Search Results (4,173)

Matrix metalloproteinase-8 (MMP-8), a neutrophil-derived collagenase responsible for the degradation of type I and III collagen, is involved in extracellular matrix remodeling, which may contribute to the destabilization of atherosclerotic plaques and thereby promote the development and progression of coronary artery disease (CAD). Single-nucleotide polymorphisms (SNPs) in the MMP-8 gene may influence the expression and activity of this enzyme, potentially affecting disease risk, clinical manifestation, and long-term prognosis. The study group included 259 patients diagnosed with CAD and 239 control blood donors. Genotyping of MMP-8 polymorphisms (rs1940475 and rs11225395) was performed using TaqMan PCR. MMP-8 gene polymorphisms showed no association with CAD risk, disease severity, or patient survival at the 5- or 10-year follow-up. All studied polymorphisms are located within the same haplotype block, where commonly co-inherited alleles (T rs1940475 and A rs11225395) may exert opposing functional effects. In conclusion, these findings suggest no significant role of the analyzed MMP-8 gene variants in CAD susceptibility or prognosis in the studied group. Full article

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic metabolic disorder associated with an elevated risk of cardiovascular disease. Mac-2 binding protein glycosylation isomer (M2BPGi), a noninvasive serum biomarker of hepatic fibrosis, has also been linked to adverse metabolic and cardiovascular outcomes. However, the association between serum M2BPGi levels and subclinical coronary atherosclerosis in individuals with MASLD remains unclear. We investigated the association between serum M2BPGi levels and coronary artery calcium score (CACS), an established imaging marker of subclinical atherosclerosis, in individuals with MASLD. Methods: This retrospective cross-sectional study included 6514 adults with MASLD who underwent health screening examinations between 2020 and 2025. Participants were categorized into quartiles according to serum M2BPGi levels: Q1 (<0.48), Q2 (0.48–0.61), Q3 (0.62–0.80), and Q4 (≥0.81). Coronary artery calcification (CAC) was defined as CACS > 0. Multivariable logistic regression analysis was performed after adjustment for age, sex, smoking status, liver enzymes, adiposity, dysglycemia, blood pressure, and lipid profile. Multivariable ordinal logistic regression analysis was additionally performed to evaluate the association between M2BPGi levels and CAC severity. Results: The prevalence of CAC increased progressively across M2BPGi quartiles (39.4%, 45.3%, 48.5%, and 57.4% for Q1–Q4, respectively; p < 0.001). In multivariable logistic regression analysis, participants in the highest M2BPGi quartile had significantly higher odds of CAC presence than those in the lowest quartile (OR, 1.32; 95% CI, 1.10–1.58; p = 0.0035). Higher M2BPGi quartiles were also independently associated with greater CAC severity in multivariable ordinal logistic regression analysis (OR, 1.33; 95% CI, 1.13–1.57; p = 0.0007 for Q4 vs. Q1). Conclusions: Higher serum M2BPGi levels were independently associated with both the presence and severity of CAC in individuals with MASLD. These findings suggest that M2BPGi may serve as a potential biomarker for identifying individuals with MASLD at increased risk of subclinical atherosclerosis and may complement conventional cardiovascular risk assessment. Full article

