The Ross procedure utilizes a pulmonary autograft for aortic valve replacement, but late autograft failure remains a clinical challenge. In this exploratory study, we characterized structural alterations in failed pulmonary autografts using digital morphometric analysis. Five autografts explanted because of regurgitation were compared with six autopsy control pulmonary valves using special stains and alpha-smooth muscle actin immunohistochemistry. One histologically most affected section per valve was evaluated using QuPath. Failed autografts showed leaflet thickening, elastosis, fibrosis, and myxomatous matrix accumulation. Compared with controls, autografts had greater maximum leaflet thickness (1.540 vs. 0.447 mm; P = 0.004), cross-sectional area (8.730 vs. 3.045 mm²; P = 0.004), α-SMA-positive area (0.707 vs. 0.046 mm²; P = 0.008), and α-SMA-positive area fraction (0.069 vs. 0.016; P = 0.017). The findings demonstrate extracellular matrix alterations and increased α-SMA immunoreactivity in hotspot regions, suggesting a myxomatous-like remodeling pattern.
Accurate assignment of myocardial territories supplied by individual coronary arteries on coronary CT angiography (CCTA) is essential for estimating myocardium at risk. Validation of coronary-based myocardial segmentation has been limited by co-registration challenges with perfusion imaging as the reference standard. By reconstructing coronary angiograms directly from the dynamic CT myocardial perfusion imaging (CT-MPI), we ensured inherent co-registration between coronaries and perfusion maps. Vessel-specific myocardial territories were assigned using a minimum cost path (MCP) and validated against MBF-derived perfusion defects from the same acquisition. In 22 patients with 27 well-defined ischemic territories MCP-assigned territories showed moderate spatial overlap with CT-MPI-derived hypoperfusion (Dice coefficient 0.72 ± 0.13) with strong surface area correlation (r = 0.81, p < 0.001). Agreement was highest in the left anterior descending (LAD) territory. MCP-based tessellation using inherently co-registered CCTA and CT-MPI enables accurate vessel-specific myocardium-at-risk assessment and offers a promising platform for anatomical-functional integration in coronary disease.
MicroRNAs may provide information about decongestion in acute decompensated heart failure (ADHF). We examined associations with residual congestion and diuretic treatment intensity. In 145 adults with ADHF, seven admission serum miRNAs were quantified by RT-qPCR. Residual congestion at 48 h required at least 2 of: VExUS score ≥ 1, clinical congestion score ≥ 3, or NT-proBNP ratio ≥ 0.70. Logistic and robust log-linear models assessed residual congestion and intravenous loop-diuretic dose intensity. Residual congestion occurred in 69 patients (47.6
Atrial fibrillation (AF) is the most common sustained arrhythmia and is strongly associated with stroke, heart failure, and mortality. Aging is a major risk factor, while atrial electrical, structural, and metabolic remodeling drive AF progression. Emerging evidence highlights protein lysine acylation as an important regulatory layer linking metabolism with epigenetic and signaling pathways in AF, including acetylation, propionylation, lactylation, 2-hydroxyisobutyrylation, succinylation, and malonylation. These modifications have been implicated in the regulation of ion channel activity, mitochondrial metabolism, oxidative stress, inflammation, and fibroblast activation, which may contribute to atrial remodeling and arrhythmogenesis. This review summarizes current advances in acylation-mediated mechanisms and discusses the potential therapeutic implications of modulating acylation-related enzymes, such as sirtuins, histone deacetylases, and acyltransferases. Understanding acylation regulatory networks may provide a basis for exploring acylation-associated biomarkers and therapeutic targets in AF. Protein lysine acylation links metabolic alterations with atrial electrical, structural, metabolic, and inflammatory remodeling. Acetylation currently has the strongest AF-specific evidence, whereas other acylations show heterogeneous levels of mechanistic support. Site-specific propionylation, lactylation, and 2-hydroxyisobutyrylation provide emerging mechanistic links to AF. Acylation-related enzymes and metabolic pathways represent potential therapeutic targets, but most evidence remains preclinical. Future studies should establish site-specific causality and validate acylation-based biomarkers and therapeutic targets in clinically relevant models and human cohorts.
Improvement of left ventricular ejection fraction (LVEF) is a relevant phenotype in heart failure with reduced ejection fraction (HFrEF), but its substrate remains unclear. In 175 HFrEF patients followed prospectively for 24 months with serial echocardiography, left atrial (LA) strain and 16 biomarkers, LVEF improvement (increase ≥ 10 points to > 40
