Search Results (4,156)

Background and Objectives: This retrospective study evaluated patients with diabetes classified according to cluster-derived diabetes phenotype groups and compared their baseline metabolic characteristics, documented complication profiles, and HbA1c course during follow-up. Materials and Methods: A total of 158 patients with type 1 or type 2 diabetes followed at Zonguldak Bülent Ecevit University Endocrinology Outpatient Clinic were included. Phenotype assignment was based on baseline domains corresponding to the Ahlqvist framework: age at diagnosis, BMI category, HbA1c, beta-cell function, insulin resistance, and autoantibody status. Complications were not used for phenotype assignment. Baseline characteristics, binary complication status, exploratory phenotype-contrast logistic regression, and longitudinal HbA1c data were evaluated. Results: The groups showed significant differences in age, age at diagnosis, HbA1c, obesity status, fasting glucose, C-peptide, fasting insulin, HOMA1-%B, HDL cholesterol, ALT, and eGFR. Hepatic steatosis/suspected NAFLD, retinopathy, nephropathy, polyneuropathy, and ketosis/ketoacidosis differed among groups when complications were analyzed as ever-positive versus negative. In exploratory phenotype-contrast logistic regression, Clusters 3–4 were associated with hepatic steatosis/suspected NAFLD, Cluster 2 with retinopathy and polyneuropathy, Cluster 3 with nephropathy, and Clusters 1–2 with ketosis/ketoacidosis; the contrast for coronary artery disease did not reach statistical significance. In a linear mixed-effects model for repeated HbA1c measurements, phenotype group was associated with HbA1c levels, whereas the time effect and group-by-time interaction were not statistically significant. Conclusions: Cluster-derived diabetes phenotype groups showed distinct baseline metabolic characteristics and different documented complication profiles. These findings should be interpreted as exploratory because of the retrospective design and incomplete follow-up data. Full article

Intravenous immunoglobulin (IVIG) resistance occurs in 10–20% of children with Kawasaki disease (KD) and is associated with a 3- to 5-fold higher risk of coronary artery lesions (CALs). Yet the mechanistic basis for why some patients progress from reversible inflammation to irreversible vascular damage after IVIG remains poorly understood. Most existing reviews have focused on risk prediction rather than the mechanistic chain linking resistance to CALs. Here, we synthesize current evidence across three interconnected pathways. First, autophagy dysfunction—particularly impaired mitophagy—sustains inflammation through cGAS-STING activation. Second, neutrophil extracellular traps (NETs) play a controversial role in KD vasculitis, with PAD2 and PAD4 possibly acting redundantly via the NLRP3 inflammasome. Third, endothelial-to-mesenchymal transition (EndMT), driven by the IL-1β/TNF axis and the USP7-TGFβ2/SMAD pathway, emerges as a core event in vascular remodeling. Building on these findings, we propose the “autophagy–inflammasome axis” as a candidate molecular switch that dictates whether inflammation resolves or persists. This hypothesis is actionable: it generates three explicit, testable predictions linking autophagic integrity to inflammatory outcomes and therapeutic response. Direct experimental validation in IVIG-resistant KD models and patient samples is now urgently needed. This review provides a systematic framework for understanding how IVIG resistance transitions to irreversible CALs. It also identifies candidate biomarkers (e.g., S100A12, mtDNA, and MCM8) and therapeutic targets (autophagy inducers, NLRP3 inhibitors, USP7 inhibitors, and anakinra) that could enable earlier intervention. Full article