Background: Autoimmune diseases (AIDs) are associated with increased cardiovascular risk. However, specific protein mediators linking AIDs to major adverse cardiovascular events (MACE) and cardiovascular death (CV death) remain unexplored. This study identifies proteomic mediators linking AIDs to MACE via high-dimensional mediation analysis in the UK Biobank. Methods: We used UK Biobank data with proteomic profiling by Olink platform. Participants with prevalent myocardial infarction (MI), stroke, and heart failure at baseline were excluded. AIDs were categorized into musculoskeletal (MSK), vasculitis, gastrointestinal (GI), neurologic, and rheumatic fever subsets. Fine–Gray models assessed associations between AIDs and MACE and CV death. Proteome-wide association studies identified proteins associated with both AIDs and cardiovascular outcomes. High-dimensional mediation analysis (HIMA) explored protein-mediated pathways. All models adjusted for age, sex, lipids, BMI, smoking, hypertension, diabetes, chronic kidney disease, atrial fibrillation, and coronary artery disease. Results: Among 400,633 participants (median follow-up 14.5 years, 44.8% male), AIDs were present in 28,754 (7.2%). All AID categories were associated with increased MACE (sHR: MSK 1.34, vasculitis 1.67, GI 1.20, neurologic 1.33, rheumatic fever 1.38; all p < 0.001). For CV death, MSK, vasculitis, and rheumatic fever showed increased risk (sHR 1.34, 1.78, 1.51; all p ≤ 0.004), but not GI or neurologic AIDs. In 43,599 participants with proteomic data, HIMA identified 66 and 32 unique potential mediators linking AIDs to MACE and CV death, respectively. Four proteins (Growth Differentiation Factor 15, Interleukin-15, urokinase plasminogen activator receptor, and Tenascin C) mediated the AID-MACE relationship across multiple AID categories. Growth Differentiation Factor 15 and Interleukin-15 were shared mediators for CV death. Conclusions: This proteomic analysis identifies specific proteins that may mediate the association between AIDs and adverse cardiovascular outcomes, offering mechanistic insights into immune-related cardiovascular risk. These findings are hypothesis-generating and require replication and validation before the identified proteins can be considered causal mediators or adopted for clinical risk stratification. Full article

Background and Objectives: Psychological distress is common in acute coronary syndrome (ACS), yet its relationship with objective coronary anatomical complexity is incompletely understood. The Kessler Psychological Distress Scale-10 (K10) is a brief self-report instrument that measures non-specific psychological distress over the preceding four weeks. We investigated whether the K10 score is associated with the anatomical SYNTAX I score and the clinical–anatomical SYNTAX II PCI score in patients hospitalized with ACS. Materials and Methods: This prospective, single tertiary-center observational study assessed 865 adult patients with suspected or confirmed ACS between 6 January 2026 and 5 June 2026. After applying predefined inclusion and exclusion criteria, 750 consecutive eligible patients with complete K10, SYNTAX I, and SYNTAX II PCI data were included in the final analytic cohort. The cohort consisted of STEMI in 337 patients (44.9%), NSTEMI in 310 (41.3%), and unstable angina pectoris in 103 (13.7%). The validated Turkish version of the K10 scale was administered after pain control and hemodynamic stabilization, within 24–48 h of admission, by trained study personnel blinded to the final SYNTAX analysis. SYNTAX I and SYNTAX II PCI scores were calculated by two blinded interventional cardiologists. The primary endpoint was SYNTAX I score ≥ 23; the key secondary endpoint was SYNTAX II PCI score ≥ 36, interpreted as a cohort-based high clinical–anatomical risk threshold. Results: Mean age was 61.3 ± 11.6 years, and 543 patients (72.4%) were men. Mean K10, SYNTAX I, and SYNTAX II PCI scores were 23.7 ± 6.7, 22.4 ± 9.5, and 31.2 ± 9.6, respectively. K10 score correlated with SYNTAX I (Spearman rho = 0.417, p < 0.001) and SYNTAX II PCI (rho = 0.348, p < 0.001). Each 5-point increase in K10 was independently associated with SYNTAX I ≥ 23 (extended model-adjusted odds ratio [OR] 1.84, 95% confidence interval [CI] 1.59–2.12; p < 0.001) and SYNTAX II PCI ≥ 36 (extended model-adjusted OR 2.26, 95% CI 1.85–2.75; p < 0.001). K10 predicted SYNTAX I ≥ 23 with an area under the curve (AUC) of 0.706 (95% CI 0.674–0.744; cutoff ≥ 24) and SYNTAX II PCI ≥ 36 with an AUC of 0.693 (95% CI 0.654–0.736; cutoff ≥ 26). Adding K10 to the extended clinical model improved cross-validated AUC for SYNTAX I ≥ 23 from 0.708 to 0.774 and for SYNTAX II PCI ≥ 36 from 0.871 to 0.905; bootstrap optimism-corrected AUCs were 0.754 and 0.899, respectively. The findings remained consistent in sensitivity analyses excluding prior CABG patients, adjusting for psychiatric history/medication use, and evaluating patients whose K10 was completed before angiography. Conclusions: In this prospective ACS cohort, early in-hospital assessment of K10-defined recent psychological distress was independently associated with both anatomical and clinical–anatomical coronary complexity. K10 should not replace angiographic risk scoring, but it may help identify a psychocardiological phenotype characterized by higher coronary disease burden and greater clinical vulnerability. Full article

