Search Results (1,829)

Late gadolinium enhancement (LGE) cardiac magnetic resonance is the reference standard for non-invasive myocardial tissue characterization. Conventional LGE analysis focuses on the presence and extent of fibrosis, yet these measures incompletely describe the spatial complexity of myocardial scar that underpins arrhythmogenesis. Entropy, derived from radiomic analysis of LGE signal-intensity distributions, has emerged as a surrogate marker of myocardial tissue heterogeneity. Mechanistically, heterogeneous fibrosis promotes electrical conduction alterations, and entropy serves as a global descriptor of this complex substrate. A growing body of evidence suggests that higher LGE entropy is associated with increased arrhythmogenicity and major adverse cardiac events. Several studies have shown that this association remains significant after adjustment for conventional clinical and imaging predictors. A smaller number of studies have gone further, demonstrating that incorporation of LGE entropy improves the discriminatory or reclassification performance of established risk-prediction models. This narrative review critically synthesizes the current evidence on LGE-derived entropy, compares methodological approaches and clinical applications, and discusses its principal limitations. After standardization and prospective validation, entropy-based phenotyping may prove useful for individualized risk stratification beyond conventional LGE metrics and guide clinical decision-making. Full article

Kawasaki disease (KD) is an acute, self-limiting systemic vasculitis that mainly affects young children. It is the leading cause of acquired heart disease in the developed world and is unique among childhood vasculitides for its predilection toward coronary artery involvement. This review describes the clinical spectrum of KD, highlighting diagnostic difficulties, especially in atypical presentations, and the challenges of managing treatment resistance. While intravenous immunoglobulin and aspirin remain the standard of care, especially in reducing coronary inflammation, early recognition and prompt therapy are crucial to preventing lifelong cardiac complications. To support this, various clinical risk scores have been developed over the decades to predict coronary artery lesions and IVIG resistance, enabling earlier intensification of treatment to prevent cardiac complications. Although the etiopathogenesis of KD remains unknown, extensive and robust research is ongoing to identify biomarkers, including epigenetic markers, innate and adaptive immunity activation markers, cytokine profiles, and to explore the influence of external triggers and the gut microbiome–immunity interplay. This review attempts to provide a concise overview of KD, aiming to assist clinicians in understanding the complexity of the problem rather than addressing all issues in detail. Full article

Background: Cerebral blood flow (CBF) is essential for maintaining cerebral metabolism in extremely preterm infants; however, no universally accepted reference standard exists for CBF velocity (CBFV). This study aimed to establish physiological reference patterns of middle cerebral artery CBFV under strictly defined physiological stability using multimodal monitoring. Methods: This post-hoc analysis included extremely preterm infants (gestational age ≤ 28⁺⁶ weeks or birthweight 500–1000 g) from a prospective cohort study. Serial Doppler ultrasonography of the middle cerebral artery was performed along with near-infrared spectroscopy and electrical cardiometry. Normal CBFV datasets were defined based on systemic stability, adequate cardiac output (>150 mL/kg/min), normal regional cerebral oxygen saturation (65–85%), and the absence of major comorbidities. Associations between Doppler parameters and postmenstrual age (PMA) and concurrent weight were analyzed using generalized estimating equations. Results: Forty infants contributed 194 normal CBFV datasets. Physiological reference ranges for peak systolic velocity (PSV), end-diastolic velocity (EDV), mean velocity (MV), resistance index (RI), and pulsatility index (PI) were established across PMA and concurrent weight strata. Both PSV and MV were associated with PMA and concurrent weight (p < 0.01), whereas EDV, RI, and PI were not. Mean blood pressure was not significantly associated with CBFV parameters. Conclusions: PSV and MV were maturation-dependent cerebral perfusion markers. Multimodally defined physiological stability provides a robust framework for establishing clinically relevant reference values for middle cerebral artery CBFV in extremely preterm infants. Full article

