Cardiovascular disease (CVD) accounts for more deaths in women than breast cancer, lung cancer and chronic lung disease combined, with a comparable mortality to that of men. Many women and physicians do not identify CVD as a major morbidity and mortality in women, resulting in significant delays in diagnosis and treatment. While advances have been made in the diagnosis, treatment and outcomes of CVD in women, there often remains insufficient evidence to guide effective, lifesaving care of women. This review of sex-specific and traditional CVD risk and risk-enhancing factors in women identifies areas of knowledge gaps to consider for investigation. A focus on the coronary vasculature reveals physiological differences of clinical relevance which can be interrogated. Inspection of and addressing disadvantage and gender bias in both the medical and lay communities should continue to be addressed. As CVD results from traditional risk factors and emerging risk-enhancing factors, a focus on the detection of preclinical cardiovascular disease may be of particular importance for women. Unique risk markers originate early in pre-menopausal women, as this is considered a healthy period of life. Awareness and implementation of the existing knowledge of sex-specific risk factors and sex-specific thresholds to educate women and physicians are needed. The anticipated life course of women supports a broadening focus on CVD toward that of lifelong care and emphasize key transitional stages for women-early risk factor onset, pregnancy, menopausal transition, and so on. This review is a call to action to re-envision a health system approach for lifespan prevention, detection, and treatment pathways to reduce CVD risk in women.

Sepsis remains one of the leading causes of death worldwide, and sepsis-induced cardiomyopathy (SICM) increases the overall mortality rate of sepsis patients. Currently, targeting therapies for SICM are lacking, due to the incomplete understanding of the pathophysiological mechanisms of SICM. Current research on the mechanisms of SICM remains at the level of the whole heart, lacking detailed studies at the single-cell levels.

Tissular gene expression profiling applicable to formalin-fixed, paraffin-embedded (FFPE) endomyocardial biopsies (EMBs) may refine the diagnosis of cardiac rejection while being easily implemented in clinical practice. This study aimed to develop and validate the first FFPE-based molecular diagnostic system dedicated to heart transplant rejection.

Osimertinib is a third-generation tyrosine kinase inhibitor targeting activating mutations of epidermal growth factor receptor with remarkable therapeutic efficacy against non-small cell lung carcinoma. However, its use has been limited by associated cardiotoxicity, primarily with heart failure. Herein, this study aims to better understand the mechanisms underlying osimertinib cardiotoxicity and explore cardioprotective strategies.

Magnesium deficiency is associated with poor outcomes in patients with heart failure (HF), but less is known about the impact of oral magnesium therapy. This study aimed to examine the association of oral magnesium with outcomes in patients with HF and whether it depends on baseline serum magnesium.

With innate immunity at the core of the pathophysiology of atherosclerosis, the discovery of new mechanisms of immune cell activation can potentially identify novel pharmacological targets to prevent or treat cardiovascular disease (CVD). One of these mechanisms is trained immunity (TRIM), defined as a recallable long-term hyperinflammatory innate immune phenotype supported by changes of metabolic and epigenetic intracellular processes. TRIM can be induced in mature innate immune cells in tissues, including monocytes/macrophages, and natural killer cells, but also in non-immune cells such as endothelial and epithelial cells (peripheral TRIM). Bone marrow haematopoietic stem and progenitor cells can also be trained (central TRIM), which explains the long-term presence of trained cells, such as monocytes and neutrophils, in the circulation. Recent experimental studies in mice revealed that central TRIM can be induced by traditional CVD risk factors (including diet-induced obesity or intermittent high-fat diet, hyperglycaemia, and hypertension), inflammatory co-morbidities (such as periodontitis and arthritis), unhealthy life-style factors (psychosocial stress and sleep disturbance), and by mechanisms activated by experimental myocardial infarction and stroke. This leads to the long-term presence of hyperinflammatory monocytes and neutrophils that can subsequently accelerate atherosclerosis development. A key mechanism that drives the development of central TRIM in many of these conditions is IL-1β signalling in the bone marrow. In addition, rewiring of cellular metabolism (e.g. activation of glycolysis and glutaminolysis) and changes in histone methylation, acetylation, and lactylation mediate the development of central and peripheral TRIM. We propose that prevention of TRIM by pharmacological targeting of these pathways in myeloid cells represents a new avenue for the prevention and treatment of cardiovascular events.

Diabetes mellitus is associated with increased risk of sudden cardiac death (SCD). However, nationwide, unselected studies are lacking. Therefore, this study aimed to estimate the incidence rates of SCD among individuals with Type 1 diabetes (T1D) and Type 2 diabetes (T2D) and to quantify the shortened life expectancy that can be attributed to SCD.

Paediatric myocardial strain analysis through echocardiography is often characterized by high variance and limited precision, highlighting the need for a standardized and vendor-agnostic approach applicable for diverse image qualities and populations, which could enhance cardiac function evaluation and enable early detection of cardiac impairment.