Coronary artery disease (CAD) is the leading cause of mortality globally. Although sub-stantial advances have been made in the diagnosis, management, and risk stratification of CAD, there is still a need for novel diagnostic biomarkers and new therapeutic targets to prevent the epi-demic of the disease. Recently, growing evidence has linked dysregulated microRNAs (miRNAs) to cardiovascular diseases, including CAD. miRNAs are endogenous, stable, single-stranded, short, non-coding RNAs, and may have utility as diagnostic and prognostic biomarkers for CAD. Dysreg-ulated miRNAs are involved in regulating lipid and glucose homeostasis pathways, renin-angiotensin-aldosterone pathways, inflammation, endothelial and vascular smooth cell phenotypes promoting atherosclerotic plaque development, progression, and instability. Additionally, miRNAs are stable and easily accessible in the extracellular space, may reside in microvesicles, and are de-tectable in serum or plasma, making them attractive biomarkers for the diagnosis and prognosis of cardiovascular disease. Accumulating studies suggest that miRNAs could be useful biomarkers for early discrimination of patients presenting with myocarditis or Takotsubo syndrome from those with a diagnosis of acute myocardial infarction, early prognostication of patients presenting with acute coronary syndromes, and accurate detection of left ventricular remodeling after a chronic or acute ischemic event. Moreover, miRNAs represent potential novel therapeutic targets for CAD or other cardiovascular diseases. This review provides an overview of the effects of the entire spec-trum of CAD, its major risk factors, and complications on levels of circulating miRNAs, as well as the limitations and challenges of their potential clinical applications.

Ischaemic heart disease (IHD) has historically been under-researched in women, leading to significant gaps in understanding sex-specific risk factors and outcomes. To address this issue, The Lancet Regional Health–Europe convened experts from a broad range of countries to evaluate sex-related cardiovascular inequalities and propose recommendations to address these disparities. Despite developing IHD a decade later than men, women experience higher mortality rates. Global Burden of Disease data highlight persistent sex differences in IHD mortality, with women showing higher mortality despite lower prevalence. Factors such as psychosocial stress, reproductive health, and physical inactivity disproportionately impact women's cardiovascular health, while caregiving responsibilities and delayed healthcare access further exacerbate these disparities. There is an urgent need to recognize chest pain symptoms in women and to reduce the time lag between symptom onset and hospital presentation. Addressing these gaps requires targeted public health interventions, expanded research, and improved clinical practices, emphasizing equitable healthcare access and greater inclusion of women in clinical trials. Tailoring treatment guidelines to account for sex differences in outcomes could significantly improve survival rates for women with IHD.

In recent years, increasing attention has been reserved to the analysis of sex-related differences in pathophysiology and prognosis of ischemic heart disease (IHD). The traditional conventional cardiovascular risk factors (hypertension, hypercholesteremia, diabetes mellitus and cigarette smoking) are still considered the major risk factors for IHD in both sexes. Nevertheless, recent studies show that they may interact with male and female coronary anatomy in a different manner. The path to sex-specific risk stratification of IHD is also supported by differences in inflammation and necrosis biomarkers (such as C-reactive protein and troponins, respectively). Indeed, large cohort studies often show different mean values of these markers in men and women. The current review summarizes the state-of-art knowledge on sex-related differences in cardiovascular risk factors and cardiac biomarkers with a prognostic value.

Cardiovascular diseases and cancer are the leading cause of morbidity and mortality globally. Cardiotoxicity from chemotherapeutic agents results in substantial morbidity and mortality in cancer survivors and patients with active cancer. Cardiotoxicity induced by 5-fluorouracil (5-FU) has been well established, yet its incidence, mechanisms, and manifestation remain poorly defined. Ischemia secondary to coronary artery vasospasm is thought to be the most frequent cardiotoxic effect of 5-FU. The available evidence of 5-FU-induced epicardial coronary artery spasm and coronary microvascular dysfunction suggests that endothelial dysfunction or primary vascular smooth muscle dysfunction (an endothelial-independent mechanism) are the possible contributing factors to this form of cardiotoxicity. In patients with 5-FU-related coronary artery vasospasm, termination of chemotherapy and administration of nitrates or calcium channel blockers may improve ischemic symptoms. However, there are variable results after administration of nitrates or calcium channel blockers in patients treated with 5-FU presumed to have myocardial ischemia, suggesting mechanisms other than impaired vasodilatory response. Clinicians should investigate whether chest pain and ECG changes can reasonably be attributed to 5-FU-induced cardiotoxicity. More prospective data and clinical randomized trials are required to understand and mitigate potentially adverse outcomes from 5-FU-induced cardiotoxicity.

Background: Existing data on female sex and excess cardiovascular mortality after myocardial infarction (MI) mostly come from high-income countries (HICs). This study aimed to investigate how sex disparities in treatments and outcomes vary across countries with different income levels. Methods: Data from the ISACS Archives registry included 22 087 MI patients from 6 HICs and 6 middle-income countries (MICs). MI data were disaggregated by clinical presentation: ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). The primary outcome was 30-day mortality. Results: Among STEMI patients, women in MICs had nearly double the 30-day mortality rate of men [12.4% vs. 5.8%; adjusted risk ratio (RR) 2.30, 95% CI 1.98–2.68]. This difference was less pronounced in HICs (6.8% vs. 5.1%; RR 1.36, 95% CI 1.05–1.75). Despite more frequent treatments and timely revascularization in MICs, sex-based mortality differences persisted even after revascularization (8.0% vs. 4.1%; RR 2.05, 95% CI, 1.68–2.50 in MICs and 5.6% vs. 2.6%; RR 2.17, 95% CI, 1.48–3.18) in HICs. Additionally, women from MICs had higher diabetes rates compared to HICs (31.8% vs. 25.1%, standardized difference = 0.15). NSTEMI outcomes were relatively similar between sexes and income groups. Conclusions: Sex disparities in mortality rates following STEMI are more pronounced in MICs compared to HICs. These disparities cannot be solely attributed to sex-related inequities in revascularization. Variations in mortality may also be influenced by sex differences in socioeconomic factors and baseline comorbidities.