Doxorubicin (DOX) remains a cornerstone of chemotherapy but is limited by dose-dependent doxorubicin-induced cardiotoxicity (DIC). Recent evidence suggests that mitochondrial dysfunction, particularly oxidative stress and ferroptosis, drives DIC progression. While the flavonoid Calycosin (CAL) is known for its cardioprotective properties, the precise mechanism by which it maintains mitochondrial homeostasis remains elusive. This study aimed to investigate the effects of CAL against DIC and to explore the mechanisms by which CAL regulates mitochondrial integrity and iron homeostasis. Using both in vitro H9c2 cardiomyocytes and in vivo C57BL/6 mice, we demonstrate that CAL significantly restores cardiac contractility and reduces myocardial damage. Transcriptomic analysis indicated that CAL protected mitochondrial function and inhibited ferroptosis. Transmission Electron Microscopy (TEM) showed that CAL preserved mitochondrial structure. Assessments of the lipid peroxidation marker malondialdehyde (MDA) and superoxide dismutase (SOD) confirmed that CAL alleviated oxidative stress, while 8-OHdG staining verified its restoration of mitochondrial DNA integrity. Molecular docking identified the affinity of CAL with NRF2 and NRF1. CAL activated the NRF2/NRF1-TFAM axis both in vivo and in vitro, promoting mitochondrial biogenesis and respiratory function, while regulating iron homeostasis via FTMT and FPN. Knockdown or inhibition of NRF2/NRF1 abolished these protective effects of CAL. Our findings suggest that CAL acts as a dual-regulator of mitochondrial transcriptional machinery and iron metabolism, offering a novel therapeutic strategy to safeguard mitochondria against ferroptosis. Full article

Atrial fibrillation (AF) and heart failure (HF) frequently coexist, but the clinical relevance of AF may differ according to whether it appears to be a potentially reversible contributor, an aggravating factor in established HF, or a marker of advanced substrate. The driver–modifier–marker lens used in this review is a provisional, nonvalidated aid to clinical reasoning and should not be interpreted as a treatment score. This narrative review was informed by dated searches of PubMed/MEDLINE, the Cochrane Library, and OpenAlex through 29 July 2026, followed by a targeted update on 30 July 2026. It considers HF with reduced, mildly reduced, and preserved ejection fraction together with AF timing, burden, ventricular-rate exposure, myocardial substrate, and reversibility. Early rhythm control may be particularly relevant when AF is recent or temporally associated with ventricular dysfunction, symptoms, decompensation, or inadequate cardiac resynchronization therapy delivery. Evidence supporting catheter ablation is most direct in suspected AF-mediated cardiomyopathy and selected HFrEF populations, whereas evidence in HFpEF more consistently supports symptom relief, improved exercise hemodynamics, and AF-burden reduction than mortality reduction. Pulmonary vein isolation remains the procedural foundation. Radiofrequency, cryoballoon, and pulsed-field ablation are effective in broad AF populations, but HF phenotype-specific prognostic superiority has not been established for any energy source. Clinical decisions should reflect the design and directness of the evidence together with expected benefit, rhythm durability, procedural risk, patient-reported outcomes, stroke prevention, guideline-directed HF therapy, risk-factor management, and patient preference. Full article