Background and Objectives: Coronary artery disease may be difficult to detect by resting echocardiography when left ventricular ejection fraction is preserved and regional wall motion abnormalities are absent. This study aimed to assess whether resting Tissue Doppler Imaging-derived mitral annular velocities can help identify CAD in patients with suspected angina pectoris. Materials and Methods: We conducted a cross-sectional observational study of 92 patients hospitalized with suspected angina pectoris who underwent elective coronary angiography at the Institute of Cardiovascular Diseases in Timișoara (January 2025–February 2026). Patients with conditions known to affect TDI-derived parameters were excluded, including previous acute coronary syndrome or myocardial revascularization, significant valvular disease, cardiomyopathies, relevant arrhythmias or conduction abnormalities, permanent pacing, reduced ejection fraction, and pericardial disease. Laboratory and echocardiographic data were collected. ROC curve analysis, univariable logistic regression and multivariable logistic regression were performed to evaluate the diagnostic performance of TDI-derived parameters and their independent association with coronary artery disease. Results: Patients with CAD had significantly lower average E′ values (7.4 ± 1.9 vs. 8.9 ± 1.8 cm/s, p < 0.001) and average S′ values [7.0 (IQR 6.0–7.5) vs. 9.0 (IQR 8.1–10.0) cm/s, p < 0.001], together with higher E/E′ ratios [9.33 (IQR 8.23–11.15) vs. 7.87 (IQR 5.93–9.51), p = 0.002]. Average S′ showed the highest discriminative ability for coronary artery disease, with an AUC of 0.899 (95% CI: 0.819–0.952, p < 0.0001). The optimal Youden-derived cut-off was ≤7.5 cm/s, yielding 77.42% sensitivity and 93.33% specificity. After adjustment for age, male sex, body mass index, diabetes, smoking status, hypertension and LVEF, dichotomized S′ remained an independent predictor of coronary artery disease (OR = 45.49, 95% CI: 8.03–257.68, p < 0.0001), with an adjusted model AUC of 0.92 and 88.04% correct classification. Conclusions: TDI, particularly S′ velocity, may be a useful resting echocardiographic parameter for identifying CAD in selected patients with preserved LVEF and no resting regional wall motion abnormalities. Rather than serving as a universal diagnostic marker, S′ should be considered a complementary, easily obtainable parameter that may improve non-invasive assessment in this specific clinical setting. Full article

Background and Clinical Significance: Iatrogenic aorto-ostial dissection is a rare but potentially life-threatening complication of percutaneous coronary intervention (PCI), most commonly involving the right coronary artery. Although ostial stenting is generally considered the standard bailout strategy, failure of initial sealing may occur in selected anatomical settings and remains poorly understood. A focused narrative review of the literature was conducted through PubMed/MEDLINE, Scopus and Web of Science to identify reports of PCI-related aorto-coronary dissection with particular attention to dissection morphology, propagation mechanisms, bailout strategies, and outcomes after ostial stenting; Case Presentation: A 76-year-old man presented with non-ST-elevation myocardial infarction. Coronary angiography showed severe ostial right coronary artery (RCA) disease and significant left anterior descending artery stenosis. Following drug-eluting stent implantation in the RCA, extensive aorto-ostial dissection with retrograde extension into the sinus of Valsalva occurred. Initial ostial stenting failed to seal the dissection and was complicated by hyperacute stent thrombosis. After successful rewiring of the true lumen, a second overlapping drug-eluting stent was implanted using a stent-in-stent technique, followed by prolonged balloon inflation, achieving complete sealing and stabilization. Serial computed tomography angiography confirmed stability, and staged PCI of the LAD was successfully performed five days later; Conclusions: Failure of primary sealing may depend not only on procedural factors but also on dissection morphology. Transverse dissections with wide entry tears may be less effectively sealed by a single ostial stent, whereas overlapping stenting with prolonged balloon inflation may represent a more effective bailout strategy. Full article

