Relentless mechanical work of the heart is powered by continuous oxygen consumption. How the heart uses oxygen is a defining feature of its health. Invasive studies have established that impaired oxygen consumption by the myocardium predicts contractile dysfunction and adverse outcomes. Despite its importance, noninvasive quantification of myocardial oxygen use remains limited. Magnetic resonance imaging (MRI) signal is known to be sensitive to blood oxygenation and has the potential to quantify myocardial oxygen consumption noninvasively, without exogenous contrast agents and free of ionizing radiation. However, its clinical translation has been impeded by the need for complex biophysical calibration, vulnerability to imaging artifacts and consistent vital motions, and the requirement of lengthy acquisition times. Here, we introduce a rapid, self-calibrated cardiac MRI framework that overcomes these barriers through high-resolution, motion-resolved coronary sinus oximetry, which can quantify myocardial oxygen extraction of the whole heart within 3 minutes. We optimized the imaging parameters via numerical simulations and validated them against invasive coronary sinus catheterization in a porcine model. We combined the method with clinical MRI sequences and demonstrated the feasibility of quantifying myocardial oxygen consumption and myocardial oxygen efficiency in patients with and without heart failure secondary to myocardial infarction in a single institution. This needle-free approach establishes a practical framework for noninvasive characterization of myocardial oxygen metabolism. It holds the potential to facilitate early disease detection, inform personalized therapeutic strategies, and guide the development of cardiometabolic therapies aimed at addressing the ongoing heart failure epidemic.
Abstract Background Coronary artery anomalies (CAAs) are rare congenital abnormalities involving the origin, course, or structure of coronary arteries. While often incidental, some variants have clinical and procedural implications. With the increasing use of computed tomography coronary angiography (CTCA), more anomalies are being detected, yet large-scale data from India remain limited. Objectives To evaluate the prevalence, anatomical patterns, and clinical relevance of CAAs over a 12-year period using CTCA at a high-volume tertiary cardiac center in India. Methods In this retrospective study, 20,243 consecutive patients undergoing multidetector CTCA between January 2011 and October 2023 were analyzed. Coronary anomalies were categorized into myocardial bridging (MB) and non-MB types based on Angelini’s classification. Each scan was independently reviewed by both a radiologist and a cardiologist. Results Coronary artery anomalies (CAAs) were identified in 1513 patients (overall prevalence 7.5%), largely driven by myocardial bridging (MB). When MB was excluded, the prevalence of non-bridging anomalies was 0.9% (n = 183), including both isolated and combined cases. Isolated myocardial bridging was the most common finding, identified in 1330 patients (87.9%), predominantly involving the mid-segment of the left anterior descending artery. Isolated non-bridging anomalies were observed in 171 patients, while 12 patients had combined MB and non-MB anomalies. Among non-bridging anomalies, the most frequent included anomalous right coronary artery origin from the left sinus with an interarterial course (26.9%), retroaortic left circumflex artery (9.9%), separate origins of the LAD and LCX (8.8%), and high take-off anomalies (7.6%). Most anomalies were classified according to Angelini’s framework, with a small subset remaining unclassified due to atypical anatomical presentations. Conclusions This 12-year retrospective cross-sectional study represents one of the largest single-center CTCA-based datasets on coronary artery anomalies (CAAs) globally. The findings highlight the utility of CTCA in detecting and characterizing both benign and potentially significant anomalies. The anatomical insights derived from this cohort have direct clinical relevance, aiding interventional cardiologists in procedural planning and risk stratification. Future multicenter studies are warranted to further refine diagnostic algorithms and management strategies across diverse populations.