Background: The Heart Rate Recovery Index (HRRI), derived from post-exercise heart rate recovery (HRR), reflects autonomic function and cardiovascular performance. Whether HRRI reflects early myocardial dysfunction and left atrial remodelling in heart failure with preserved ejection fraction (HFpEF) has not been previously examined. The H₂FPEF score, which integrates clinical and echocardiographic parameters, is used to assess the likelihood of HFpEF. This study investigates the relationship between HRRI, H₂FPEF score, and echocardiographic markers of longitudinal systolic function, including mitral annular plane systolic excursion (MAPSE), as well as left atrial volume index (LAVI), in patients with preserved left ventricular ejection fraction. Methods: A prospective observational study included 241 patients referred for cardiac exercise testing at the Institute of Cardiovascular Diseases Timisoara and the Clinical County Hospital of Sibiu. HRRI was calculated as the ratio of heart rate acceleration time (AT) to deceleration time (DT) during exercise testing. A comprehensive echocardiographic assessment was performed on all patients. Statistical analysis involved univariate testing and multivariable logistic regression with stepwise selection. Results: HRRI was significantly lower in HFpEF patients compared with those without heart failure (1.97 ± 0.66 vs. 2.73 ± 1.08, p < 0.01). HRRI correlated significantly with exercise performance, age, H₂FPEF score, and echocardiographic markers of diastolic and longitudinal systolic dysfunction. ROC analysis identified an HRRI cut-off value of 2.25 for HFpEF detection (AUC = 0.748), while HRRI remained significantly associated with HFpEF after adjustment for the covariates included in the model. The combined HRRI–H₂FPEF score improved diagnostic discrimination compared with the H₂FPEF score alone (AUC 0.897 vs. 0.858), achieving an overall classification accuracy of 82.2%. Conclusions: In our study, HRRI is significantly reduced in HFpEF and distinguishes patients with and without heart failure. It shows associations with echocardiographic markers of diastolic and longitudinal systolic dysfunction, exercise capacity, and H₂FPEF score. Full article

Background: This study aims to assess the effectiveness and safety of modified parasternal nerve block (MPSB) in providing perioperative analgesia and improving postoperative recovery in patients undergoing off-pump coronary artery bypass grafting (OPCABG). Methods: Sixty-five patients scheduled for OPCABG were randomly assigned to either the intervention group (MPSB group), which received a preoperative modified parasternal block, or the control group. The primary outcome measured was intraoperative opioid consumption. Secondary outcomes included levels of inflammatory markers, postoperative pain scores (assessed using the Visual Analog Scale, VAS), incidence of postoperative nausea and vomiting (PONV), total plasma ropivacaine concentration, gastrointestinal recovery parameters, mobilization metrics, intensive care unit (ICU) parameters (mechanical ventilation duration, ICU length of stay, requirement for rescue analgesics), length of hospital stay, incidence of postoperative pulmonary complications (PPCs), and chronic pain. Results: Intraoperative sufentanil consumption was significantly reduced in the MPSB group (130.0 [IQR, 110.0–167.5] μg vs. 280.0 [IQR, 192.5–327.5] μg; p < 0.01). Inflammatory markers were consistently lower in the MPSB group. Pharmacokinetic analysis revealed a mean peak plasma ropivacaine concentration of 0.88 μg/mL, with the maximum individual concentration reaching 1.76 μg/mL at 5 min post-administration. The MPSB group demonstrated superior postoperative outcomes, including lower VAS pain scores, earlier return of gastrointestinal function, reduced duration of mechanical ventilation, decreased rescue analgesic requirements in the ICU, shorter hospital stays, and lower incidence of PPCs. Conclusions: Preoperative modified parasternal block significantly reduced perioperative opioid consumption in cardiac surgery patients. This intervention demonstrated benefits in facilitating rapid postoperative recovery. The conventional ropivacaine dosing regimen was a safe and effective analgesic approach, associated with a low risk of local anesthetic systemic toxicity. Full article

