Scientists at the University of Augsburg have discovered a particularly active subgroup of blood platelets that may cause heart attacks in people with coronary heart disease despite drug therapy. This discovery may open up new prospects for customized therapies. The research results are published in the European Heart Journal and were presented on August 31 at Europe’s largest cardiology congress.
Despite modern medication, many people with coronary heart disease continue to suffer heart attacks. A research team from the University of Augsburg, together with colleagues from Munich and Milan, has now found a possible explanation for this and has also provided a very promising therapeutic approach.
Their work focused on so-called “reticulated platelets”: particularly young, RNA-rich and reactive thrombocytes. “We have discovered that they play a central role in the formation of blood clots in patients with coronary heart disease,” explains Prof. Dr. Dario Bongiovanni, Professor at the Faculty of Medicine and Head of the Study Center of the First Medical Clinic at Augsburg University Hospital.
“In our work, we were able to comprehensively characterize the biological mechanisms of these cells for the first time. This allows us to explain why these platelets remain overactive in many patients even under optimal therapy,” continues Bongiovanni. The reason is that these young platelets have a particularly large number of activating signaling pathways that make them more sensitive and reactive than mature platelets.
Coronary heart disease (CHD) is the most common heart disease worldwide. It occurs when the coronary arteries narrow due to buildup of fatty deposits and the heart is no longer supplied with sufficient oxygen. The consequences can be chest pain, heart attack or sudden cardiac death.
The results come from a multidimensional, using various methods, analysis of the blood of over 90 patients with coronary heart disease. Among other things, the researchers found signaling pathways that can be used to specifically inhibit the activity of such blood cells, in particular two target structures called GPVI and PI3K. Initial laboratory experiments confirmed that inhibiting these signaling pathways can reduce platelet hyperactivity.
“Our results could pave the way for personalized platelet inhibition, i.e. tailored therapies that are adapted to the individual characteristics of a patient’s platelets,” emphasizes Bongiovanni.
The study was presented at the ESC Congress 2025 on August 31 in Madrid, Spain.
More information:
Kilian Kirmes et al, Reticulated platelets in coronary artery disease: a multidimensional approach unveils prothrombotic signalling and novel therapeutic targets, European Heart Journal (2025). DOI: 10.1093/eurheartj/ehaf694
The content is provided for information purposes only.