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Patient immune response could potentially prevent heart failure

Antibodies were found in plasma and heart muscle of end-stage heart failure patients

Heart Failure


 

Vienna, Austria – 22 April 2018: Patients’ own immune response has the potential to prevent the development and progression of heart failure, according to research presented today at Frontiers in CardioVascular Biology (FCVB) 2018, a European Society of Cardiology congress(1). The study found antibodies in the plasma and heart muscle of end-stage heart failure patients.

“The role of the immune response in the development of heart failure is unknown,” said Patricia van den Hoogen, a PhD student at the University Medical Centre Utrecht / Netherlands Heart Institute in Utrecht, the Netherlands. “We investigated the immune response in patients with end-stage heart failure to see if this might be a new target for treatment.”

This study looked at whether patients with end-stage heart failure show signs of inflammation. After a heart attack, inflammation, which is the body’s normal immune response to injury, clears dead cells and other resulting debris. Heart attacks damage the heart muscle and may eventually lead to heart failure, which is a progressive disease. For patients with end-stage heart failure, heart transplantation may be the only treatment option.

The study included 20 patients with end-stage heart failure and three healthy controls. Heart failure was caused by ischaemic heart disease (heart attack) in ten patients and by dilated cardiomyopathy in ten patients.

The researchers analysed heart tissue and plasma samples to see which antibodies and other immune cells were present. Next they tested the samples with different epitopes to see if they could find the targets of the antibodies.

The investigators found increased levels of antibodies in the heart and plasma of end-stage heart failure patients compared to healthy controls .Interestingly, antibody levels were higher in patients with ischaemic heart failure compared to those with dilated heart failure.

Levels of other types of immune cells, including T cells, B cells, and macrophages, were significantly higher in the heart tissue of heart failure patients compared to healthy controls. In the plasma, heart failure patients had different types of B cells than healthy controls. Specifically, heart failure patients had more plasma B cells, which produce antibodies, and fewer regulatory B cells, which are immunosuppressive.

The epitope screening to identify antibody targets is ongoing. Based on their initial results, the researchers have selected 200 epitopes for follow-up studies.

Ms van den Hoogen said: “We observed more inflammation in patients with end-stage heart failure than in healthy people. Heart failure patients had higher levels of antibodies, and more of the cells that produce antibodies. This suggests that the inflammatory response is activated and might play an important role in heart failure.”

“These patients were in the final stage of heart failure,” she added. “In future studies we will investigate whether there is an inflammatory response in the early phase of heart failure, and whether the response becomes more pronounced as heart failure worsens.”

She concluded: “We now know there is an inflammatory response in patients with end-stage heart failure. This paves the way for creating new therapies to prevent the development or progression of heart failure by targeting the immune response. If we identify the targets of the antibodies through our epitope screening, personalised treatments could be designed.”

ENDS

Notes to editor

Authors: ESC Press Office

Tel: +33 (0)4 89 87 24 83 

Mob: +33 (0)6 24 71 28 96
Email: press@escardio.org

 

 

SOURCES OF FUNDING:  We acknowledge the support from Innovation and the Netherlands CardioVascular Research Initiative (CVON): The Dutch Heart Foundation, Dutch Federation of University Medical Centers, the Netherlands Organization for Health Research and Development, and the Royal Netherlands Academy of Science. Additionally, the ZonMW Translational Adult Stem Cell grant 1161002016, grant of the PLN foundation and Horizon2020 ERC-2016-COG EVICARE (725229).

 

DISCLOSURES: None.

 

References and notes

(1) The abstract ‘The potential pathological role of cardiac autoantibodies in the development of heart failure’ will be presented during the Poster session: Basic Science – Cardiac Diseases which takes place on 22 April from 08:30 to 16:30 CEST in the Poster Area.

 

 

 

About Frontiers in CardioVascular Biology

Frontiers in CardioVascular Biology (FCVB) is a comprehensive basic science conference organised every two years by the ESC Council on Basic Cardiovascular Science, whose mission is to enhance the importance of basic science to clinical cardiology. FCVB is organised in collaboration with 12 European cardiovascular science societies.


About the European Society of Cardiology

The European Society of Cardiology brings together health care professionals from more than 150 countries, working to advance cardiovascular medicine and help people lead longer, healthier lives.

 

Information for journalists attending FCVB 2018

FCVB 2018 will be held from 20 to 22 April at the Austria Centre Vienna in Vienna, Austria. The full scientific programme is available here

  • To register on-site please bring avalid press card or appropriate letter of assignment with proof of three recent published articles (cardiology or health-related, or referring to a previous ESC Event).
  • Press registration is not available to industry or its public relations representatives, event management, marketing or communications representatives.