The autoimmune basis of dilated cardiomyopathy. 1995

F Cetta, and V V Michels
Section of Pediatric Cardiology, Mayo Clinic, Rochester, MN 55905, USA.

Dilated cardiomyopathy is a form of heart disease characterized by ventricular dilatation and reduced systolic function. In most patients, dilated cardiomyopathy is a sporadic disease. However, 20% of dilated cardiomyopathy patients may have a familial form of the disease. The aetiologies of both the sporadic and familial forms of dilated cardiomyopathy are unknown in most cases. Dilated cardiomyopathy has a spectrum of clinical and subclinical presentations. During the last 10 years, there have been many investigations concerning the possible aetiologic role of immune factors in dilated cardiomyopathy. It is plausible that an antecedent viral infection initiates an immunological cascade which in turn leads to production of autoimmune antibodies resulting in dilated cardiomyopathy. However, in most dilated cardiomyopathy patients, an antecedent viral infection cannot be identified. Similarly, the trail of immunological research has diverged as different groups have identified distinct autoantibodies or other immune factors in heterogeneous subsets of dilated cardiomyopathy and control patients. In this manuscript, we review the studies which have contributed supportive and confounding evidence to the theoretical autoimmune basis of dilated cardiomyopathy.

UI MeSH Term Description Entries
D002311 Cardiomyopathy, Dilated A form of CARDIAC MUSCLE disease that is characterized by ventricular dilation, VENTRICULAR DYSFUNCTION, and HEART FAILURE. Risk factors include SMOKING; ALCOHOL DRINKING; HYPERTENSION; INFECTION; PREGNANCY; and mutations in the LMNA gene encoding LAMIN TYPE A, a NUCLEAR LAMINA protein. Cardiomyopathy, Congestive,Congestive Cardiomyopathy,Dilated Cardiomyopathy,Cardiomyopathy, Dilated, 1a,Cardiomyopathy, Dilated, Autosomal Recessive,Cardiomyopathy, Dilated, CMD1A,Cardiomyopathy, Dilated, LMNA,Cardiomyopathy, Dilated, With Conduction Defect 1,Cardiomyopathy, Dilated, with Conduction Deffect1,Cardiomyopathy, Familial Idiopathic,Cardiomyopathy, Idiopathic Dilated,Cardiomyopathies, Congestive,Cardiomyopathies, Dilated,Cardiomyopathies, Familial Idiopathic,Cardiomyopathies, Idiopathic Dilated,Congestive Cardiomyopathies,Dilated Cardiomyopathies,Dilated Cardiomyopathies, Idiopathic,Dilated Cardiomyopathy, Idiopathic,Familial Idiopathic Cardiomyopathies,Familial Idiopathic Cardiomyopathy,Idiopathic Cardiomyopathies, Familial,Idiopathic Cardiomyopathy, Familial,Idiopathic Dilated Cardiomyopathies,Idiopathic Dilated Cardiomyopathy
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D001323 Autoantibodies Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them. Autoantibody
D001327 Autoimmune Diseases Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides. Autoimmune Disease,Disease, Autoimmune,Diseases, Autoimmune
D015551 Autoimmunity Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES. Autoimmune Response,Autoimmune Responses,Autoimmunities

Related Publications

F Cetta, and V V Michels
December 2016, International journal of cardiology,
F Cetta, and V V Michels
April 2009, Circulation journal : official journal of the Japanese Circulation Society,
F Cetta, and V V Michels
January 1987, Kardiologia polska,
F Cetta, and V V Michels
January 1995, Journal of molecular and cellular cardiology,
F Cetta, and V V Michels
January 1994, Texas Heart Institute journal,
F Cetta, and V V Michels
February 1997, Trends in cardiovascular medicine,
F Cetta, and V V Michels
February 1992, Harefuah,
F Cetta, and V V Michels
February 2017, International journal of cardiology,
F Cetta, and V V Michels
December 2002, Herz,
F Cetta, and V V Michels
February 2002, Biochemical and biophysical research communications,
Copied contents to your clipboard!