The entire process of atherogenesis, including initiation, growth, and complication, can be seen as an inflammatory response to injury. Factors, such as cigarette smoking, hypertension, atherogenic lipoproteins, and hyperglycemia, are well-known contributors. However, the expanding scientific knowledge demonstrates that the interface of inflammation/cardiovascular disease extends further. In more recent years, the role of immune checkpoints has been identified in regulating atherosclerosis. Studies targeting PD-1 programmed death ligand 1, and CTLA-4 have shown that they act as critical negative regulators of atherosclerosis. These findings have consequences for approved therapies in certain indications. Moreover, events like myocardial ischemia and venous thromboembolism can be provoked during CAR-T cell therapy, further underscoring the connection between inflammation and cardiovascular risk. Changes in cardiac function, leading to heart failure and cardiogenic shock, can also be associated with CAR-T cell therapy, although not directly linked to a cytokine release syndrome.
Autoimmune diseases are also linked to increased cardiovascular morbidity and mortality. Conditions such as rheumatoid arthritis, and psoriasis, along with over 100 other known autoimmune diseases, collectively affecting 5–9% of the global population, also exhibit similar inflammatory mechanisms contributing to cardiovascular risk. Validated risk stratification tools tailored to these groups are still lacking, as well as tools to identify the residual inflammatory risk for secondary prevention.

The objective of this Research Topic is to assemble a comprehensive collection of papers aimed at discussing and identifying inflammatory pathways that elevate the risk of cardiovascular outcomes not only in patients with classic risk factors like diabetes but also in chronic-inflammatory conditions such as HIV, cancer, or autoimmune diseases. Additionally, we aim to explore innovative approaches for stratifying the risk in the latter group, recognizing that most available risk stratification tools were originally designed for the former group. Furthermore, this Research Topic seeks to encompass manuscripts addressing the assessment of inflammation-associated risk in secondary prevention, ranging from bioassays to state-of-the-art cardiovascular imaging techniques. By delving into these diverse methodologies, we hope to gain deeper insights into the mechanisms underlying inflammation-related cardiovascular complications. Lastly, we welcome papers focusing on the cardiovascular effects of immunomodulatory therapies, such as immune checkpoint inhibitors (ICIs) and chimeric antigen receptor (CAR)-T cell therapy. Additionally, investigations into drugs with inflammation-modulating properties, such as PCSK-9 inhibitors or GLP-1 agonists, are encouraged as they can shed light on potential novel strategies for managing inflammation-related cardiovascular risk.

We welcome the submission of manuscripts including, but not limited to, the following topics.
Special focus will be given (but is not restricted) to:
• Randomized clinical trials using novel drugs capable of attenuating residual inflammatory cardiovascular risk or describing mechanisms by which risk may be increased.
• Large observational studies aimed at identifying new inflammation-associated markers of cardiovascular disease progression.
• Experimental studies dedicated to investigating mechanisms involved in shared pathways between classic and novel risk factors, such as immune dysregulation, cytokine signaling, or endothelial dysfunction, and exploring how these mechanisms contribute to long-term cardiovascular complications.
• Observational studies that assess and propose risk stratification tools to address inflammation-driven risk in different population groups.

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Frontiers in Cardiovascular Medicine

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