Background: Patients with Kawasaki disease (KD) who develop coronary artery aneurysms (CAAs) are at increased risk of future fatal coronary events. Pharmacotherapeutic strategies to prevent coronary stenosis are still lacking. In this exploratory study, the therapeutic effect of the angiotensin receptor blocker (ARB) losartan on coronary artery (CA) stenosis was investigated in a murine model. Methods: Five-week-old male C57BL/6J mice were intraperitoneally injected with 1000 μg of Lactobacillus casei cell wall extract (LCWE) (n = 12) to induce CA stenosis. Two weeks later, the LCWE-injected mice (n = 12) were divided into two groups: six received drinking water containing losartan (100 mg/L) (LCWE+ARB), while six received normal drinking water (LCWE group). A control group (n = 5) received phosphate-buffered saline (PBS) instead of LCWE. Sixteen weeks after LCWE administration—corresponding to the peak of CA stenosis and 14 weeks after treatment initiation—the mice were euthanized for histological evaluation of the coronary arteries. Results: Losartan treatment significantly reduced the coronary arteritis score (median [IQR (interquartile range)]: 0 [0–9.5] vs. 21.5 [15–24.3], p = 0.003). LCWE-induced neointimal formation with vascular smooth muscle cell proliferation and subsequent CA stenosis were markedly attenuated in losartan-treated mice (25% vs. 100%, p < 0.001). Losartan-associated attenuation of CA stenosis was accompanied by the preservation of medial calponin expression, a reduction in the number of proliferating cell nuclear antigen (PCNA)-positive cells in the neointima, and a decrease in serum MMP-9 (matrix metalloproteinase-9) levels. Conclusions: These findings from a murine model of KD provide preliminary evidence that losartan may attenuate coronary artery remodeling. Further mechanistic studies are warranted to clarify its potential translational relevance. Full article

Background and Objectives: Coronary computed tomography angiography (CCTA) has become a central non-invasive imaging modality for the evaluation of suspected chronic coronary syndromes. Nevertheless, referral patterns and sex-related differences in real-world CCTA utilization may vary according to demographic structure, healthcare accessibility, and regional clinical practice. The present study aimed to evaluate age- and sex-related patterns in CCTA referrals and coronary atherosclerotic burden within a real-world Eastern European single-center CCTA referral cohort. Materials and Methods: We performed a retrospective analysis of 2742 consecutive CCTA examinations at a tertiary center in Sibiu, Romania, between March 2019 and January 2025. The demographic profile of the referral cohort was compared with the adult population structure of Sibiu County. Subsequently, an age- and sex-stratified proportional subsample of 397 cases was selected from the CCTA cohort for detailed analysis of sex-related differences regarding coronary artery calcium score (CACS), significant coronary stenoses, and significant cardiovascular event risk. Results: The age distribution of the CCTA referral cohort differed significantly from that of the adult county population (p < 0.01), with referrals concentrated predominantly between 55 and 79 years of age. Female patients were overall more frequently represented within the referral cohort compared with the underlying county population; however, males demonstrated significantly higher coronary artery calcium scores, a greater prevalence of significant coronary stenoses, and higher revascularization risk compared with females—particularly between 50 and 79 years of age—within the stratified proportional subsample. In contrast, patients younger than 40 years demonstrated very low rates of significant coronary disease regardless of sex. Conclusions: This study provides a real-world perspective on age- and sex-related patterns in CCTA utilization and coronary atherosclerotic burden within an Eastern European imaging center. The findings highlight the interaction between demographic structure, guideline-directed diagnostic strategies, and coronary imaging utilization in routine clinical practice. Full article

