Coronary artery calcium clinical utilization: An update.

IgG4 related coronary artery involvement: A scoping review of the literature.

Optimization of drug diffusion in drug-eluting stents for coronary artery based on deep reinforcement learning.

Introduction: Acute Coronary Syndrome (ACS) remains a major cause of morbidity and mortality worldwide, primarily driven by plaque rupture and thrombotic occlusion in coronary arteries. Traditional biomarkers provide limited insight into the inflammatory and lipid-driven mechanisms underlying plaque instability. Soluble Triggering Receptor Expressed on Myeloid Cells 2 (sTREM2), a shed form of a membrane-bound receptor expressed on macrophages and other myeloid cells, has been implicated in lipid metabolism, immune regulation and tissue homeostasis. Although its role in neurodegenerative and metabolic disorders has been increasingly recognised, its relevance in atherosclerosis and acute coronary events is still being elucidated. Exploring sTREM2 in this setting may offer novel perspectives on immune-metabolic activity in coronary artery disease. Aim: To investigate the association between serum sTREM2 levels and ACS, as well as disease severity. Materials and Methods: The present observational crosssectional study was conducted at the Department of Biochemistry, SRM Medical College Hospital and Research Centre, Potheri, SRM Nagar, Kattankulathur, Tamil Nadu, India, between December 2023 and August 2024. A total of 180 participants were enrolled, including 90 newly diagnosed ACS patients and 90 age- and gender-matched healthy controls. Inclusion criteria for the ACS group included adults aged over 25 years with a confirmed diagnosis of ACS {STElevation Myocardial Infarction (STEMI), Non ST-Elevation Myocardial Infarction (NSTEMI), or unstable angina} based on clinical presentation, Electrocardiographic (ECG) changes and cardiac biomarkers. Controls were healthy volunteers with no history of cardiovascular disease. Serum sTREM2 levels, lipid profile, Apolipoprotein B (ApoB) and high-sensitivity C-Reactive Protein (hs-CRP) were measured. ACS severity was assessed using the Synergy Between Percutaneous Coronary Intervention With TAXUS and Cardiac Surgery (SYNTAX I) score. Demographic parameters including age, gender, Body Mass Index (BMI). Statistical analysis was performed using Statistical Package for the Social Sciences (SPSS) version 22.0. Data normality was assessed using the Shapiro-Wilk test. Group comparisons were conducted using the Mann-Whitney U test and Kruskal-Wallis test. Spearman’s correlation was used to evaluate relationships between variables and Receiver Operating Characteristic (ROC) curve analysis assessed the diagnostic utility of biomarkers. A p-value <0.05 was considered statistically significant. Results: Serum sTREM2 levels were significantly higher in ACS patients {115.19 (78.18-191.67) pg/mL} compared to controls {70.74 (51.16-89.03) pg/mL} (p<0.001). ACS patients also exhibited elevated hs-CRP, ApoB, Total Cholesterol (TC), LowDensity Lipoprotein (LDL) and Very Low-Density Lipoprotein (VLDL), along with reduced High-Density Lipoprotein (HDL) levels. A positive correlation was identified between sTREM2 and body weight, BMI, TC, LDL and the TC/HDL ratio, while a negative correlation was noted with HDL. sTREM2 levels increased progressively with ACS severity as determined by the SYNTAX I score. No significant correlation was found between sTREM2 and hs-CRP or ApoB. ROC analysis demonstrated moderate diagnostic accuracy for sTREM2, with an Area Under the Curve (AUC) of 0.771. Conclusion: The present study demonstrates that serum sTREM2 levels are significantly elevated in ACS patients and correlate with disease severity. These findings suggest that sTREM2 may serve as a novel biomarker for ACS stratification, providing insights into the inflammatory and lipid-related mechanisms driving disease progression. Further longitudinal studies are required to validate its prognostic and clinical utility.