Cardiovascular disease (CVD) prevention depends on accurate risk stratification before symptoms develop. Standard tools such as the Pooled Cohort Equations, QRISK3, and SCORE2 require laboratory data and are less informative in borderline-risk individuals, creating a role for accessible adjuncts. Retinal imaging directly visualizes the systemic microvasculature, and deep-learning oculomics may provide complementary risk information. Reti-CVD generates a three-tier classification from a retinal photograph and is among the more extensively validated retinal-AI tools. This narrative review evaluates its clinical positioning and implementation as an exemplar rather than a product endorsement, organizing evidence by cohort, comparing the approach with established scores and subclinical atherosclerosis markers, and considering implementation, regulation, and equity. RetiCAC was trained using coronary artery calcium as a surrogate label; subsequent Reti-CVD studies included UK Biobank, Singapore SEED, and CMERC-HI. Reported discrimination was approximately 0.75 by the Harrell C-index, with modest reclassification improvement, particularly in borderline-risk groups. As the commercial product DrNoon for CVD, the tool holds marketing authorization from Korea’s Ministry of Food and Drug Safety (MFDS) and, according to the manufacturer, CE certification under the EU Medical Device Regulation (MDR); in Korea it entered outpatient practice through a time-limited non-covered (out-of-pocket) assessment-deferral pathway, and it has not yet received US FDA authorization. Most evidence originates from one research group and one commercial algorithm, and no randomized or outcome-based study has shown that Reti-CVD-guided care improves clinical outcomes. These observational findings remain hypothesis-generating rather than evidence of established clinical utility. Reti-CVD is therefore best regarded as a non-invasive risk enhancer for borderline/intermediate-risk reclassification, not as a tool of established clinical utility; independent validation, intervention trials, and cost-effectiveness and reimbursement evidence are needed before broad integration. Full article

Background/Objectives: Atrial fibrillation (AF) and chronic kidney disease (CKD) frequently coexist and are associated with a high risk of cardiovascular complications. Previous studies have primarily focused on differences in clinical profiles by anticoagulant therapy or arrhythmia. Only a limited number of studies have evaluated the impact of CKD severity on patients’ clinical characteristics. Methods: This retrospective observational study aimed to characterize the clinical profile of contemporary patients with AF and CKD with an estimated glomerular filtration rate (eGFR) of 15–49 mL/min/1.73 m². The analysis included patients with AF from the CRAFT registry (NCT02987062). Patients were divided into two groups according to eGFR: 15–49 mL/min/1.73 m² and ≥50 mL/min/1.73 m². The groups were compared with respect to demographic characteristics, comorbidities, and treatment patterns. Statistical analyses included the Mann–Whitney U test, the chi-square test and multivariable logistic regression analysis. Results: A total of 3203 patients with AF were included, of whom 1153 had eGFR < 50 mL/min/1.73 m². Compared with patients with eGFR ≥ 50 mL/min/1.73 m², those with lower eGFR were significantly older, more often female, and had a higher burden of comorbidities, including arterial hypertension, heart failure, coronary artery disease, and diabetes mellitus. Direct oral anticoagulants were the predominant anticoagulant therapy, irrespective of renal function. Conclusions: Patients with AF and moderate-to-severe CKD present a distinct clinical profile characterized by advanced age and a higher burden of comorbidities. These findings improve the understanding of the clinical profile of patients with AF and moderate-to-severe CKD and may support risk assessment and clinical decision-making. Full article

Coronary artery aneurysm (CAA) and ectasia (CAE) are characterized by an abnormal dilation exceeding 1.5 times the reference diameter of the adjacent normal vessel segment. Usually, these vascular anomalies are detected incidentally during coronary computed tomography angiography or invasive coronary angiography. Their clinical significance has become increasingly recognized over time because they may be associated with myocardial ischemia, thrombosis, distal embolization, acute coronary syndromes, and adverse long-term outcomes. In adults, atherosclerosis remains the most frequent cause, while Kawasaki disease is the leading etiology in children. Many patients remain asymptomatic, and the diagnosis is often incidental. Given their variable natural history and poorly delineated prognostic implications, individualized clinical risk stratification is essential. Coronary angiography remains the gold standard for invasive assessment. Management remains controversial in the absence of randomized controlled trials establishing an optimal therapeutic strategy. Full article