Background/Objectives: High-sensitivity cardiac troponin I (hs-cTnI) has shown inconsistent diagnostic performance for acute cellular rejection (ACR) after heart transplantation. We evaluated whether time-normalized hs-cTnI kinetics provide incremental diagnostic value beyond the concurrent concentration for detecting ACR grade ≥ 2R and whether this association varies with time after transplantation. Methods: This retrospective single-center study included 1237 biopsy episodes from 139 heart transplant recipients. Two generalized linear mixed-effects logistic regression models with patient-specific random intercepts were compared. M1 included concurrent log₂-transformed hs-cTnI, whereas M2 additionally included the time-normalized change in log₂-transformed hs-cTnI per 7 days. Discrimination was assessed using leave-one-patient-out cross-validation with patient-level cluster bootstrap confidence intervals. Exploratory analyses examined early (≤90 days), late (>90 days), and continuous post-transplant time. Results: In the overall cohort, M1 showed modest discrimination (AUC 0.641, 95% CI 0.592–0.689), whereas M2 provided no improvement (AUC 0.635; ΔAUC −0.007). Within 90 days, neither model was informative (M1 AUC 0.503; M2 AUC 0.494). Beyond 90 days, M1 showed moderate discrimination (AUC 0.758, 95% CI 0.664–0.838), but M2 again provided no improvement (AUC 0.746; ΔAUC −0.012). Continuous-time modeling showed that the association between concurrent hs-cTnI and ACR strengthened with increasing time after transplantation, whereas the kinetic term remained non-informative. Conclusions: Time-normalized hs-cTnI kinetics did not provide incremental diagnostic value beyond concurrent hs-cTnI. Concurrent hs-cTnI may warrant further evaluation as an adjunctive late-period marker, but the 90-day threshold remains exploratory and requires external validation. Neither hs-cTnI concentration nor its kinetics should replace endomyocardial biopsy. Full article

Background/Objectives: Type 2 diabetes mellitus (T2DM) is a global epidemic strongly associated with an increased risk of heart failure, independent of coronary artery disease or hypertension. This condition, historically termed diabetic cardiomyopathy (DCM) and recently redefined as “diabetic myocardial disorder,” remains frequently underdiagnosed in its subclinical stages. The objective of this non-systematic review is to synthesize current evidence on the pathophysiological mechanisms, diagnostic advancements, and evolving therapeutic strategies for diabetic myocardial involvement. Methods: A comprehensive review of contemporary literature was conducted, focusing on recent consensus statements from the ESC and AHA, large-scale epidemiological data (IDF/WHO), and pivotal clinical trials (EMPA-REG, DAPA-HF, and LEADER). We analyzed the role of multimodal imaging—specifically speckle-tracking echocardiography (STE) and multiparametric cardiac magnetic resonance (CMR)—and circulating biomarkers in early phenotyping. Results: Pathophysiological drivers include lipotoxicity, oxidative stress, and AGE-mediated fibrosis. Advanced imaging techniques, such as global longitudinal strain (GLS) and CMR T1-mapping/ECV quantification, demonstrate superior sensitivity over LVEF in detecting early subendocardial dysfunction and diffuse fibrosis. Furthermore, NT-proBNP serves as a robust prognostic marker for the HFpEF-like trajectory typical of diabetes. Clinically, the therapeutic landscape has shifted with SGLT2 inhibitors and GLP-1 receptor agonists, which provide significant cardioprotection and reduction in heart failure hospitalizations through mechanisms beyond glycemic control. Conclusions: Diabetic myocardial disorder represents a complex continuum within the cardiometabolic spectrum. Early detection through multimodal imaging and biomarkers is essential for risk stratification. Integrating novel glucose-lowering therapies with proven cardiovascular benefits is now mandatory to alter the natural history of the disease and prevent progression to overt heart failure. Full article

