Dear Members, Colleagues, and Friends,
We hope this first newsletter of 2025 finds you well and off to a great start!
As we step into a promising new year, we want to thank you for your continued dedication and enthusiasm. Together, we achieved remarkable milestones in 2024, and we’re excited to embark on another productive journey in 2025. This newsletter outlines our shared vision for the year ahead, along with opportunities to grow and contribute to our vibrant community.
Our Goals for 2025
Through our programmes, grants and partnerships, we work to elevate early career success. As we set out into a year of growth, we wanted to share some of our short- and long-term goals with you.
Expand Membership and Engagement: We aim to welcome more professionals, women and young researchers, diversifying and strengthening our Working Group on Coronary Pathophysiology and Microcirculation. Being a member enhances your scientific and clinical impact while fostering collaborations and a sense of belonging. Membership is free, and valid for one year, but you can set it to auto-renew so you don’t have to worry about losing it or reapplying later. Join today and be part of this rewarding community!
Early-Career Support: We continue to prioritise early-career development through programmes like the Mobility Travel Grants and the ESC Abstract Award — stay tuned for application details!
Enhance Knowledge Sharing: Our Working Group Talks and panel discussions will facilitate innovation and disseminate cutting-edge research — more updates coming soon.
We would like to draw your attention to the upcoming meetings, abstract submission deadlines and awards:
ESC Congress 2025 together with World Congress of Cardiology, Madrid & Online will run from 29 August - 1 September. This year’s deadline for submitting Abstracts is Saturday, 1 March 12:00 noon CET, for Clinical Cases 7 March, and from 26 March to 6 June for Late-Breaking Science.
Featured Commentary. In this issue, Prof. Daphne Merkus provides insights on the paper “[SGLT2 expression in human vasculature and heart correlates with low-grade inflammation and causes eNOS-NO/ROS imbalance]”, which offers novel perspectives on SGLT2 inhibitors and potential role of oxidative stress in INOCA. Presence of SGLT2 was observed in the endothelium of the thoracic aorta and in the coronary microcirculation as well as in cardiomyocytes. Inflammation and oxidative stress are key components of coronary microvascular dysfunction and INOCA. Interestingly, higher expression of SGLT2 was associated with increased oxidative stress. Read the full commentary here
You are the heart of our community, and your contributions make everything possible. We look forward to engaging with you through our activities and initiatives throughout the year!
Edina Cenko, Chairperson 2024-2026
Ines Drenjančević, Communication Coordinator
Our mission: To reduce the burden of cardiovascular disease.