Optimal management of coronary artery disease (CAD) requires tailoring treatment strategies to lesion characteristics. Intracoronary pullback enables hemodynamic mapping of coronary lesions, potentially improving therapeutic decision-making, particularly in distinguishing focal from diffuse disease. To evaluate how pullback measurement influences overall treatment strategy-optimal medical therapy (OMT), percutaneous coronary intervention (PCI), or coronary artery bypass grafting (CABG)-in patients with significant CAD. We conducted a retrospective, multicenter cohort study including 842 patients with stable angina, unstable angina, or non-ST-elevation myocardial infarction (NSTEMI) and functionally significant left anterior descending artery (LAD) disease. Patients were stratified into two groups: one group (PB group, n=561) had pullback measurement, and the other (Conventional group, n=281) not. Outcomes included treatment strategy, major adverse cardiovascular events (MACE), and all-cause mortality at 1year. Pullback led to more Heart Team discussions (66.3% vs. 58.7%; p=0.033), greater adoption of OMT (51.5% vs. 40.9%; p=0.004), and lower PCI rates (27.1% vs. 36.3%; p=0.007). CABG rates remained unaffected. Pullback independently increased the odds of OMT and reduced the odds of PCI (OR = 0.58, p=0.003), while three-vessel disease strongly predicted CABG (OR = 2.51; p<0.001). At 1year, the PB group had higher mortality (4.3% vs. 1.1%, p=0.013), but similar MACE compared to the Conventional group. However, clinical outcomes did not differ between treatment groups. Intracoronary pullback favours a conservative treatment strategy. MACE rates are not increased at 1year.

Exercise training-induced plaque stabilization in rabbits associated with restored β2-adrenergic receptor signaling and reduced ectopic trypsin.

Coronary artery spasm (CAS), which can be epicardial and/or microvascular, is highly prevalent in patients with angina and non-obstructive coronary artery disease (ANOCA) undergoing coronary function testing (CFT). The CFT is invasive and limits larger diagnostics studies. We studied if Holter monitoring with symptom tracking identifies Holter-based CAS features with diagnostic potential in ANOCA patients. 42 ANOCA patients (88% female) were recruited in the UMCU-IMPRESS pilot study and wore a 12-lead Holter device for 2-7days prior to CFT, with simultaneous symptom tracking. We compared symptoms and Holter-ECG characteristics between patients with and without CAS and calculated diagnostic measures for CAS using several thresholds for ischemia-related parameters. 33 Patients were diagnosed with CAS (79%). These patients more often had≥1min of ST depression in total per day compared to patients without CAS (≥0.035mV: 88% vs 44%, p=0.013; ≥0.040mV: 73% vs 33%, p=0.049), but discriminative ability was limited (AUC (95% CI): 0.65 (0.48-0.68)). Furthermore, patients with CAS had periods of lower heart rates and longer PQ and QT times than patients without CAS, most evident at night and early morning. Patients with CAS more often demonstrated at least one minute of ST depression in total per day and exhibited periods of lower heart rates and longer PQ times mainly during the night and early morning compared to patients without CAS. Although discriminative ability was limited, we show that Holter monitoring may reveal signals in CAS patients, substantiating the need of large (AI-based) studies.

Impact of using the 2024 ESC guideline-recommended method to estimate the likelihood of obstructive coronary disease - a cardiac CT study.