Cardiovascular and vascular diseases remain major causes of morbidity and mortality worldwide, despite substantial advances in prevention, diagnosis, and treatment. In recent years, cardiovascular imaging has moved beyond the traditional assessment of anatomy and morphology toward a multidimensional evaluation of function, tissue composition, haemodynamics, inflammation, and individualized risk. This evolution has been driven by technological progress in echocardiography, cardiovascular magnetic resonance, computed tomography, nuclear imaging, intravascular imaging, and point-of-care ultrasound, together with the rapid development of artificial intelligence, radiomics, and predictive analytics. Advanced echocardiographic techniques, including contrast stress echocardiography and emerging methods for myocardial scar detection, may improve functional and prognostic assessment in patients with suspected or established coronary artery disease. Cardiac magnetic resonance, through tissue mapping, late gadolinium enhancement, and 4D flow imaging, provides unique information on myocardial fibrosis, perfusion, ventricular remodelling, and vascular haemodynamics. Computed tomography, particularly with the introduction of photon-counting technology, is expanding the non-invasive characterization of coronary plaques, vascular calcification, and thromboembolic disease. Hybrid imaging with PET/CT and PET/MR offers additional insight into vascular inflammation, myocardial metabolism, and active disease processes. At the same time, intravascular ultrasound, optical coherence tomography, and augmented-reality-supported imaging are refining interventional guidance, while point-of-care ultrasound is broadening access to rapid bedside cardiovascular and vascular assessment. The integration of imaging findings with circulating biomarkers, clinical scores, lipid profiles, coagulation parameters, and machine-learning models represents a promising strategy for personalized risk stratification, particularly in complex conditions such as coronary artery disease, venous thromboembolism, pulmonary embolism, and bleeding risk during antithrombotic therapy. This review summarizes current advances in cardiovascular imaging, discusses their translational implications, and highlights future directions for integrating imaging, artificial intelligence, and precision medicine into daily clinical practice. Full article

Obstructive sleep apnea (OSA)-induced hypoxia modulates inflammatory mediators associated with atherosclerosis and cardiovascular diseases. ICAM-1, VCAM-1, TNF-α and IL-6 are involved in atherogenesis, but their expression in the aortic walls of OSA patients remains unknown. This study aimed to determine the relationship between OSA severity and inflammatory markers expression in aortic tissue from patients undergoing coronary artery bypass grafting (CABG). This study included 46 patients who underwent CABG. OSA severity was assessed using the WatchPAT™ home sleep apnea test, classifying patients into control and mild (0 < AHI < 15) and moderate-to-severe (AHI ≥ 15) OSA groups. Aortic wall samples were collected intraoperatively, and ICAM-1, VCAM-1, TNF-α and IL-6 expression was evaluated using immunohistochemistry. Statistical analysis compared protein expression across OSA severity groups. Compared with control and mild OSA, in aorta of the moderate-to-severe OSA group, significant differences for ICAM-1 (p = 0.001) and VCAM-1 (p = 0.006) expression were demonstrated. This study provides novel evidence of significantly increased ICAM-1 and VCAM-1 expression in the aortic walls of patients with moderate-to-severe OSA. No statistically significant differences were observed for TNF-α and IL-6. Our findings offer a rationale for integrating vascular inflammation markers into cardiovascular risk stratification in OSA. They also support the concept of OSA as a systemic inflammatory disorder, with tangible effects on large-vessel morphology. Full article

Background: Transradial access has become a preferred strategy for chronic total occlusion (CTO) percutaneous coronary intervention (PCI) because of lower access site complication rates and increasing feasibility for complex CTO techniques using large-bore slender or sheathless systems. However, long-term outcomes after successful transradial CTO recanalization and their predictors remain incompletely defined. We aimed to identify long-term clinical and procedural predictors of major adverse cerebrovascular and cardiac events (MACCEs) after successful transradial CTO PCI. Methods: We performed a prospective dual-center cohort study including 227 consecutive patients who underwent successful transradial CTO PCI at two high-volume catheterization laboratories with dedicated CTO programs. A total of 405 CTO PCI procedures were screened; all femoral access cases were excluded and only transradial cases were eligible. Baseline clinical characteristics, left ventricular ejection fraction (LVEF), lesion complexity including J-CTO score, coronary disease extent, and procedural variables were prospectively collected and/or verified from institutional databases. The primary endpoint was MACCEs, defined as a composite of all-cause death, non-fatal myocardial infarction, target vessel revascularization, and stroke/transient ischemic attack. Event rates were estimated using Kaplan–Meier methods. Predictors were explored using Cox proportional hazards regression with clinically relevant covariates and procedural characteristics entered into multivariable models. Results: Among 227 patients with successful transradial CTO recanalization and complete 5-year follow-up among survivors, cumulative MACCEs and all-cause mortality were 44.0% and 21.5%, respectively. In multivariable Cox analysis, prior myocardial infarction, right coronary artery target vessel, and a higher number of implanted stents were independently associated with increased MACCE risk, whereas previous PCI and preserved LVEF (≥40%) were associated with lower MACCE risk. For all-cause mortality, preserved LVEF was independently protective, while right coronary artery target vessel intervention was associated with increased mortality risk; severe chronic kidney disease showed a significant univariable association and remained a strong signal after multivariable adjustment. Conclusions: After successful transradial CTO PCI, long-term MACCEs appear to be driven primarily by baseline comorbidity and coronary disease burden. No deaths were related to access site bleeding, and vascular access was not associated with fatal complications. These findings contribute to personalized cardiovascular medicine by identifying readily available clinical, anatomical, and procedural factors that enable individualized long-term risk stratification following successful transradial CTO recanalization. Integrating these predictors into post-procedural assessment may support tailored secondary prevention, follow-up strategies, and patient management according to individual risk profiles. Full article

