Cardiovascular disease remains the leading cause of morbidity and mortality worldwide, especially in regions like Eastern Europe, South Asia, and Latin America. A significant portion of these cases (80%) is linked to atherosclerosis, which can lead to severe conditions like ischemic heart disease and stroke, with atherosclerosis (ATS) responsible for the majority of cases. This review explores the multifaceted relationship between insulin resistance (IR) and ATS, highlighting their roles as both independent and interrelated contributors to cardiovascular risk. ATS is characterized by lipid accumulation and chronic inflammation within arterial walls, driven by factors such as hypertension, dyslipidemia, and genetic predisposition, with endothelial dysfunction as a key early event. The early detection of subclinical ATS is critical and can be achieved through a combination of non-invasive imaging techniques—such as coronary artery calcium scoring and carotid ultrasound—and comprehensive risk profiling. IR, marked by impaired glucose uptake in liver, muscle, and adipose tissue, often precedes early diabetes and is associated with metabolic disturbances, including dyslipidemia and chronic inflammation. The diagnosis of IR relies on surrogate indices such as HOMA-IR, the QUICKI, and the TyG index, which facilitate screening in clinical practice. Compelling evidence indicates that IR independently predicts the progression of atherosclerotic plaques, even in non-diabetic individuals, and operates through both traditional risk factors and direct vascular effects. Understanding and targeting the IR–ATS axis is essential for the effective prevention and management of cardiovascular disease.

Inflammation plays a pivotal role in the pathogenesis of acute coronary syndromes (ACS), contributing to plaque instability, thrombosis, and myocardial injury. This review aims to comprehensively examine the inflammatory mechanisms underlying ACS and evaluate current and emerging anti-inflammatory therapeutic strategies. We conducted a comprehensive literature review examining the role of inflammatory pathways in ACS pathophysiology, including innate and adaptive immune responses, key inflammatory mediators, and cellular mechanisms. We analyzed current evidence for anti-inflammatory therapies and their clinical outcomes in ACS management. Inflammatory processes in ACS involve complex interactions between innate immune cells (neutrophils, macrophages, monocytes) and adaptive immune cells (T lymphocytes, B cells). Key mechanisms include neutrophil extracellular trap (NET) formation, macrophage polarization, T cell subset imbalances (Th1/Th17 predominance with regulatory T cell dysfunction), and complement activation. Inflammatory biomarkers such as C-reactive protein, interleukin-6, and NET-specific markers demonstrate prognostic value. Anti-inflammatory therapies including colchicine, canakinumab (IL-1β inhibition), and methotrexate have shown cardiovascular benefits in clinical trials. Emerging targets include NET inhibition, T cell modulation, and precision inflammatory profiling approaches. Inflammation represents a critical therapeutic target in ACS beyond traditional risk factor modification. While colchicine and IL-1β inhibition have demonstrated clinical efficacy, future strategies should focus on precision medicine approaches targeting specific inflammatory pathways based on individual patient profiles. Integration of anti-inflammatory therapy with lipid management and antithrombotic strategies offers promise for improving ACS outcomes through comprehensive targeting of the multifactorial pathophysiology underlying coronary artery disease.

