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Disturbed protective mechanism makes heart susceptible to dangerous arrhythmias, as Freiburg heart researchers demonstrate. New therapeutic targets for sudden cardiac death discovered.
It never rains but it pours: Many people who have suffered a heart attack subsequently develop life-threatening complications like ventricular fibrillation. Now an international research team from the University of Freiburg’s Faculty of Medicine and Dalhousie University Halifax in Canada have found out why this is the case. In a study published on 2 June 2025 in Circulation Research, the researchers demonstrate that a natural mechanism that protects healthy hearts from mechanically induced arrhythmias collapses during a heart attack – with dangerous consequences. The researchers describe this mechanism for the first time on the basis of an animal model and show initial points of departure for possible therapies.
‘Electrical and mechanical relaxation of the heart after a heartbeat are closely coupled. This coupling is disturbed during a heart attack, which can lead to cardiac arrhythmias. As a result, the heart does not fill up properly and pumps too little blood’, says co-study leader Prof. Dr. Peter Kohl, director of the Institute for Experimental Cardiovascular Medicine at the University Heart Center of the Medical Center – University of Freiburg and a member of the University of Freiburg’s Faculty of Medicine. Kohl is also spokesperson of collaborative research centre 1425, ‘Make Better Scars’, which studies scar formation in the heart. The study was conducted in collaboration with a team led by Prof. Dr. Alex Quinn from the Department of Physiology and Biophysics at Dalhousie University. ‘Our studies explain for the first time why mechanically induced cardiac arrhythmias can appear after a heart attack – in a time window that was previously regarded as “protected”,’ The researchers call the newly described connection repolarization-relaxation coupling.
New therapeutic targets
The team was able to demonstrate at the molecular level what is responsible for the disturbance. As a result of the heart attack, the duration of electrical excitation shortens to such an extent that the mechanical processes cannot follow it. An unexpected additional strain in this phase – caused, for example, by uneven contractions – can trigger electrical misfires.
Fortunately, the team also identified potential therapeutic targets. The blocking of particular ion channels, the buffering of calcium, or the reduction of oxygen radicals reduced the development of arrhythmias in the laboratory experiments. ‘This knowledge can now help us to develop new medications that lower the risk of dangerous arrhythmias after a heart attack’, explains the lead author, Dr. Breanne A. Cameron, who researches at both locations. As the previous experiments were conducted on rabbit hearts and animal cells, the team is now planning studies on larger animal models and targeted testing of appropriate active agents as their next step.
Original title of the publication:
Disturbed repolarization-relaxation coupling during acute myocardial ischaemia permits systolic mechano-arrhythmogenesis
DOI: 10.1161/CIRCRESAHA.124.326057
Link to the study: https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.124.326057
https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.124.326057
Every heart is different – and yet the mechanisms involved in the relaxation of the heart are simila ...
Quinn & Kohl
Medical Center – University of Freiburg
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Every heart is different – and yet the mechanisms involved in the relaxation of the heart are simila ...
Quinn & Kohl
Medical Center – University of Freiburg
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