Inflammatory dilated cardiomyopathy

Maisch, Bernhard; Pankuweit, Sabine

doi:10.1007/s00059-020-04900-8

Cited by 26 publications

(9 citation statements)

References 77 publications

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“…To test the hypothesis that circulating c-Met + memory T cells mark the presence of myocardial inflammation, we first assessed their presence in the peripheral blood of patients presenting with presumed myocardial infarction but were subsequently diagnosed with AM as a cause of their acute myocardial injury. Additional groups included patients with apparently idiopathic DCM, often associated with cardiac inflammation 21 : patients with first-time STEMI for whom acute myocardial injury is a manifestation of coronary atherosclerosis in which inflammation localizes to the arteries but not the heart 22 ; patients undergoing elective cardiac surgery but with no evidence of inflammation; patients with IHF; and HCs. A cohort of patients with active Sjögren syndrome, a noncardiac autoimmune condition, was also included as a control.…”

Section: Resultsmentioning

confidence: 99%

Circulating c-Met–Expressing Memory T Cells Define Cardiac Autoimmunity

et al. 2022

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BACKGROUND: Autoimmunity is increasingly recognized as a key contributing factor in heart muscle diseases. The functional features of cardiac autoimmunity in humans remain undefined because of the challenge of studying immune responses in situ. We previously described a subset of c-mesenchymal epithelial transition factor (c-Met)–expressing (c-Met + ) memory T lymphocytes that preferentially migrate to cardiac tissue in mice and humans. METHODS: In-depth phenotyping of peripheral blood T cells, including c-Met + T cells, was undertaken in groups of patients with inflammatory and noninflammatory cardiomyopathies, patients with noncardiac autoimmunity, and healthy controls. Validation studies were carried out using human cardiac tissue and in an experimental model of cardiac inflammation. RESULTS: We show that c-Met + T cells are selectively increased in the circulation and in the myocardium of patients with inflammatory cardiomyopathies. The phenotype and function of c-Met + T cells are distinct from those of c-Met–negative (c-Met − ) T cells, including preferential proliferation to cardiac myosin and coproduction of multiple cytokines (interleukin-4, interleukin-17, and interleukin-22). Furthermore, circulating c-Met + T cell subpopulations in different heart muscle diseases identify distinct and overlapping mechanisms of heart inflammation. In experimental autoimmune myocarditis, elevations in autoantigen-specific c-Met + T cells in peripheral blood mark the loss of immune tolerance to the heart. Disease development can be halted by pharmacologic c-Met inhibition, indicating a causative role for c-Met + T cells. CONCLUSIONS: Our study demonstrates that the detection of circulating c-Met + T cells may have use in the diagnosis and monitoring of adaptive cardiac inflammation and definition of new targets for therapeutic intervention when cardiac autoimmunity causes or contributes to progressive cardiac injury.

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Section: Resultsmentioning

confidence: 99%

Circulating c-Met–Expressing Memory T Cells Define Cardiac Autoimmunity

et al. 2022

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“…In these individuals, if viruses are detected, the suggested description is inflammatory viral cardiomyopathy , but in the absence of inflammation, the disease process is described as viral cardiomyopathy. 65 …”

Section: Cardiac Autoimmunity In Viral Myocarditismentioning

confidence: 99%

The knowns and unknowns of cardiac autoimmunity in viral myocarditis

Mone,

Reddy

2023

Reviews in Medical Virology

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Myocarditis can result from various infectious and non‐infectious causes that can lead to dilated cardiomyopathy (DCM) and heart failure. Among the infectious causes, viruses are commonly suspected. But the challenge is our inability to demonstrate infectious viral particles during clinical presentations, partly because by that point, the viruses would have damaged the tissues and be cleared by the immune system. Therefore, viral signatures such as viral nucleic acids and virus‐reactive antibodies may be the only readouts pointing to viruses as potential primary triggers of DCM. Thus, it becomes hard to explain persistent inflammatory infiltrates that might occur in individuals affected with chronic myocarditis/DCM manifesting myocardial dysfunctions. In these circumstances, autoimmunity is suspected, and antibodies to various autoantigens have been demonstrated, suggesting that immune therapies to suppress the autoimmune responses may be necessary. From this perspective, we endeavoured to determine whether or not the known viral causes are associated with development of autoimmune responses to cardiac antigens that include both cardiotropic and non‐cardiotropic viruses. If so, what their nature and significance are in developing chronic myocarditis resulting from viruses as primary triggers.