Dyslipidemia is a major modifiable risk factor in patients with acute coronary syndrome (ACS), and effective management is essential to reduce the risk of recurrent cardiovascular events. Recent guidelines emphasize early, intensive lipid-lowering therapy (LLT) and increasingly recommend combination regimens to achieve ambitious low-density lipoprotein cholesterol (LDL-C) targets. This review evaluates current evidence and recommendations for dyslipidemia treatment in ACS, with a focus on the rationale, timing, and selection of combination therapy. We conducted a comprehensive review of recent clinical guidelines, randomized controlled trials, and observational studies addressing lipid management in ACS. The analysis included data on LDL-C targets, efficacy and safety of high-intensity statins, adjunctive non-statin therapies (ezetimibe, PCSK9 inhibitors), and the impact of dietary interventions. Early and intensive LLT, initiated within 24–48 h of ACS, is associated with significant reductions in recurrent events and mortality. High-intensity statins (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) are first-line, with combination therapy (statin plus ezetimibe and/or PCSK9 inhibitor) recommended for patients not achieving LDL-C < 1.4 mmol/L (50% reduction from baseline. Evidence supports further LDL-C lowering (<1.0 mmol/L) in very high-risk patients. The Mediterranean and DASH diets provide additional benefit in lipid profile optimization and risk reduction. Statins also confer pleiotropic effects, including anti-inflammatory and plaque-stabilizing actions. Recent studies and real-world data confirm the efficacy and safety of combination approaches but highlight the need for individualized therapy based on residual risk, comorbidities, and tolerability. Achieving guideline-recommended LDL-C targets in ACS patients often requires early initiation of combination lipid-lowering therapy. Optimal management should be individualized considering both LDL-C levels and broader risk profiles. Ongoing research is needed to refine patient selection for combination therapy and to integrate novel agents into clinical practice.

Background: NT-proBNP levels with a wide range at admission play both a diagnostic and a prognostic role in patients with HF. The differences regarding the clinical profiles and demography in decompensated HF patients according to NT-proBNP levels at admission are not clear. Methods: This study aimed to analyze and compare clinical profiles and demographics in patients hospitalized for decompensated heart failure according to levels of NT-proBNP at admission. The study included 302 patients hospitalized for decompensated HF who were divided into three groups based on admission NT-proBNP levels: group A (n = 46, with NT-proBNP level < 3000 pg/mL), group B (n = 130, NT-proBNP level between 3000–10,000 pg/mL), and group C (n = 126, NT-proBNP level > 10,000 pg/mL). Results: Patients hospitalized with decompensated HF and very high levels of NTproBNP, above 10,000 pg/mL at admission, are older, have a lower LVEF, higher NYHA class, more renal dysfunction, and longer hospital stay, resulting in a more severe clinical profile. Conclusions: The presence of very high levels of NT-proBNP may identify a category of patients with a more severe prognosis that requires more aggressive management and closer follow-up.

Background: Transcatheter aortic valve implantation is established for severe calcific tricuspid aortic stenosis, but its application in bicuspid aortic valve (BAV) stenosis, pure native aortic regurgitation (AR), and small aortic annulus anatomy remains limited by heterogeneous morphology, device-specific constraints, and uncertain long-term outcomes. These settings require decisions that extend beyond immediate procedural success to encompass coronary access, reintervention, valve durability, and associated aortopathy. This review synthesizes current evidence and proposes an anatomy-driven framework integrating imaging, device selection, procedural planning, and lifetime management. Methods: A structured narrative review was conducted in accordance with the Scale for the Assessment of Narrative Review Articles (SANRA) criteria. PubMed/MEDLINE, Embase, and the Cochrane Central Register of Controlled Trials were searched from 1 January 2010 to 31 March 2026 for studies addressing TAVI in BAV stenosis, pure native AR, and small aortic annulus anatomy. Randomized trials, meta-analyses, multicenter registries, pivotal device studies, and guideline or consensus documents were prioritized. After screening 2663 records and assessing 330 full-text reports, 101 records were retained for qualitative synthesis. Evidence was appraised by anatomical substrate, imaging phenotype, device strategy, procedural hazards, and implications for lifetime management. Results: In BAV stenosis, contemporary registry and prospective cohort data support high device success and acceptable early and mid-term outcomes in carefully selected patients; however, calcified raphe, bulky asymmetric leaflet or left ventricular outflow tract calcification, annular eccentricity, and concomitant aortopathy identify higher-risk phenotypes that often favor surgery. Randomized evidence in younger low-risk BAV patients remains limited and exploratory, with the NOTION-2 trial showing a numerically higher 3-year composite event rate after TAVI than surgical aortic valve replacement (20.4% vs. 7.8%; hazard ratio 2.9, 95% confidence interval 0.9–9.0) in the small bicuspid subgroup. In pure native AR, lack of annular calcification and frequent root dilatation impair anchoring of conventional transcatheter heart valves, increasing risks of migration, embolization, residual AR, and second-valve implantation. Dedicated leaflet-anchoring devices have improved outcomes: in ALIGN-AR, the JenaValve Trilogy system achieved procedural success above 95% in high-surgical-risk patients, although evidence remains single-arm and nonrandomized. In small annuli, the strongest comparative evidence comes from the SMART trial, in which supra-annular self-expanding valves were non-inferior to balloon-expandable valves for the 12-month clinical composite and reduced moderate/severe prosthesis–patient mismatch at 30 days (11.2% vs. 35.3%). Across all three phenotypes, electrocardiography-gated computed tomography is fundamental for defining anchoring, sizing, calcium distribution, root and coronary anatomy, anticipated coronary re-access, and the feasibility of redo-TAVI. Surgery remains particularly relevant when aortic repair, annular/root enlargement, or a more durable lifetime strategy is required. Conclusions: TAVI is feasible in selected patients with BAV stenosis, pure native AR, and small aortic annuli, but the evidentiary strength and optimal procedural strategy differ substantially across these anatomies. Treatment should be guided by an anatomy-driven, computed-tomography-based Heart Team assessment that integrates immediate procedural feasibility with age, surgical candidacy, aortopathy, prosthesis–patient mismatch risk, coronary access, durability, and future reintervention options. Surgery remains the more established strategy for many younger, operable patients with unfavorable BAV morphology or aortopathy, AR with root dilatation, or very small annuli amenable to enlargement. Dedicated randomized trials, standardized imaging criteria, and long-term durability data are needed to refine lifetime management in complex aortic valve anatomy.

