and H. Watkins Evidence for Microvascular Dysfunction in Hypertrophic Cardiomyopathy: New Insights From Multiparametric Magnetic Resonance Imaging Circulation, May 8, 2007; 115(18): 2418 - 2425. [Abstract] [Full Text] [PDF]
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C. Marcassa, R. Campini, E. Verna, L. Ceriani, and P. Giannuzzi Assessment of cardiac asynchrony by radionuclide phase analysis: Correlation with ventricular function in patients with narrow or prolonged QRS interval Eur J Heart Fail, May 1, 2007; 9(5): 484 - 490. [Abstract] [Full Text] [PDF]
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R. Macedo, K. Prakasa, C. Tichnell, F. Marcus, H. Calkins, J. A. C. Lima, and D. A. Bluemke Marked Lipomatous Infiltration of the Right Ventricle: MRI Findings in Relation to Arrhythmogenic Right Ventricular Dysplasia Am. J. Roentgenol., May 1, 2007; 188(5): W423 - W427. [Abstract] [Full Text] [PDF]
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A. Staudt, P. Eichler, C. Trimpert, S. B. Felix, and A. Greinacher Fc{gamma} Receptors IIa on Cardiomyocytes and Their Potential Functional Relevance in Dilated Cardiomyopathy J. Am. Coll. Cardiol., April 24, 2007; 49(16): 1684 - 1692. [Abstract] [Full Text] [PDF]
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A. L.P. Caforio, N. G. Mahon, M. K. Baig, F. Tona, R. T. Murphy, P. M. Elliott, and W. J. McKenna Prospective Familial Assessment in Dilated Cardiomyopathy: Cardiac Autoantibodies Predict Disease Development in Asymptomatic Relatives Circulation, January 2, 2007; 115(1): 76 - 83. [Abstract] [Full Text] [PDF]
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A. Perrot, R. Dietz, and K. J. Osterziel Is there a common genetic basis for all familial cardiomyopathies? Eur J Heart Fail, January 1, 2007; 9(1): 4 - 6. [Full Text] [PDF]
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M. Medin, M. Hermida-Prieto, L. Monserrat, R. Laredo, J. C. Rodriguez-Rey, X. Fernandez, and A. Castro-Beiras Mutational screening of phospholamban gene in hypertrophic and idiopathic dilated cardiomyopathy and functional study of the PLN -42 C>G mutation Eur J Heart Fail, January 1, 2007; 9(1): 37 - 43. [Abstract] [Full Text] [PDF]
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P. Alter and B. Maisch Non-compaction cardiomyopathy in an adult with hereditary spherocytosis Eur J Heart Fail, January 1, 2007; 9(1): 98 - 99. [Abstract] [Full Text] [PDF]
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