Long non-coding RNAs (lncRNAs) constitute an important group of regulatory RNA molecules involved in the control of gene expression at the epigenetic, transcriptional, and post-transcriptional levels. In recent years, their crucial role in the pathophysiology of cardiovascular diseases, particularly coronary heart disease, has become increasingly evident. The aim of this review is to present current knowledge regarding the mechanisms of lncRNA action in the cardiovascular system, their involvement in the molecular processes associated with myocardial ischaemia, and their potential diagnostic and therapeutic applications. We discuss the molecular mechanisms responsible for the regulation of cardiomyocyte apoptosis, oxidative stress, mitochondrial dysfunction, angiogenesis, coronary vessel remodelling, and cardiac fibrosis. Particular attention is paid to selected lncRNAs involved in coronary heart disease, including MIAT, MALAT1, ANRIL, and H19, which influence inflammatory processes, vascular smooth muscle cell proliferation, responses to hypoxia, and cardiac fibrosis. The potential of lncRNAs as diagnostic and prognostic biomarkers in coronary artery disease is also discussed. Current evidence suggests that molecules such as MALAT1, MIAT, LIPCAR, and HCG11 may have considerable diagnostic and prognostic value, including for predicting major adverse cardiovascular events and the no-reflow phenomenon following percutaneous coronary intervention. Furthermore, contemporary therapeutic strategies targeting lncRNAs are presented, including antisense oligonucleotides, siRNAs, and CRISPR/Cas9 genome-editing technologies. Despite promising preclinical findings, the clinical application of lncRNA-based therapies remains limited by challenges related to safety, delivery of therapeutic molecules, and translation of experimental findings into clinical practice. Nevertheless, lncRNAs represent a promising avenue for the development of precision medicine and may play an important role in the future diagnosis and treatment of cardiovascular diseases. Full article

Coronary artery calcification (CAC) is a pressing issue in cardiology. Mesenchymal stem cells (MSCs) derived from epicardial adipose tissue (EAT) may serve as a source of osteoblasts in the cardiovascular system. This study aimed to evaluate and compare the immunophenotype, proliferation, and osteogenic potential of EAT-MSCs from patients with coronary artery disease (CAD) and those with aortic stenosis (AS). The immunophenotype of MSCs was analyzed based on key markers: CD105, CD90, CD73, CD31, CD34, CD45, HLA-DR. Cell proliferation was assessed by the doubling time of the population and the specific growth rate of the cultures. The osteogenic potential was evaluated by the expression levels of the RUNX2, SPP1, ALPL, and BGLAP genes using PCR, as well as the protein levels in supernatants via ELISA. Qualitative detection of osteogenic proteins in cells by immunofluorescence staining. The intensity of extracellular matrix mineralization was measured using photometric methods. CD73 expression in EAT-MSCs from CAD patients was nearly 50% lower than in EAT-MSC cultures from AS patients. Following osteogenic induction, EAT-MSCs from CAD patients showed increased expression of osteogenic marker genes and their corresponding proteins. The intensity of extracellular matrix mineralization by osteoblasts derived from EAT-MSCs of CAD patients was higher than in the comparison group. EAT-MSCs from CAD patients with coronary calcification demonstrated reduced CD73 expression in culture and enhanced osteogenic potential compared to patients without coronary artery involvement. Full article