Background: Non-invasive biomarkers may facilitate early risk stratification in patients with coronary artery disease (CAD). Although the uric acid-to-HDL cholesterol ratio (UHR) has been identified as a novel marker associated with coronary atherosclerosis, the relationship between the uric acid-to-magnesium ratio (UA/Mg ratio) and the angiographic burden of coronary artery disease has not been sufficiently investigated. This study evaluated the association between the UA/Mg ratio and angiographic coronary artery disease burden in patients undergoing elective coronary angiography and compared its discriminative performance with that of the UHR and the frontal QRS-T angle. Methods: In this retrospective cross-sectional study, patients who underwent elective coronary angiography between 2022 and 2025 were evaluated. Patients with atrial fibrillation, left ventricular ejection fraction <50%, eGFR < 50 mL/min/1.73 m², severe valvular disease, uric acid-lowering therapy, or acute coronary syndrome were excluded. A total of 351 patients were included in the study and divided into three groups—low (n = 117), intermediate (n = 117), and high (n = 117)—based on their Gensini scores. Independent associations were evaluated using multivariable ordinal logistic regression analysis. Receiver operating characteristic (ROC) analysis was performed to evaluate discrimination of the high Gensini tertile. Results: The UA/Mg ratio was strongly correlated with the Gensini score (ρ = 0.699, p < 0.001), showing a correlation comparable to that of the UHR (ρ = 0.717, p < 0.001) and stronger than that of the frontal QRS-T angle (ρ = 0.546, p < 0.001). In the multivariable ordinal logistic regression analysis, the UA/Mg ratio remained independently associated with higher Gensini tertiles (OR = 2.34, 95% CI: 1.23–4.45; p = 0.009). In the ROC analysis, the UA/Mg ratio demonstrated excellent discriminative performance for identifying the high Gensini tertile (AUC = 0.907, 95% CI: 0.877–0.938). The AUC of the UA/Mg ratio was comparable to that of the UHR (DeLong p = 0.978), whereas it was significantly higher than that of the frontal QRS-T angle (DeLong p < 0.001). Conclusions: The uric acid-to-magnesium ratio was strongly and independently associated with the burden of angiographic coronary artery disease in patients undergoing elective coronary angiography. The UA/Mg ratio demonstrated discriminative performance comparable to that of the UHR and superior to the frontal QRS-T angle. These findings suggest that the UA/Mg ratio may serve as a complementary biomarker for assessing angiographic coronary artery disease burden. Further prospective studies are warranted to validate its clinical utility. Full article

Background: Invasive coronary angiography has historically been the reference standard for coronary, valvular, and structural heart disease. Over the past decade, coronary computed tomography angiography (CCTA), CT-derived fractional flow reserve (CT-FFR), photon-counting detector computed tomography (PCCT), and cardiac magnetic resonance (CMR) have expanded the range of clinical questions answerable without an intra-arterial catheter, but this shift has been uneven across clinical domains. Methods: We performed a narrative review and synthesis of randomized trials, registries, society guidelines, and consensus documents (2009–2026) identified through PubMed and major cardiovascular guideline databases, written from a joint cardiology and cardiac-surgical standpoint. Results: The boundary has shifted asymmetrically, by which we mean a domain-dependent rather than uniform displacement of invasive angiography. Non-invasive imaging is now established as the first-line approach for stable chest pain at low-to-moderate pretest probability, for pre-transcatheter aortic valve replacement (TAVR) and structural procedural planning, and for aortic disease. It remains contested for stable multivessel disease and pre-coronary artery bypass grafting (CABG) planning, where CCTA- or CT-FFR-only planning is still investigational. Invasive angiography stays first-line for ST-elevation myocardial infarction (STEMI), cardiogenic shock, and complex percutaneous coronary intervention (PCI), where diagnosis and therapy are inseparable. Conclusions: Invasive and non-invasive modalities are complementary rather than competing. The appropriate first-line investigation depends on the disease domain, pretest probability, anatomical complexity, imaging quality, and whether diagnosis and treatment can be separated. We propose a complexity-stratified, heart-team framework and identify the surgical research gaps that remain. Full article