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“…Brazilian Journal of Development, Curitiba, v.9, n.4, p. 12705-12720, apr., 2023 Em relação às causas da CMD, podemos dividi-las entre adquiridas ou genéticas, embora em alguns casos essas podem se sobrepor. Causas genéticas estão relacionadas a mutações em aproximadamente 40 genes.…”

Section: Etiologia E Fisiopatologiaunclassified

“…Além disso, alguns achados ecocardiográficos também desempenham um papel fundamental para ajudar na diferenciação entre uma forma idiopática aparente de RCM de formas secundárias, como na doença cardíaca sarcóide, síndrome hipereosinofílica, cardiomiopatia diabética, entre outras. Além de fornecer dados adicionais para distinção com pericardite constritiva (MAISCH; PANKUWEIT, 2020, CIARAMBINO et al, 2021, FAGGIANO et al, 2021, MUHAMMED et al, 2022.…”

Section: Diagnósticounclassified

Cardiomiopatia dilatada: aspectos epidemiológicos, fisiopatológicos e manejo terapêutico

Duarte¹,

Rodrigues²,

Bothrel³

et al. 2023

Braz. J. Develop.

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A Cardiomiopatia Dilatada (CMD) é uma doença cardíaca caracterizada pela dilatação do coração e diminuição da função contrátil, que pode levar a insuficiência cardíaca e morte súbita. A fisiopatologia da CMD envolve um processo de remodelação ventricular que leva à dilatação e enfraquecimento do músculo cardíaco. Múltiplos fatores, como estresse oxidativo, inflamação, disfunção mitocondrial e alterações no citoesqueleto celular, contribuem para essa remodelação ventricular. Quanto à epidemiologia, trata-se de uma doença rara, que afeta principalmente homens na terceira e quarta década de vida. Em crianças, a maior incidência ocorre em menores de 12 meses, com uma prevalência de 0,57 a cada 100.000 crianças e é mais comum em meninos. A prevalência da doença varia em diferentes países e populações, havendo uma predisposição genética para o desenvolvimento da CMD. O diagnóstico da CMD envolve avaliação clínica, exames laboratoriais, eletrocardiograma, ecocardiograma e ressonância magnética cardíaca. Já a abordagem terapêutica tem como objetivo controlar os sintomas, melhorar a função cardíaca e reduzir o risco de morte súbita. O manejo terapêutico inclui o uso de medicamentos como inibidores da enzima conversora de angiotensina, betabloqueadores e diuréticos, além de intervenções não medicamentosas, como restrição de sal, controle do peso, exercícios físicos supervisionados e nos casos mais graves o implante de um desfibrilador cardíaco ou transplante cardíaco. O prognóstico da CMD melhorou significativamente nos últimos anos com tratamentos farmacológicos, não farmacológicos e diagnósticos precoces por meio de pesquisas familiares. Assim, o acompanhamento regular com um cardiologista e a adesão ao tratamento são essenciais para o controle da doença e melhora da qualidade de vida do paciente.

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Inflammatory dilated cardiomyopathy

Cited by 26 publications

References 77 publications

Circulating c-Met–Expressing Memory T Cells Define Cardiac Autoimmunity

Circulating c-Met–Expressing Memory T Cells Define Cardiac Autoimmunity

The knowns and unknowns of cardiac autoimmunity in viral myocarditis

Cardiomiopatia dilatada: aspectos epidemiológicos, fisiopatológicos e manejo terapêutico

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