Coronary artery disease (CAD) and mental health disorders, particularly depression and anxiety, exhibit a complex, bidirectional relationship that adversely influences clinical outcomes and mortality. Mental illnesses account for approximately 8 million deaths annually, while cardiovascular diseases, including CAD, contribute to about 17 million deaths, with CAD alone responsible for one-third of deaths among individuals aged ≥35 years. This review offers a structured synthesis of current knowledge focusing on the (1) epidemiology, emphasizing the reciprocal risk between CAD and psychiatric conditions; (2) pathophysiological insights, including inflammation, neurohormonal dysregulation, platelet hyperactivation, and shared genetic determinants; and (3) therapeutic approaches, encompassing pharmacological management, psychotherapeutic interventions, and integrated care models. Selective serotonin reuptake inhibitors (SSRIs) remain the pharmacologic agents of choice in patients with CAD and depression due to their favorable cardiac profile, while cognitive behavioral therapy (CBT) offers psychological benefit. However, evidence for mortality reduction remains limited. Emerging research highlights the importance of biomarker-driven care, gut–brain–heart axis modulation, and AI-enabled clinical integration.

The sex-specific effect of skeletal muscle mass (SMM) index (SMI) on 4-year first fatal/non-fatal cardiovascular disease (CVD) event in free-of-disease individuals was examined. In 2009, n = 1411 inhabitants (mean age = 64(12)) from Ikaria were selected. Follow-up was performed in 2013. SMI was created to reflect SMM through appendicular skeletal muscle mass (indirectly calculated through formulas) divided by body mass index (BMI). Fifteen and six tenths percent of participants exhibited CVD (19.8% in men/12% in women, p = 0.002). Significant U-shape trends were observed in participants >65 years old and women irrespective to age confirmed through multi-adjusted Cox regression analysis; in age >65 years, Hazard Ratio (HR)_{(2nd vs. 1st SMI tertile)} = 0.80, 95% Confidence Interval (95%CI) (0.45, 0.96) and in women HR_{(2nd vs. 1st SMI tertile)} = 0.71, 95% CI (0.33, 0.95), while, as for the 3rd SMI tertile, no significant trends were observed. Mediation analysis revealed that mediators of the aforementioned associations in men were the arterial distensibility and total testosterone, while, in women, inflammation, insulin resistance, and arterial distensibility. High SMM accompanied by obesity may not guarantee lower CVD risk. Specific cardiometabolic factors seem to explain this need for balance between lean and fat mass.

Background/Objectives: The ankle-brachial index (ABI) is a non-invasive diagnostic tool for peripheral artery disease (PAD) and a marker of systemic atherosclerosis, predictive of cardiovascular (CV) events. The ambulatory arterial stiffness index (AASI), derived from 24-h blood pressure monitoring, also predicts CV morbidity and mortality, particularly stroke. However, their combined prognostic utility in acute myocardial infarction (AMI) remains underexplored. This study aimed to assess the predictive value of ABI and AASI in patients with AMI. Methods: We conducted a single-center observational cohort study including 441 consecutive patients with AMI (79% male; mean age 62 years). ABI was measured using an automated device, with ≤0.9 defined as abnormal. AASI was calculated from 24-h blood pressure recordings. The primary endpoint was a composite of all-cause and CV death and major CV events, assessed in-hospital and over a 3-year follow-up. Results: Median ABI was 1.10 (IQR 1.00–1.18); 10.4% had abnormal ABI. Abnormal ABI was associated with a threefold higher risk of in-hospital adverse events (OR 2.93, 95% CI: 1.48–5.81, p = 0.002). In Cox regression, abnormal ABI predicted long-term all-cause mortality (HR 2.88, 95% CI: 1.53–5.42, p = 0.001), independent of traditional risk factors. Each 0.1 increase in AASI was linked to a 21% higher risk of the composite outcome (p = 0.001) and 25% increased risk of recurrent AMI or urgent revascularization (p = 0.001). Conclusions: In this prospective cohort of patients with AMI, ABI and AASI were associated with adverse outcomes, suggesting their potential role in risk stratification. These exploratory findings require validation in larger, multicenter cohorts to assess their incremental prognostic value and generalizability.

The personalized applications of 3D printing in interventional cardiology and cardiac surgery represent a transformative paradigm in the management of structural heart diseases. This review underscores the pivotal role of 3D printing in enhancing procedural precision, from preoperative planning to procedural simulation, particularly in valvular heart diseases, such as aortic stenosis and mitral regurgitation. The ability to create patient-specific models contributes significantly to predicting and preventing complications like paravalvular leakage, ensuring optimal device selection, and improving outcomes. Additionally, 3D printing extends its impact beyond valvular diseases to tricuspid regurgitation and non-valvular structural heart conditions. The comprehensive synthesis of the existing literature presented here emphasizes the promising trajectory of individualized approaches facilitated by 3D printing, promising a future where tailored interventions based on precise anatomical considerations become standard practice in cardiovascular care.

Cardiovascular disease remains the leading cause of mortality among women worldwide, yet coronary syndromes in women continue to be under-recognized and insufficiently represented in clinical research. This review summarizes sex-specific pathophysiological mechanisms, risk factors, clinical presentation, and management considerations in women with coronary syndromes. Women are more likely than men to present with non-obstructive and non-atherosclerotic ischemic phenotypes, including ischemia or angina with non-obstructive coronary arteries, coronary microvascular dysfunction, myocardial infarction with non-obstructive coronary arteries, spontaneous coronary artery dissection, vasospastic angina, and Takotsubo syndrome. These entities often require diagnostic strategies beyond the detection of flow-limiting epicardial stenosis, including cardiac magnetic resonance imaging, intracoronary imaging, and coronary function testing. Traditional cardiovascular risk factors remain important, but several female-specific risk enhancers, including premature menopause, adverse pregnancy outcomes, polycystic ovary syndrome, autoimmune disease, and psychosocial stressors, further modify risk and remain incompletely integrated into routine clinical assessment. Women may also experience diagnostic delays due to symptom misclassification, lower baseline troponin concentrations, and clinical algorithms historically derived from male-predominant populations. Management should follow guideline-directed therapy when appropriate, while recognizing sex-related differences in pharmacology, bleeding risk, revascularization outcomes, and the need for phenotype-specific treatment in INOCA, MINOCA, SCAD, and Takotsubo syndrome. Finally, transgender and gender-diverse individuals remain largely absent from cardiovascular trials, highlighting the need for inclusive research frameworks that distinguish sex, gender identity, and hormone exposure. Improved recognition of sex- and gender-related differences is essential to advance equitable cardiovascular care.