Background: Coffee contains bioactive compounds associated with cardiometabolic benefits, which modulate metabolic pathways of Sirtuin-1. The AGEs–RAGE axis promotes Sirtuin-1 degradation, but soluble RAGE (sRAGE) acts as a decoy receptor, modulating this signaling pathway. In this hypothesis-generating study, we explore whether relatively higher versus lower body mass index (BMI) phenotypes are associated with differential sRAGE responses to caffeinated and decaffeinated coffee in patients with coronary artery disease (CAD). Methods: Thirty patients were allocated into two intervention-sequence groups that differed in mean BMI (n = 15). Group A (higher BMI) received caffeinated coffee followed by decaffeinated coffee; group B (lower BMI) received the inverse sequence. Biomarkers were measured at baseline, 28, and 56 days. Multiple regression models were constructed using sRAGE as the dependent variable and glucose, glycated hemoglobin (HbA1c), homocysteine, lipoprotein(a) (Lp(a)), Sirtuin-1, and small dense LDL (sdLDL) as predictors. Results: Serum biomarkers remained unchanged; only Sirtuin-1 increased after caffeinated coffee (p = 0.033) in group B. Regression analyses revealed distinct metabolic profiles between groups. Group A: Baseline sRAGE was inversely associated with glucose and Lp(a) (R² = 0.748; p = 0.009). After coffee exposure, these associations disappeared. In group B, homocysteine and sRAGE were associated across all conditions. Furthermore, sRAGE was positively associated with sdLDL and inversely with HbA1c and Sirtuin-1 (R² = 0.862; p = 0.021) after decaffeinated coffee. After caffeinated coffee, sRAGE was positively associated with glucose and SIRT-1, and inversely associated with Lp(a) (R² = 0.908; p = 0.009). Conclusions: BMI appears to modulate the sRAGE response to coffee intake in CAD patients, with leaner individuals exhibiting a response that is highly dependent on the type of coffee consumed. Full article

Percutaneous coronary intervention (PCI) using drug-coated balloons (DCBs) may provide outcomes comparable to drug-eluting stents (DESs) due to the absence of a permanent implant and improved coronary artery remodelling. This study compared clinical outcomes of DCB-only angioplasty with DESs in a real-world setting. All patients undergoing PCI with DCBs or DESs for de novo disease were included in a propensity score-matched analysis using prospective and retrospective collected data from a single centre. The primary outcome was target lesion revascularisation (TLR) at 12 months. The secondary outcomes were major adverse cardiac events (MACEs) defined as a composite of all-cause death, myocardial infarction, or TLR at 12 months. Propensity matching produced 904 DCB lesions (719 patients) matched to 1424 DES lesions (1271 patients). The DCB group had smaller coronary arteries, shorter treated segments, and more bifurcation lesions. The mean age was 65 years, 22% of patients had prior MI, 16% had diabetes, and 58% had acute coronary syndromes. The rate of TLR at 12 months was as follows: 2.3% with DCBs; 2.5% with DESs (OR 0.86, p = 0.726, 95% CI 0.37–2.02). MACE was 8.2% with DCBs and 7.3% for DESs (OR 1.04, 95% CI 0.73–1.47). Results suggest comparable outcomes in patients who received paclitaxel DCBs compared to DESs without excess MACE, highlighting the need for randomised controlled trials. Full article

Background/Objectives: Severe mitral regurgitation (MR) is associated with chronic atrial stretch, chamber enlargement, pulmonary pressure elevation, and atrial fibrosis, yet the relationship between tissue inflammatory/profibrotic signaling, histologically quantified fibrosis, and echocardiographic remodeling remains incompletely characterized. This study aimed to compare biatrial tissue remodeling in patients with severe MR undergoing mitral valve surgery with a practical non-valvular surgical comparator group undergoing isolated coronary artery bypass grafting (CABG). Methods: This single-center, observational, cross-sectional comparative study included 36 elective cardiac-surgery patients: 22 with severe MR and 14 undergoing isolated CABG without significant valvular disease. Left- and right-atrial tissue samples were collected intraoperatively. IL-6, TNF-α, and TGF-β expression was assessed by quantitative real-time PCR using pooled atrial samples stratified by atrial side and study group, whereas atrial fibrosis was quantified histologically on individual tissue specimens using Masson’s trichrome staining and digital image analysis. Clinical, laboratory, and echocardiographic parameters were compared between groups, and exploratory associations were assessed with cautious interpretation. Results: Compared with the CABG comparator group, patients with severe MR showed a pooled molecular profile compatible with higher aggregate atrial expression of IL-6, TNF-α, and TGF-β; because qPCR was performed on pooled tissue preparations, these molecular findings were interpreted descriptively and were not used for patient-level inferential statistics. Histologically quantified fibrosis was significantly increased in severe MR in both the left atrium (29.69 ± 12.26% vs. 12.17 ± 4.56%, p < 0.0001) and the right atrium (25.25 ± 11.33% vs. 9.01 ± 4.46%, p < 0.0001). The MR group also showed more pronounced echocardiographic remodeling, including larger estimated left atrial volume, higher pulmonary artery systolic pressure, and greater right ventricular diameter. Exploratory individual-level analyses were restricted to histological fibrosis and echocardiographic variables. Conclusions: Severe MR was associated with marked echocardiographic remodeling and significantly greater histologically quantified biatrial fibrosis compared with a CABG surgical comparator group. Pooled qPCR findings support an aggregate inflammatory/profibrotic signal, but they should be interpreted descriptively because individual-level molecular variability could not be assessed. These findings are hypothesis-generating and do not establish causality. Full article

