BMC Cardiovascular Disorders was delighted to attend the 2024 European Society of Cardiology (ESC) Congress in London, where over 31,800 cardiovascular professionals gathered to explore the latest research and build connections. Focusing on 'Personalising Cardiovascular Care', the bustling event featured 12 hotline sessions introducing the primary endpoints of 38 novel clinical trials, 26 late-breaking science sessions, interactive ESC guideline sessions, numerous poster presentations and 378 clinical cases. In a record-breaking year, 4,451 abstracts were presented by 3700 presenters from 92 countries.
In an introductory video, ESC Program Chair John McMurray celebrated a significant milestone — women now make up 50% of the faculty. In another stride to support the professional development of women, the ESC partnered with the 'Women As One' network to launch RISE, an annual conference initiated in 2023 to ‘Regroup, Inspire, Strengthen and Energize’ women in cardiology. RISE @ ESC Congress 2024 included insightful discussions led by experts in cardiology and business, designed to facilitate the elevation of women cardiologists into leadership roles.
Here, Editor Jennifer Harman of BMC Cardiovascular Disorders shares her highlights.
Women and cardiovascular disease: addressing the gender gap
One of the challenges which accompanies an event such as the ESC Congress is choosing which presentations to attend, especially when you're an editor of a journal with such a broad scope like BMC Cardiovascular Disorders. While I inevitably missed some great talks, I was fortunate to attend several thought-provoking sessions across various disciplines. With the efforts of the ESC to support women cardiologists in my mind, I was attracted to a number of sessions discussing the latest research on cardiovascular disease (CVD) in women. The Congress hosted five ePoster sessions on the topic, with eight abstracts each. It was fantastic to see so much research on the topic to help bridge the gender gap in cardiovascular research as advocated by the ESC.
Endometriosis is a prevalent chronic gynaecological disease affecting 1 in 10 women, which can lead to systemic inflammation - a risk factor for CVD. Therefore, Dr. Eva Havers-Borgersen explored whether there is an association between endometriosis and cardiovascular events. The retrospective Danish nationwide cohort study of almost 300,000 women found that women with endometriosis face a 20% greater associated risk of acute myocardial infarction or ischemic stroke compared to those without the disease. The study, recently published in the European Heart Journal, highlights that sex-specific risk factors, such as endometriosis, should be considered for inclusion in cardiovascular risk prediction models. Dr Eva Havers-Borgersen commented,"Future studies are needed to examine the exact underlying mechanism driving this association. However, endometriosis is known to be linked to chronic systemic inflammation with oxidative stress, endothelial dysfunction, and a pro-atherogenic lipid profile - factors which may affect the risk of CVD."
When I asked Dr Eva Havers-Borgersen what was her most memorable experience at the ESC Congress, she said, "What I was most excited about was the number of brilliant women presenting their research and especially the number of studies on women - but I do hope that someday, there won't be a need for specific sessions labelled as "special populations" for women, and instead, that studies on women will be a natural part of the studies overall."
Another highlight from these scientific sessions was a presentation by Dr Elizabeth Paratz (St Vincent's Institute of Medical Research, Auatralia). Dr Paratz presented her work on "Sex disparities in bystander defibrillation for out-of-hospital cardiac arrest", which examined the role of bystanders in more than 32,500 out-of-hospital cardiac arrests using data from 2002 – 2021 from the Victorian Ambulance Cardiac Arrest Registry. It found that women who have a cardiac arrest in Victoria, Australia, are only half as likely as men to receive defibrillation from a bystander. Studies such as those carried out by Eva and Elizabeth are needed to ensure that risk factors and symptoms of CVD in women are recognised and reported.
Dr Paratz commented "This year, I have been fortunate enough to be presenting a lot of research, and I have loved the period immediately after where there is extreme enthusiasm from future collaborators, discussion of how our research might fit into future projects and the design of the next collaboration. Everyone here is so passionate about high-quality research and the next project."
Clonal hematopoiesis as an emerging risk factor of atherosclerosis
I enjoyed rekindling my former research interests learning about clonal hematopoiesis as a risk factor for atherosclerotic CVD via several experts in the field, including Professor Jose Javier Fuster (Spanish National Centre for Cardiovascular Research).