Background: Myocardial ischemia–reperfusion during cardiac surgery is associated with complex metabolic alterations that reflect both myocardial injury and recovery. This prospective study aimed to characterize intraoperative lactate, pH, and bicarbonate dynamics in paired coronary sinus (CS) and peripheral blood samples and to explore whether these responses could be integrated into a composite marker of reperfusion-related metabolic burden (RMB). Methods: We prospectively studied 101 patients undergoing cardiac surgery with cardiopulmonary bypass. Simultaneous blood samples from the CS and peripheral circulation were obtained before aortic cross-clamping (T0), immediately after declamping (T1), and 10 min after reperfusion (T2). Temporal changes and transmyocardial gradients of lactate, pH, and bicarbonate were analyzed. RMB was calculated from standardized changes in these variables. As an exploratory analysis, associations with in-hospital mortality were evaluated using receiver operating characteristic (ROC) analysis. Results: Significant temporal variations in metabolic parameters were observed, with the most pronounced transmyocardial disturbances occurring at aortic declamping. Lactate demonstrated the largest gradient during early reperfusion, accompanied by transient acidosis and bicarbonate consumption. The RMB framework integrated these coordinated metabolic responses into a single measure of reperfusion stress. In exploratory outcome analyses, higher RMB values were observed among non-survivors, with the largest observed AUC for peripheral RMB measured 10 min after reperfusion (AUC 0.87). However, these estimates were based on only seven deaths and should be considered hypothesis-generating. Conclusions: Paired CS and peripheral sampling revealed dynamic metabolic adaptations during myocardial ischemia–reperfusion. The exploratory RMB framework integrates coordinated metabolic changes into a single descriptive measure of reperfusion-related stress. Its observed associations with in-hospital mortality remain preliminary and require confirmation through external validation and evaluation in larger independent prospective cohorts. Full article

Objectives: Heart failure (HF) arises from multiple interrelated pathological processes. Among these, lysosomal impairment and loss of autophagic homeostasis are increasingly recognized as important contributors to myocardial damage and ventricular remodeling. This study sought to identify lysophagy-associated signature genes in HF and to define their biological roles, cellular origins, and potential diagnostic relevance. Methods: Bulk myocardial transcriptome datasets, including GSE16499, GSE57338, and GSE76701, were integrated with the human cardiac single-cell dataset GSE145154. Differential expression analysis was first performed to identify lysophagy-related differentially expressed genes (DEGs). Candidate hub genes were then screened using support vector machine-recursive feature elimination (SVM-RFE) and least absolute shrinkage and selection operator (LASSO) regression. Functional enrichment analysis, Gene Set Enrichment Analysis (GSEA), immune infiltration assessment, single-cell transcriptomic mapping, and regulatory network analysis were subsequently conducted. The expression profiles of the selected genes were validated in a murine HF model, and VAMP8 overexpression assays were performed in H9c2 cells. Results: Five hub genes, namely VAMP8, STX2, MCOLN1, DERL1, and PTP4A2, were consistently and markedly decreased in failing myocardial tissue. These genes were mainly linked to SNARE-dependent vesicle trafficking and lysophagy regulation. A diagnostic model incorporating these hub genes demonstrated good discriminatory performance in both the training dataset and a small independent validation cohort, supporting further evaluation of their potential diagnostic value. Single-cell analysis further indicated that these genes were primarily enriched in cardiac FOLR2⁺ tissue-resident macrophages (TRMs). Pseudotime and cell–cell communication analyses associated this module with FOLR2⁺ TRM cell states and predicted interactions with cardiac stromal cells. In the HF mouse model, the mRNA levels of all five hub genes were decreased, with concurrent reductions in VAMP8, MCOLN1 and DERL1 protein expression. In Ang II/LLOMe-induced H9c2 cells, VAMP8 overexpression was associated with reduced cardiomyocyte injury, attenuation of changes in the abundance of lysosome- and autophagy-related proteins, and fewer ultrastructural abnormalities, suggesting a potential cardioprotective effect. Conclusions: VAMP8, STX2, MCOLN1, DERL1, and PTP4A2 were identified as candidate molecular markers of HF that reflect alterations in a lysophagy- and vesicular-transport-related program associated with FOLR2⁺ tissue-resident macrophages. These findings provide new insights into immune-microenvironment remodeling in HF and suggest potential directions for mechanistic and therapeutic investigations. Full article