More children are undergoing congenital or non-congenital cardiac surgery today which can impact outcomes for subsequent thoracic surgery. However, post-lung transplant (LTx) outcomes of children with previous cardiac surgery are unknown, so we explored this important issue using a publicly available database. A retrospective analysis was performed using the Scientific Registry of Transplant Recipients (SRTR). First-time pediatric LTx candidates without and with history of prior cardiac surgery, excluding previous cardiothoracic transplantation, from 2003 to 2024 were enrolled into our study. Univariate analyses, multivariable Cox regression, and Kaplan–Meier plots were performed for a comprehensive analysis. We identified 1333 and 144 LTx candidates without and with prior cardiac surgery (52 with congenital surgery, 92 with non-congenital surgery) with more children with cardiac surgery being listed for LTx over time. There were 811 LTx recipients without prior cardiac surgery compared to 63 with prior cardiac surgery (14 congenital, 49 non-congenital). Children with prior congenital cardiac surgery were much younger, and pulmonary vascular disease (PVD) was the most common indication for LTx. Prior non-congenital cardiac surgery did not negatively impact short- or long-term post-LTx outcomes in children. However, history of congenital cardiac surgery was associated with high waitlist mortality (31
Background: Postoperative delirium complicates up to one-quarter of cardiac surgery patients and increases morbidity and mortality. A validated prognostic model could guide targeted prevention. Methods: In this prospective cohort study, 158 adults undergoing cardiac surgery were enrolled. Delirium was assessed daily for five days using CAM-ICU, RASS, and ICDSC. Univariate predictors (p<0.05) entered multivariate logistic regression. Model discrimination was assessed by ROC analysis; internal validity by 500-sample bootstrapping and ten-fold cross-validation. Results: The mean age was 60.4 +/- 10.8 years and 53.2% were female. Delirium occurred in 38 patients (24.1%), peaking on day 1 (15.2%), with hyperactive subtype in 91.7%. Univariate risk factors: female gender (73.7% vs 15.6%, p=0.004), minimally invasive surgery (44.2% vs 20.0%, p<0.001), mechanical ventilation (36.7 +/- 34.3 vs 28.7 +/- 20.9 h, p=0.002), sedation (32.3 +/- 31.7 vs 19.7 +/- 16.7 h, p<0.001), propofol (25.9 +/- 20.1 vs 14.2 +/- 9.1 h, p<0.001), infection (42.1% vs 24.2%, p=0.033), stroke (18.4% vs 5.3%, p=0.009). Multivariate independent predictors: Female gender (OR 2.68; p=0.048; AUC 0.635; p=0.012); Minimally invasive surgery (OR 4.14; p=0.005; AUC 0.650; p=0.005); Propofol duration per hour (OR 1.07; p=0.011; AUC 0.747; p<0.001); Postoperative infection (OR 3.45; p=0.046; AUC 0.590; p=0.096). Apparent model (female gender, minimally invasive surgery, propofol sedation duration, and postoperative infection) AUC was 0.828 (95% CI 0.759-0.897; p<0.001). Bootstrap mean optimism was 0.038, yielding an optimism-corrected AUC of 0.790. Ten-fold cross-validation produced a mean AUC of 0.79 +/- 0.04. Conclusions: Postoperative delirium affects nearly one-quarter of cardiac surgery patients. A prognostic model including female gender, minimally invasive surgery, propofol sedation duration, and postoperative infection demonstrates robust discrimination (optimism-corrected AUC 0.790) and internal stability. Implementation may enable early risk stratification and optimization of sedation and infection-prevention protocols.
RATIONALE:Acute cellular rejection (ACR) remains a significant challenge in lung transplantation, with incomplete understanding of its molecular mechanisms and pathways linking ACR to chronic lung allograft dysfunction (CLAD). OBJECTIVES:To characterize the cellular and molecular mechanisms underlying ACR in lung allografts using single cell genomics and identify potential therapeutic targets for CLAD. METHODS:Single cell RNA-sequencing of freshly collected lung tissue was performed across 8 pediatric and adult patients with ACR, Resolved ACR, and surveillance biopsies without ACR. Validation included gene microarray analysis, immunofluorescence, and single cell ATAC-seq. MEASUREMENTS AND MAIN RESULTS:Gene set enrichment analysis revealed persistent TGF-β signaling and PI3K/AKT/mTOR pathway activation in both ACR and Resolved samples, validated by immunofluorescence showing sustained elevation of mTOR activation marker phosphorylated-S6 ribosomal protein and COL3A1. Fibrogenic cells exhibited myofibroblast gene signatures via mesenchymal state transitions rather than epithelial- or endothelial-to-mesenchymal transition. Cell communication analysis showed increased Type II Interferon signaling, with Jak/Stat pathway activation in endothelial and basal cells, and reduced VE-Cadherin staining in ACR. Compositional analysis revealed increased cytotoxic, memory T cells and dendritic cells, with persistent reduction of natural killer cells in ACR and Resolved. Donor/recipient analysis revealed predominantly recipient-derived immune cells in ACR. CONCLUSIONS:Persistent TGF-β and mTOR pathway activation following histologic ACR resolution provides molecular insight into ACR-CLAD linkage and suggests mTOR inhibition and TGF-β blockade as potential therapeutic mechanisms to prevent CLAD.