Background: Cardiovascular disease (CVD) remains the leading cause of mortality across the European Union (EU), with a fourfold to fivefold east–west gradient in standardized circulatory-disease mortality. Romania ranks second highest in the EU (787 per 100,000 inhabitants in 2023). Primary-prevention practice is organized around two quantitative frameworks—the 2021 European Society of Cardiology (ESC) SCORE2/SCORE2-OP system and the 2018/2019 American College of Cardiology/American Heart Association (ACC/AHA) Pooled Cohort Equations (PCE)—which converge on therapy but diverge on patient selection. Methods: We conducted a structured narrative review (SANRA-compliant) of contemporary primary-prevention guidelines, validation studies, key trials of risk-modifier interventions, and Romanian epidemiological data through April 2026. On this basis, we developed ROMA-CV (Risk Of Multifactorial Atherosclerosis—CardioVascular) as a conceptual, country-specific risk-stratification framework anchored to existing Class I/IIa recommendations or Level A/B evidence, rather than as a fully developed, ready-to-use clinical tool Results: Four structural limitations of SCORE2 are clinically consequential in Romania: (i) an age floor of 40 years that excludes the population in which premature myocardial infarction is most preventable; (ii) a country-level calibration coefficient applied to individuals; (iii) permissive treatment of lipoprotein(a) [Lp(a)]; and (iv) an under-emphasis of subclinical-atherosclerosis imaging. We propose ROMA-CV (Risk Of Multifactorial Atherosclerosis—Cardiovascular), a four-step algorithm retaining SCORE2 as the quantitative spine while embedding once-in-a-lifetime Lp(a) measurement, a mandatory amplifier checklist, and selective coronary artery calcium (CAC) or carotid/femoral ultrasound imaging. Conclusions: ROMA-CV is a hypothesis-generating proposal that operationalizes existing evidence-based recommendations into a deterministic Romanian pathway aligned with the 2025–2030 Romanian National Plan for Non-Communicable Diseases and the EU Cardiovascular Health Plan. The algorithm is not a validated clinical decision tool and requires prospective external validation in Romanian cohorts—alongside feasibility, cost-effectiveness, and implementation studies—before any consideration of routine clinical adoption. Full article

Background: Micro- and nanoplastics (MNPs) are emerging contaminants increasingly detected in human tissues and biological fluids. Their presence in blood, vascular tissues, thrombi, and atherosclerotic plaques raises concern about their possible association with cardiovascular disease. This systematic review synthesized evidence on associations between MNPs and cardiovascular pathology. Methods: A systematic search was conducted in October 2025 in PubMed, Scopus, Web of Science, and Embase according to PRISMA guidelines and a PICOS-based strategy. Original human studies from the last 10 years were eligible. Fourteen studies were included. Due to methodological heterogeneity, a narrative synthesis was performed. Risk of bias was assessed using ROBINS-E, and certainty of evidence was evaluated using a GRADE-informed approach. Results: MNPs were detected in multiple cardiovascular-related matrices. Included studies suggested possible associations with major adverse cardiovascular events, acute coronary syndrome, myocardial infarction, arterial stenosis, vascular calcification, thromboembolic disease, hypertension, inflammatory markers, coagulation-related parameters, and lipid profiles. However, the certainty of evidence was very low, and most studies had a high or very high risk of bias. Conclusions: Current evidence suggests a possible association between MNPs and cardiovascular pathology, but causality remains unproven. Larger prospective studies using standardized detection protocols, rigorous contamination control, and adjustment for confounders are needed. Full article