Heart failure and diabetes mellitus are major contributors to global morbidity and mortality, with their prevalence continuously rising, primarily due to aging populations and improvements in healthcare. These conditions often coexist or develop sequentially, leading to complex interactions that significantly influence the progression and management of both diseases. Furthermore, heart failure and diabetes are commonly associated with coronary artery disease, which presents a unique challenge in clinical management, particularly in the context of myocardial revascularization. The presence of diabetes exacerbates atherosclerotic progression and impairs endothelial function, while heart failure complicates the perfusion and recovery of myocardial tissue post-intervention. This narrative review delves into the underlying mechanisms contributing to revascularization failure in patients with heart failure and diabetes, emphasizing the importance of understanding these interactions for optimal treatment. The review also summarizes key findings from randomized controlled trials, examining evidence both in the general population and in specific subgroups, including the elderly and patients with left main coronary artery disease, chronic kidney disease, peripheral artery disease, and chronic obstructive pulmonary disease. Understanding these complexities is critical for improving patient outcomes.

Background/Objectives: Diagnostic performance of angiography-derived physiological measures has been benchmarked against two-dimensional (2D) and three-dimensional (3D) quantitative coronary angiography (QCA), which are known for their poor correlation with hemodynamic lesion severity. Relying on the statistical concept of the wisdom of the crowd, we devised a human-performance reference for FFR surrogates, called vox populi FFR (vpFFR), and examined the comparative diagnostic performance of vpFFR, as well as 2D- and 3D-QCA, using invasively measured FFR as the gold standard. Methods: Analyses were performed in a single-center, prospective registry of consecutive FFR procedures. We calculated vpFFR as a mean of five independent, blinded predictions of the invasively measured FFR. Pearson’s correlation coefficient and receiver operating characteristic (ROC) curve analyses were used for diagnostic performance comparisons. Results: In 116 patients (156 vessels), Pearson’s correlation coefficients for vpFFR, 2D-, and 3D-QCA with invasively measured FFR are 0.56, −0.26, and −0.01, respectively (p < 0.001, p = 0.001 and p = 0.918). vpFFR has a sensitivity of 56%, specificity of 84%, positive predictive value of 67%, and negative predictive value of 76%. It correctly classified hemodynamic severity of lesions in 73% of vessels compared to 65% and 51% for 2D- and 3D-QCA, respectively. vpFFR has a larger area under the ROC curve than 2D- and 3D-QCA for predicting positive FFR (0.78, 0.63, and 0.45, respectively, p < 0.001). Conclusions: vpFFR, a mean value of five predictions of invasively measured FFR, has moderate diagnostic performance, superior to 2D- and 3D-QCA using FFR as the gold standard, and can be used as a human-performance reference for existing and emerging angiography-derived physiological measures.

Coronary artery calcification (CAC) represents a clear sign of advanced atherosclerosis and a strong indicator of coronary artery disease burden and cardiovascular risk. Beyond its established prognostic value, CAC significantly influences plaque biology, lesion morphology, and the technical complexity of percutaneous coronary intervention (PCI). This review summarizes current knowledge on the mechanisms of vascular calcification, its clinical determinants, diagnostic assessment, and therapeutic implications. Vascular calcification is now understood as an active, regulated process involving osteogenic transdifferentiation of vascular smooth muscle cells, inflammatory signaling pathways, extracellular vesicle release, and disturbances in mineral metabolism. Distinct calcification phenotypes exert different effects on plaque stability: micro- and spotty calcifications are frequently linked to plaque vulnerability, whereas dense, sheet-like calcification is more typical of stable fibrocalcific lesions. The prevalence of CAC increases with age and differs between sexes, while cardiometabolic risk factors, chronic kidney disease, systemic inflammation, and genetic predisposition further contribute to its development. Noninvasive computed tomography remains the cornerstone for CAC detection and quantification, enabling reliable cardiovascular risk stratification. Intravascular imaging techniques, particularly intravascular ultrasound and optical coherence tomography, provide detailed characterization of calcified plaque morphology and support optimal procedural planning. In patients with heavily calcified lesions, intravascular imaging-guided lesion preparation and stent optimization represent the most effective strategy for improving PCI outcomes.

Introduction: Acute ST-segment elevation myocardial infarction (STEMI) remains a major cause of cardiovascular morbidity and mortality. Despite successful primary percutaneous coronary intervention (pPCI), early myocardial injury and stress may contribute to left ventricular dysfunction. The optimal timing of biomarker assessment after STEMI remains uncertain. Objective: To characterize the early kinetics of soluble suppression of tumorigenicity-2 (sST2), galectin-3 (Gal-3), mid-regional pro-adrenomedullin (MR-proADM), and growth differentiation factor 15 (GDF-15) during the first 96 h after STEMI and identify potentially informative sampling time points for future prognostic assessment. Secondary, exploratory objectives were to evaluate differences in biomarker concentrations according to symptom duration, left ventricular ejection fraction (LVEF), and infarct-related artery. Methods: In this prospective, single-center, exploratory pilot study, patients aged 18–75 years with first STEMI treated with pPCI within 6 h of symptom onset were enrolled between September 2024 and November 2025. Blood samples were collected at admission and 12 ± 4, 24 ± 4, 48 ± 8, and 96 ± 8 h after pPCI. Biomarkers were measured by ELISA, with high-sensitivity cardiac troponin I (hs-cTnI) as a reference marker of myocardial injury. Results: Of 46 enrolled patients, 16 were excluded, mostly due to early discharge, and 30 patients with complete samples at all five time points were included in the analysis (mean age 57.9 ± 11.1 years; 66.7% male). sST2, MR-proADM, and hs-cTnI showed significant temporal variation (all p < 0.001), with the highest measured concentrations of sST2 at 12 h and of MR-proADM at 24 h. No significant change over time was found for Gal-3 and GDF-15. In exploratory analyses, sST2 and MR-proADM concentrations were higher in patients with LVEF < 40%, and sST2 concentrations were higher in patients with left anterior descending artery (LAD) infarction. Symptom duration was not associated with biomarker concentrations. Conclusions: sST2 and MR-proADM show distinct early post-STEMI kinetics, suggesting potentially informative sampling windows for future prognostic studies. Larger prospective studies are needed to confirm these kinetics and the exploratory differences according to left ventricular function and infarct location, and to evaluate the prognostic value of these sampling windows with echocardiographic and clinical follow-up.