Background: Coronary in-stent restenosis (ISR) remains a major limitation of percutaneous coronary intervention (PCI) with drug-eluting stents (DES), adversely affecting long-term outcomes. Most available prediction models rely on invasive procedural variables and have been developed predominantly in high-income populations, limiting their generalizability. This study aimed to identify independent predictors of coronary ISR and to develop and internally validate a clinically applicable risk stratification model based on routinely available clinical, laboratory, and procedural factors in a cohort of patients from Kazakhstan. Methods: In this retrospective case–control study, 910 patients with coronary artery disease (CAD) who underwent follow-up coronary angiography after PCI between January 2018 and July 2025 were included. The study comprised 455 patients with angiographically confirmed coronary in-stent restenosis and 455 patients without restenosis selected using a consecutive sampling approach. Clinical characteristics, laboratory parameters, echocardiographic findings, and angiographic data were analyzed. Independent predictors were identified using multivariable binary logistic regression. Model discrimination was assessed using receiver operating characteristic (ROC) curve analysis, and internal validation was performed using bootstrap resampling. Results: The mean age was 62.9 ± 8.9 years, and 75.2% of patients were male. Restenosis was independently associated with prior myocardial infarction (MI) (OR 2.20; 95% CI 1.65–2.80), type 2 diabetes mellitus (T2DM) (OR 2.60; 95% CI 1.93–3.47), and smoking (OR 1.40; 95% CI 1.01–1.89). Patients with restenosis demonstrated a less favorable inflammatory and metabolic profile, including higher NLR, MHR, atherogenic index, and TyG index (all p < 0.05). LVEF was significantly lower, while multivessel disease and the number of implanted stents was higher (p < 0.001). A risk stratification model incorporating T2DM, the number of implanted stents, MPV, neutrophil count, HDL-C, LVEF demonstrated good discrimination (AUC 0.828) and 74.4% accuracy. Conclusions: The proposed model demonstrated good discrimination and satisfactory internal validity with limited optimism after internal bootstrap validation. It may serve as a useful tool for patient risk stratification after PCI. External validation in independent cohorts is required before widespread clinical implementation. Full article

This narrative review critically summarizes the literature on the associations of Type A and Type D personality, together with related personality traits, with cardiovascular disease (CVD) onset, prognosis, cardiac surgery, and rehabilitation outcomes. For the past half a century, there has been a consistent interest in the question of whether or not there is a connection between personality qualities and CVD. At the same time as individuals with a Type A personality who were angry, competitive, and excessively motivated were overrepresented among patients seeking treatment for CVD, it was also noted that these individuals were more likely to acquire coronary artery disease or syndrome. Anger and animosity were among the unfavorable impacts that were found to be connected with worse cardiovascular outcomes, according to the findings of research. After that, a new personality entity was brought into existence, which was referred to as the type D “distressed” personality. This personality type coupled negative affectivity and social inhibition. Type D personality subsequently became a major focus of research, and several studies reported associations with poorer patient-reported health and adverse cardiac outcomes. However, these findings have not been consistently replicated, and the stability, incremental predictive value, and independence of Type D personality from depression, disease severity, and other psychosocial factors remain debated. As a result, there are a number of criticisms that pertain to the current knowledge of the connection between personality construct and the risk of developing cardiovascular diseases as well as the outcome of these diseases. This review provides a critical narrative synthesis of supportive and conflicting evidence and highlights the methodological limitations that currently prevent definitive causal or prognostic conclusions. Full article

Objective: This study investigated the modifying effect of time to admission (TTA) on the relationship between admission to operation time (ATO) and outcomes in elderly patients with hip fractures. Methods: This retrospective cohort study included elderly patients with hip fractures treated at the trauma center. We collected data on patient characteristics, comorbidities, TTA, ATO, and all-cause mortality. Statistical analyses were conducted using R and EmpowerStats software. Results: Two thousand three hundred and sixty patients were included, with a median follow-up duration of 39.00 (29.05–50.79) months. Patients were stratified into four groups by ATO: ATO ≤ 2 d; 2 < ATO ≤ 4 d; 4 < ATO ≤ 6 d; and ATO > 6 d. The median TTA for each ATO group was as follows: 24 (4–168), 8 (4–48), 10.5 (4–48), and 10 (4–48) h, respectively. During follow-up, 733 patients (31.07%) died. Interaction analyses further stratified patients by TTA: ≤24 h vs. >24 h. The results demonstrated that TTA exerted a significant modifying effect on the ATO–mortality association. In the TTA ≤ 24 h group, each 1 d ATO delay was associated with a 5% increased risk of mortality (HR = 1.05; 95% CI: 1.01–1.09, p = 0.0095). In contrast, ATO delay was not associated with higher mortality in the TTA > 24 h group (HR = 0.98; 95% CI: 0.93–1.02, p = 0.3050). Notably, the TTA–ATO–mortality interaction remained statistically significant across several high-risk subgroups: females, those with femoral neck fractures, age-adjusted Charlson comorbidity index ≤ 4, hypertension, coronary artery disease, arrhythmia, and absence of chronic obstructive pulmonary disease. Conclusions: TTA is an important effect modifier of the association between ATO and mortality among elderly patients with hip fractures. Full article