Contemporary intensive care operates in an environment with high-complexity cases, large volumes of information, and vast physiological, biological, and therapeutic data, collected from laboratory results, investigations, and therapies for organ support, as well as from systems that operate in parallel. The lack of interoperability contributes to information overload, alarm fatigue, and delayed decision-making. The Smart ICU concept has been developed to address these limitations by integrating medical devices, information systems, and artificial intelligence into a unified system that allows interoperable data integration and predictive analytics. Aim: The purpose of this article is to provide a narrative review of the Smart ICU concept, with a specific focus on the cardiac intensive care unit. It summarizes Smart ICU architecture, data integration, clinical support, and applicability in monitoring perioperative inflammation in cardiac surgery. We describe the Smart ICU architecture, from data acquisition to storage and analytics, highlighting the differences between Smart ICU, artificial intelligence, and Tele-ICU, and we underline predictive analytics as a supportive tool, as well as its influence on clinical outcomes. Cardiac ICU application: Cardiac ICUs offer a data-dense, temporally well-defined model following cardiac surgery with cardiopulmonary bypass, where data concerning patients’ hemodynamics, perfusion data, and biological and inflammatory markers intertwine. Cardiac Smart ICU models could recognize early signs of hemodynamic compromise and low cardiac output states and identify early indicators of post-cardiac surgery complications. Neutrophil activation and complete blood count-derived indices may be used as dynamic biological data for Smart Cardiac ICU models. Conclusion: The Smart Cardiac ICU may support earlier risk stratification, and therefore earlier diagnostic and therapeutic interventions, but its clinical value requires prospective, multicenter validation. Cardiopulmonary bypass-induced inflammation may offer an ideal setting to integrate physiological, procedural, and immunological data into bedside predictive models. Full article

Background: Wearable sensing technologies enable continuous monitoring of physiological states in athletes, yet age-related differences in autonomic and mechanical load among professional soccer players remain insufficiently characterized. This study investigated whether heart rate variability (HRV) indices and accelerometry-derived physical load differ between younger and older professional players during routine morning training sessions. Methods: Fourteen male professional soccer players were monitored using a wrist-worn biosensor. Participants were divided into two age groups: Group A (≤23 years, n = 7) and Group B (≥24 years, n = 7). The device was attached at 08:30 and recorded tri-axial acceleration and cardiac signals continuously until 11:30 (≈3 h). Extracted metrics included root mean square of successive differences (RMSSD), percentage of NN intervals differing by more than 50 ms (pNN50), heart rate recovery (HRR), maximum heart rate, and total beat count. Group differences and position-based differences were evaluated. Results: Accelerometry-based physical load showed no significant difference between age groups. In contrast, HRV indices demonstrated age-related divergence: RMSSD was significantly higher in Group A compared to Group B (p = 0.031), suggesting greater parasympathetic activity in younger players. Total beat count was significantly higher in Group B (p = 0.015). pNN50 showed no group difference (p = 0.918). Pre- and post-session HRR did not differ significantly between groups, whereas maximum heart rate was significantly higher in Group A (p = 0.0017). Position-based comparisons revealed no consistent differences across metrics. Conclusions: Although mechanical load was comparable between age groups, autonomic markers—particularly RMSSD—indicated higher parasympathetic modulation in younger professional players. These findings align with established sports physiology literature but provide preliminary evidence derived from real-world data collected in professional soccer athletes using a compact wrist-worn biosensor. The results support the utility of wearable HRV monitoring for age-related physiological profiling in elite sports environments. Full article