Background: The optimal duration of dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) of the left main coronary artery remains uncertain because this lesion involves a large myocardial territory and requires a careful balance between ischemic protection and bleeding risk. This review aimed to provide an updated, left-main-focused synthesis of the evidence on DAPT duration after PCI and to clarify how treatment should be individualized according to clinical presentation, lesion complexity, procedural strategy, intravascular imaging, and validated ischemic and bleeding risk scores. Methods: This narrative review with a structured literature search examined studies published from January 2010 through May 2026 in PubMed/MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, and Google Scholar. From 248 identified records, 62 studies met the eligibility criteria and were included in the qualitative synthesis, comprising 38 randomized controlled trials and 24 observational studies or pooled analyses. The review prioritized direct left-main-specific evidence while also incorporating broader PCI studies with left-main subgroups and indirect contextual evidence relevant to antiplatelet decision-making. Independent screening, duplicate data extraction, and qualitative risk-of-bias assessment were performed, but the review was not prospectively registered, and no meta-analysis was conducted. Results: The available evidence supports an individualized rather than fixed DAPT strategy after left main PCI. In stable patients with anatomically simple left main lesions and acceptable bleeding risk, 6–12 months of DAPT appears generally sufficient, whereas patients with acute coronary syndromes, two-stent distal bifurcation strategies, high thrombotic burden, or other high-ischemic-risk features may derive greater benefit from extending therapy beyond 12 months when bleeding risk is low. Contemporary guideline recommendations are broadly aligned with this risk-adapted approach, and recent trials further refine decision-making: PARTHENOPE provided randomized support for risk-score-guided personalization of DAPT duration, whereas NEO-MINDSET cautioned against immediate aspirin withdrawal after PCI in acute coronary syndromes. Intravascular imaging, especially IVUS and OCT, improves procedural optimization and may help contextualize post-PCI thrombotic risk, although current data do not validate imaging findings alone as a stand-alone criterion for abbreviated DAPT. Conclusions: DAPT duration after left main PCI should be individualized by integrating clinical presentation, lesion and procedural complexity, intravascular imaging, and validated ischemic and bleeding risk tools. A personalized, risk-adapted strategy currently offers the most appropriate framework for balancing ischemic benefit against bleeding harm in this high-risk population.