Immunosuppressive Therapy for Heart Failure

Wojnicz, Romuald

doi:10.1016/j.hfc.2005.06.009

Cited by 1 publication

(2 citation statements)

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“…[14][15][16][17][18] Conversely, general inhibition of the immune response by corticosteroids or intravenous immunoglobulin (IVIG) administration showed no effect on mortality in HF patients compared with conventional treatment. [19][20][21][22][23] These previous observations suggest a pathogenic role of a specific antibody-mediated immune response. In line with this hypothesis, deposits of antibodies (mainly IgG1 and IgG3) in the myocardium of HF patients have been observed.…”

Section: Introductionmentioning

confidence: 75%

“…Clinical trials targeting the chronic pro‐inflammatory response by immuno‐adsorption showed beneficial effects on mortality in patients with DCM as clearance of all four immunoglobulin G (IgG) subclasses improved cardiac performance . Conversely, general inhibition of the immune response by corticosteroids or intravenous immunoglobulin (IVIG) administration showed no effect on mortality in HF patients compared with conventional treatment . These previous observations suggest a pathogenic role of a specific antibody‐mediated immune response.…”

Section: Introductionmentioning

confidence: 99%

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Increased circulating IgG levels, myocardial immune cells and IgG deposits support a role for an immune response in pre‐ and end‐stage heart failure

Hoogen

Jager

Huibers

et al. 2019

J Cellular Molecular Medi

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The chronic inflammatory response plays an important role in adverse cardiac remodelling and the development of heart failure (HF). There is also evidence that in the pathogenesis of several cardiovascular diseases, chronic inflammation is accompanied by antibody and complement deposits in the heart, suggestive of a true autoimmune response. However, the role of antibody‐mediated immune responses in HF progression is less clear. We assessed whether immune cell infiltration and immunoglobulin levels are associated with HF type and disease stage, taking sex differences into account. We found IgG deposits and increased infiltration of immune cells in the affected myocardium of patients with end‐stage HF with reduced ejection fraction (HFrEF, n = 20). Circulating levels of IgG1 and IgG3 were elevated in these patients. Furthermore, the percentage of transitional/regulatory B cells was decreased (from 6.9% to 2.4%) compared with healthy controls (n = 5). Similarly, increased levels of circulating IgG1 and IgG3 were observed in men with left ventricular diastolic dysfunction (LVDD, n = 5), possibly an early stage of HF with preserved EF (HFpEF). In conclusion, IgG deposits and infiltrates of immune cells are present in end‐stage HFrEF. In addition, both LVDD patients and end‐stage HFrEF patients show elevated levels of circulating IgG1 and IgG3, suggesting an antibody‐mediated immune response upon cardiac remodelling, which in the early phase of remodelling appear to differ between men and women. These immunoglobulin subclasses might be used as marker for pre‐stage HF and its progression. Future identification of auto‐antigens might open possibilities for new therapeutic interventions.

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