Clonal hematopoiesis of indeterminate potential (CHIP) is driven by acquired somatic mutations in hematopoietic stem and progenitor cells, leading to a significant proportion of mutant immune cells that may influence inflammatory responses central to CVD. Studies in humans and mouse models have shown that multiple CHIP-associated genes contribute to atherosclerosis. At the "Emerging risk factors in CVD" session, Fuster introduced two new research articles from his group on the topic that were published simultaneously with his presentation.
Fuster explained that inactivating mutations in TET2, a transcriptional regulator, are frequent in clonal hematopoiesis. Previous studies using atherosclerosis-prone, transgenic mice found that bone marrow reconstitution with TET2-deficient cells was sufficient for their clonal expansion and increased atherosclerotic plaque size. Further mechanistic studies showed that this accelerated atherosclerosis may be due to the exacerbated production of IL-1β by TET2-deficient mutant macrophages. IL-1β stimulation of many different types of cells in arteries increases the expression level of inflammation-responsive genes associated with atherosclerotic CVD.
In humans, evidence suggesting that TET2 mutations cause atherosclerosis came from a post hoc analysis of the CANTOS trial led by Eric Svensson (Novartis Institutes for BioMedical Research), published in JAMA Cardiology. CANTOS importantly found that Canakinumab, a therapeutic monoclonal antibody targeting IL-1β, led to a significantly lower rate of recurrent cardiovascular events than placebo. The post hoc analysis showed a 9-fold greater response to Canakinumab in TET2 mutation carriers.
In view of Canakinumab's high cost and numerous side effects, Fuster and colleagues investigated the use of the more affordable and accessible drug Colchicine, publishing their findings in the European Heart Journal. Studies have shown that Colchicine inhibits IL-1β induced inflammatory responses. The drug is approved or recommended by a number of regulatory bodies, including the FDA, for secondary CVD prevention in high-risk patients with atherosclerosis.
Experiments using mice found that Colchicine doesn't affect the expansion of TET2 mutant cells, but it suppresses the increased production of IL-1β, suppressing accelerated atherosclerosis. In line with these findings, analysis of 37,181 Mass General Brigham Biobank patients and 437,236 UK Biobank participants revealed that a history of Colchicine treatment is associated with a substantial attenuation of the effect of TET2 mutations on myocardial infarction risk.
Researchers have argued that developing prospective clinical trials does not make sense if CHIP is a symptom rather than a cause of atherosclerosis. To resolve this debate, Fuster and his team conducted a longitudinal study using data from the PESA study, publishing their findings in Nature Medicine. PESA (Progression of Early Subclinical Atherosclerosis) is a prospective longitudinal study of approximately 4000 apparently healthy middle-aged participants. The participants have undergone periodic examinations using various noninvasive imaging techniques since 2010 to detect the presence and progression of asymptomatic atherosclerosis. The researchers used high-sensitivity DNA sequencing technology to detect somatic mutations in blood samples from these patients and assessed the presence and progression of atherosclerosis using the imaging data. Interesting, the results demonstrate that participants who had somatic mutations linked to CHIP at the start of the study were more likely to develop atherosclerosis in the following years. However, the presence and extent of atherosclerosis did not influence the expansion of mutant blood cells. These findings suggest there is a unidirectional association of clonal hematopoiesis with atherosclerosis development, supporting the need for further research to develop personalised therapeutic strategies for managing the risk of atherosclerotic CVD.
When I asked Professor Fuster what his most memorable moment was, he said "Celebrating these two new publications with colleagues and the very positive feed-back that we got during the conference were probably the most memorable experiences during the ESC congress. It was great to learn about how our work will help others working on clonal hematopoiesis and CVD."
Recently, BMC Cardiovascular Disorders published an article Collection showcasing research on the role of immunity and inflammation in cardiovascular disorders. To read open-access research on the topic, visit: https://www.biomedcentral.com/collections/IICD.
Thanks to an exceptional and diverse programme, it is impossible to mention all of the highlights. The extensive material from the Congress will be available online on ESC 365 with unlimited year-long access for FESC and ESC Professional Members. BMC Cardiovascular Disorders eagerly anticipates the 2025 event, which will be held in Madrid.
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