Background/Objectives: In-hospital cardiac arrest (IHCA) remains associated with poor survival, while the contribution of arrest etiology and early physiological markers to outcome remains incompletely defined. We examined associations between clinical, neurological, metabolic, and etiological factors and sustained return of spontaneous circulation (ROSC) lasting >20 min, 28-day survival, and 60-day mortality. Methods: This retrospective single-center cohort included 134 adults with confirmed IHCA requiring cardiopulmonary resuscitation at a tertiary university hospital with advanced transplant care between 2011 and 2015. Sustained ROSC and 28-day survival were analyzed using parsimonious Firth penalized logistic regression models, and 60-day mortality using Cox proportional hazards regression. Selected neurological and biomarker analyses were considered exploratory. Results: Sustained ROSC was achieved in 91 patients (67.9%), 33 (24.6%) survived to day 28, and 30 (22.4%) survived to day 60. Initial non-shockable rhythm was associated with lower odds of sustained ROSC (aOR 0.26, 95% CI 0.09–0.69) and 28-day survival (aOR 0.27, 95% CI 0.10–0.68), and with higher 60-day mortality (aHR 1.96, 95% CI 1.25–3.08). The presence of a potentially reversible cause was associated with more favorable outcomes, whereas active hematologic malignancy was associated with higher 60-day mortality (aHR 1.89, 95% CI 1.15–3.10). Exploratory analyses also showed associations of initially dilated pupils with lower 28-day survival and higher lactate with 60-day mortality. Among patients who survived beyond 24 h, higher BNP was associated with subsequent mortality. Conclusions: Non-shockable rhythm and the presence of a potentially reversible cause were consistently associated with outcomes following IHCA, while active hematologic malignancy was associated with poorer longer-term survival. Exploratory findings from lactate, initial pupillary assessment, and BNP may provide complementary prognostic information, although the BNP analysis was limited to patients who survived beyond 24 h. These findings require confirmation in contemporary multicenter cohorts and do not establish validated clinical prediction tools. Full article

Background: Perioperative cardiovascular complications remain a major concern in patients undergoing noncardiac surgery. Coronary computed tomography (CT)-based imaging, including coronary artery calcium (CAC) scoring, coronary CT angiography (CCTA), and CT-derived fractional flow reserve (CT-FFR), enables noninvasive assessment of coronary plaque burden, anatomic stenosis, and functional ischemia. However, the comparative prognostic value of these CT-based imaging markers for predicting perioperative major adverse cardiac events (MACE) has not been systematically evaluated. Methods: We performed a systematic review and meta-analysis of studies evaluating CT-based coronary imaging before noncardiac surgery. PubMed, Embase, and Cochrane CENTRAL were searched from inception through December 2025. Studies were included if they assessed CAC, CCTA, or CT-FFR and reported perioperative MACE. Risk of bias was independently assessed by two reviewers using the Quality In Prognosis Studies (QUIPS) tool. Pooled effect estimates were calculated using a random-effects model. The CT-FFR analysis was pre-specified as exploratory given the limited number of eligible studies. Results: A total of 13 studies including 10,100 patients undergoing noncardiac surgery were included in the systematic review, and 9 studies were eligible for quantitative meta-analysis. Obstructive coronary artery disease detected by CCTA was strongly associated with perioperative MACE (pooled odds ratio [OR] 7.18, 95% confidence interval [CI] 3.89–13.25). CAC burden was also significantly associated with perioperative cardiac risk (pooled OR 2.48, 95% CI 1.76–3.50). One study evaluating CT-FFR demonstrated a strong association between CT-FFR-defined ischemia and perioperative events (OR 10.77, 95% CI 4.64–25.02). These findings suggest that different CT-based imaging markers provide complementary prognostic information, with anatomic and functional assessment offering higher point estimates than plaque burden scoring. Conclusions: CT-based coronary imaging markers are significantly associated with perioperative MACE in patients undergoing noncardiac surgery. CAC burden and obstructive CAD detected on CCTA demonstrated consistent prognostic associations with perioperative cardiovascular events across multiple studies. CT-FFR showed a strong exploratory signal in a single eligible study, suggesting a potential additional role for functional ischemia assessment, although further validation in larger prospective cohorts is required. CT-based coronary imaging may therefore provide valuable complementary information for perioperative cardiovascular risk stratification. Full article