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.

(1) Aims: This study aimed to compare cardiovascular outcomes in patients older than 75 years with those of younger patients who underwent interventional treatment for acute coronary syndrome (ACS) at a tertiary university hospital. (2) Methods and Results: This was a retrospective, observational study conducted between January 2016 and December 2021, including 1846 consecutive patients with ACS (older than 75 years n = 203, 11%; younger than 75 years n = 1643, 89%). After admission, patients underwent coronary angiography and subsequently received percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), or medical therapy. The mean age in the older group (O75) was 80 ± 4 years versus 59 ± 9 years in the younger group (Y75) (p < 0.001). Older patients more frequently presented with multivessel coronary disease (O75: 114 [56%] vs. Y75: 727 [44%], p = 0.004), and the left anterior descending artery (LAD) was more often the culprit vessel (O75: 105 [52%] vs. Y75: 684 [41%]). Major adverse cardio-cerebral events (MACCEs) occurred more frequently in patients older than 75 years, mainly due to higher mortality (O75: 14 [6.9%] vs. Y75: 27 [1.6%], p < 0.001) and stroke (O75: 3 [1.5%] vs. Y75: 2 [0.1%], p < 0.001). Multivessel disease was the only factor independently associated with MACCEs (HR 1.417, 95% CI 1.058–1.898, p = 0.02). The incidence of significant bleeding (Bleeding Association Research Consortium (BARC) class ≥ 3) was similar between groups (Y75: 123/1643 [7.5%] vs. O75: 13/203 [6.5%], p = 0.587). (3) Conclusions: Patients older than 75 years have worse short- and long-term prognoses following ACS compared with younger patients. Special attention and a multidisciplinary, personalized approach are required to optimize outcomes in this population.