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http://dx.doi.org/10.1097/01.chi.0000138361.59594.90 | DOI Listing |
Front Immunol
February 2024
The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
J Cardiovasc Dev Dis
September 2023
Department of Cardiology, National Defense Medical College, Tokorozawa 359-8513, Japan.
A wide range of anti-myocardial autoantibodies have been reported since the 1970s. Among them, autoantibodies against the β-adrenergic receptor (βAR-AAb) have been the most thoroughly investigated, especially in dilated cardiomyopathy (DCM). ΒAR-Aabs have agonist effects inducing desensitization of βAR, cardiomyocyte apoptosis, and sustained calcium influx which lead to cardiac dysfunction and arrhythmias.
View Article and Find Full Text PDFBMC Cardiovasc Disord
June 2019
Department of Cardiology, Gansu Provincial Hospital, Lanzhou University, Lanzhou, 730000, People's Republic of China.
Background: Familial hypercholesterolemia (FH) can lead to premature coronary heart disease. Anticardiolipin antibody may be a contributor for thrombosis. Here, we report an adult with possible FH suffered from premature myocardial infarction that may be triggered by transient increased anticardiolipin antibody.
View Article and Find Full Text PDFRinsho Shinkeigaku
December 2016
Department of Neurology, Fukuoka University School of Medicine.
Objective: Myasthenia gravis (MG) is an immunological disorder of the neuromuscular junction, characterized by easy fatigability and weakness of the skeletal muscles. However, it has sometimes been reported that heart diseases including cardiomyopathies leading to sudden death have been observed in patients with MG. We studied the prevalence of electrocardiographic (ECG) abnormalities and heart disease in patients newly diagnosed with MG who had not received immunotherapy.
View Article and Find Full Text PDFAlthough genetic abnormalities play a pivotal role in the development of dilated cardiomyopathy (DCM), acquired infection and autoimmune abnormalities, or both, appear to be predominant underlying disorders. Of these, viral infection causes target organ damage via perforin produced by suppressor T cells. Thereafter, various antigens released from damaged myocytes are presented on the major histocompatibility complex II, which is expressed in antigen-presenting cells, resulting in activation of both cellular (Th1) and humoral (Th2) immunity.
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