Vascular smooth muscle cells (VSMCs) are the primary contractile component of blood vessels and can undergo phenotypic switching from a contractile to a synthetic phenotype in vascular diseases such as coronary artery disease (CAD) and restenosis. This process leads to decreased expression of SMC lineage genes and increased proliferative, migratory and secretory abilities that drive disease progression. Super-enhancers (SE) and lineage-specific transcription factors are believed to drive expression of genes that maintain cell identity and homeostasis. The goal of this study is to identify novel regulators of VSMC homeostasis by screening for SE-regulated transcription factors in arterial tissues. We characterized human artery SEs by analyzing the enhancer histone mark H3K27ac ChIP-seq data of multiple arterial tissues. We unexpectedly discovered the transcription factor PRDM16, a GWAS-identified CAD risk gene with previously well-documented roles in brown adipocytes but with an unknown function in vascular disease progression, is enriched with artery-specific SEs. Further analysis of public bulk RNA-seq and scRNA-seq datasets, as well as qRT-PCR and Western blotting analysis, demonstrated that PRDM16 is highly expressed in arterial tissues and in contractile VSMCs but not in visceral SMCs, and down-regulated in phenotypically modulated VSMCs. To explore the function of Prdm16 in vivo, we generated both inducible and constitutive Prdm16 SMC-specific knockout mice and performed bulk RNA-Seq analysis of aortic tissues and left carotid artery ligation to assess neointima formation. SMC-deficiency of Prdm16 does not affect the aortic morphology at baseline but significantly alters expression of many genes involved in VSMC homeostasis and cardiovascular disease, and suppresses VSMC proliferation and neointima formation in male mice. Specifically, Prdm16 negatively regulates the expression of Tgfb2 that encodes an upstream ligand of the TGF-β signaling pathway, by suppressing its promoter activity. Our results suggest that the CAD risk gene PRDM16 is highly expressed in VSMCs and is a novel regulator of VSMC homeostasis and neointima formation.

ROS disrupt COP9 signalosome-mediated ABCA1 protection and trigger its ubiquitination and degradation by cullin3 inhibiting cholesterol efflux and promoting foam cell formation in response to GPCR agonists.

Geometric deep learning-based coronary wall shear stress estimation from real-world patients.

Machine learning-based prediction of three-year mortality in elderly inpatients with coronary artery disease combined with heart failure.

Clinician-level variation in lipid management for secondary prevention of atherosclerotic cardiovascular disease: Opportunities for practice improvement.

Synchronising coronary artery system via physics-informed neural feedback control

Coronary computed tomography angiography (CCTA) enables a non-invasive, comprehensive assessment of coronary artery disease, and artificial intelligence (AI) offers the potential to improve CCTA image interpretation. This study aimed to evaluate the performance of an AI-powered method for automatic plaque quantification from CCTA, with optical coherence tomography (OCT) as reference standard. Patients who underwent CCTA within 6 months prior to OCT were retrospectively enrolled. AI-assisted automatic plaque quantification was performed on CCTA with specific plaque composition classification based on adaptive Hounsfield unit thresholds. Qualitative high-risk plaque features were also assessed. Automated co-registration of CCTA and OCT was performed with the link of invasive coronary angiography. A total of 91 patients with 153 co-registered lesions were evaluated. The AI-assisted automatic CCTA analysis showed significant correlations with OCT for quantifying plaque volume/burden and different plaque compositions (all P values <0.001); of which, the correlation coefficient for plaque volume was 0.84. Vulnerable plaque, defined as lipid-to-cap ratio >0.33 on OCT, was identified in 39 (25.5%) lesions. CCTA-derived plaque volume >82.5 mm3 [odds ratio (OR), 9.39], maximal plaque burden >76.4% (OR, 3.70), lipidic tissue volume >16.3 mm³ (OR, 4.42), all P < 0.001, and high-risk plaque features ≥2 (OR, 2.70, P = 0.009) were independent predictors of OCT-derived vulnerable plaques. The average time for automatic CCTA plaque quantification was 1.8 min per patient. The novel AI-powered method facilitated fully automatic plaque quantification and correlated well with co-registered OCT.

Linggui Zhugan Decoction mitigates post-myocardial infarction heart failure through modulation of cardiomyocyte F-actin cytoskeletal organization.

Fast cardiac magnetic resonance (CMR) protocol for biventricular functional assessment and tissue characterisation.

Transcriptome-wide association study of cardiovascular outcomes in chronic kidney disease: The chronic renal insufficiency cohort.

Liver fibrosis scores predict cardiovascular outcomes in myocardial infarction and non-obstructive coronary arteries patients with and without diabetes or prediabetes.

Analysis of arterial wall mechanics in right coronary artery obstructive disease: FSI modelling and non-invasive FFR validation