Epicardial adipose tissue (EAT) is a distinct form of visceral adipose tissue that lies within the pericardium and directly adjacent to the myocardium. Individuals with type 2 diabetes mellitus (T2DM) exhibit excessive and metabolically active EAT, which contributes to the development of early diabetic myocardial disease, formerly referred to as diabetic cardiomyopathy. Recent studies have demonstrated that excess EAT is characterized by a proinflammatory profile that may adversely affect the underlying myocardium, leading to impaired diastolic and systolic function. In this review, we discuss the role of excessive EAT as a source of proinflammatory and profibrotic cytokines that influence adjacent ventricular and atrial myocardium through local tissue crosstalk. In addition to metabolic alterations, enlarged EAT induces hemodynamic changes that result in pericardial constraint and enhanced ventricular interdependence, both of which are hallmarks of diabetic pericardial disease. We further analyze the interplay among T2DM, inflammation, obesity, and increased EAT on the one hand, and myocardial dysfunction characterized by myocardial stiffness, elevated filling pressures, and diastolic and systolic dysfunction on the other. We emphasize that the distinct immunometabolic activity of perivascular adipose tissue may lead to a paradigm shift in the understanding of coronary artery disease, moving from a predominantly endoluminal to an exoluminal perspective. A wide range of dietary, lifestyle, and pharmacological interventions are available within this emerging diabeto-cardiometabolic continuum, each with a potential role; however, the timing of intervention is crucial. This review also explores the potential effects of antidiabetic and other pharmacological agents that modulate EAT thickness, volume, and/or activity, and discusses directions for future mechanistic and clinical research. Full article

Background: Exercise habits are unknown in pediatric patients with anomalous aortic origin of coronary arteries (AAOCA). In this study, we aim to identify differences in exercise habits and their relationship to BMI and other demographic factors in pediatric patients with AAOCA. Methods: A single-center, cross-sectional study of 573 patients with AAOCA (mean age = 10.5 years, SD 6.3, 63% males) was conducted. Exercise habits were classified as recreational or organized/competitive. BMI percentiles were stratified as normal (5th to ≤85th), overweight (85th to ≤95th), and obese (≥95th). Exercise habits and BMI were compared by demographic factors, presence of ischemia, and surgery status. Means were compared using two-tailed t-tests and multivariate linear regression with a false discovery rate correction. χ² tests were used for categorical variables. Results: Nearly two-thirds (63.5%) of patients exercise recreationally, and 35% of the total cohort are overweight or obese (BMI > 85th%ile). Those who exercise competitively (29%) were more likely to have had surgery (24% vs. 15%, p = 0.019) and less likely to be exercise-restricted (3% vs. 8.5% p = 0.018). BMI in right-AAOCA is significantly elevated compared to left-AAOCA (63.1 vs. 53.1 percentile, p = 0.018). There was no difference in BMI percentile in those restricted from exercise or in those who exercised competitively. BMI and exercise habits are unrelated to ischemia, AAOCA subtype, exercise habits or restriction on multivariate analysis. Conclusions: One-third of AAOCA patients are overweight or obese, and BMI is not associated with exercise habits in this cohort. Surgical patients were more likely to exercise competitively, and this may have implications for personal choices to engage in exercise. Future studies are needed to determine optimal exercise recommendations to promote active lifestyles while minimizing the risk of sudden death. Full article