Cardiac arrest is a major medical emergency with survival rates below 10%. Among care components after the return of spontaneous circulation (ROSC), sedation remains poorly standardized. Initial sedation may be withheld from the most severely ill patients in order to facilitate the early identification of neurological recovery. We analyzed data from the prospective AfterROSC1 and AfterROSC2 cohort studies. We compared post-cardiac arrest patients in whom sedation was vs. was not started during pre-hospital care. Patients' characteristics, day-90 survival, and day-90 survival with a favorable neurological outcome were analyzed (modified Rankin scale 0-3). The day-90 neurological outcome was adjusted for disease severity (modified Cardiac Arrest Hospital Prognosis score [mCAHP]) and for center effect. Of the 1596 included patients, 1324 (83%) were and 272 (17%) were not sedated before intensive-care-unit (ICU) admission. In both groups, males and cardiac arrest at home predominated. The mCAHP score was higher in the group without pre-ICU sedation (median: 90 [70-106] vs. 105 [90-116], P=0.001). The pre-ICU sedated group had a higher proportion of patients with a favorable day-90 outcome (32.4% vs. 11.8%; P=0.001). This difference remained significant after adjustment for the mCAHP score and center (adjusted odds ratio, 2.19; 95% confidence interval, 1.31-3.65; P=0.003) but not after propensity score adjustment: 1.40 [95%CI: 0.70 ; 2.09] (P = 0.26). The decision of sedation started after ROSC and before ICU admission was associated with a good functional recovery on day 90. However, the design of this study does not allow us to establish a causal link between pre-hospital sedation and improved neurological recovery. In particular, it is not possible to formally rule out residual indication bias. A randomized trial assessing the effect of early sedation on treatment strategies and patient outcomes is needed.
The roles of Contactin-2 (CNTN2) and ferroptosis in heart failure and cardiac remodeling remain incompletely understood. CNTN2 was significantly upregulated in hypertrophic cardiomyopathy patients and heart failure mice. In cardiomyocyte specific CNTN2 conditional knockout (CNTN2 cKO) mice, transverse aortic constriction (TAC) induced markedly exacerbated heart failure, cardiac remodeling and ferroptosis compared to control mice. Ferroptosis inhibition substantially attenuated heart failure in CNTN2 cKO mice subjected to TAC, indicating that enhanced ferroptosis contributes to the detrimental effects of CNTN2 deficiency. RNA sequencing identified NUPR1, a ferroptosis repressor, as a downstream molecule of CNTN2. Mechanistically, CNTN2 activated the Lyn/eIF2α/ATF4 pathway to regulate NUPR1. CNTN2 overexpression attenuated Angiotensin II-induced cardiomyocyte ferroptosis and pathological remodeling, whereas these protective effects were abolished by Lyn or NUPR1 inhibitors. We further revealed CNTN2 and Lyn interacted with each other, and that CNTN2 interacted with Lyn through its 1-328aa domain. In vivo NUPR1 overexpression via AAV9 significantly mitigated TAC-induced heart failure and cardiac remodeling in CNTN2 cKO mice. Our study demonstrates that CNTN2 protects against pressure overload induced heart failure and cardiac remodeling by regulating ferroptosis through the Lyn/eIF2α/ATF4/NUPR1 pathway, suggesting CNTN2 as a potential therapeutic target.
This study aimed to evaluate the impact of perioperative respiratory muscle training on respiratory muscle strength, pulmonary function, functional capacity and prognostic outcomes in patients undergoing surgery. A randomized controlled trial. Cardiac surgery ward and cardiac surgery intensive care unit of a tertiary Grade A hospital in Fuzhou, China. Eighty-two participants. Perioperative respiratory muscle exercise. Eighty-two patients were randomly assigned to either the intervention group (n = 42), who performed perioperative respiratory muscle training, or the control group (n = 40). Patients completed one session per day from admission to discharge (except during mechanical ventilation). Respiratory muscle strength was assessed upon admission, the day before surgery, on the third day post-intensive care unit transfer, and at discharge. Each patient underwent a lung function test, six-minute walk test, self-efficacy for exercise scale, anxiety and depression test, and quality of life questionnaire, before and after intervention. The intervention group showed significantly greater improvements in maximal inspiratory pressure (57.69 ± 10.85 cmH2O vs. 48.28 ± 10.30 cmH2O), pulmonary function, functional capacity, postoperative pulmonary complications (38.1% vs. 65.0%), inspiratory muscle weakness (42.9% vs. 85.0%), duration of mechanical ventilation and intensive care unit stay, level of anxiety and depression, quality of life, and length of post-operative hospitalization. Additionally, the incidence of postoperative pulmonary (9.5% vs. 22.5%) and re-hospitalization within six months (9.5% vs. 17.5%) was reduced, though not statistically significant. Perioperative respiratory muscle training could contribute to improved respiratory muscle strength, pulmonary function, functional capacity, prognostic outcome, and quality of life in elderly cardiac surgery patients. Continuous activation of the respiratory muscles could provide multiple benefits for these individuals.
Sudden arrhythmic death remains a major clinical risk in ischemic heart disease (IHD), underscoring the need for improved risk stratification. Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) provides measures of scar burden and heterogeneity, but its incremental prognostic value beyond conventional markers such as left ventricular ejection fraction remains uncertain. We analysed two independent IHD cohorts (Dataset 1: n = 399, 54 events; National Research Ethics Service approvals 07/H0708/83 and 09/H0504/104+5; Dataset 2: n = 424, 50 events; derived from the prospectively registered REVIVED-BCIS2 trial, ISRCTN45979711, registered 20 November 2012)using clinical and LGE-CMR-derived variables to evaluate the contribution of LGE-CMR features, and compare machine learning-based survival modelling approaches. A brute-force feature-selection strategy identified optimal predictor subsets for Cox proportional hazards models, Random Survival Forests, and DeepSurv, evaluated using cross-cohort and pooled validation strategies. Scar entropy consistently emerged as a strong predictor of major arrhythmic events. Non-linear approaches outperformed Cox regression, with DeepSurv demonstrating superior generalization across cohorts and Random Survival Forests showing robust performance in pooled analyses. These findings support scar heterogeneity as an important prognostic marker and suggest that machine-learning survival models may improve arrhythmic risk prediction in patients with IHD.
Electrocardiogram (ECG) provides four-dimensional view to the electrical properties of the heart. We performed a comprehensive multi-domain screening to find the most significant lead-specific ECG features associated with sudden cardiac death (SCD). We analyzed retrospective data from 21,176 consecutive patients undergoing coronary angiography in Tampere University Hospital between 2007 and 2018. 937 ECG variables provided by the 12SL algorithm were used for the analysis. From those, the significant lead-specific ECG variables were categorized into three subgroups: P-wave, QRS complex, and ST-segment/T-wave. The most significant (i.e., lowest P-value) independent lead-specific ECG variables were tested in multivariate analysis after filtering correlating variables with weaker associations with SCD. Among ventricular depolarization (QRS complex) variables, the strongest associations with SCD were observed for QRS intrinsicoid deflection (lead I) (p = 4.6 × 10-8), QRS peak-to-peak amplitude (lead aVR) (p = 1.9 × 10-5), and Q-wave amplitude (lead V1) (p = 7.6 × 10-6). Among repolarization (ST-segment and T-wave) variables, the strongest predictors of SCD were T-wave amplitude (lead aVR) (p = 3.5 × 10-7) and ST-segment end amplitude (lead aVL) (p = 8.1 × 10-5). The strongest associations with SCD among atrial depolarization (P-wave) variables were P-wave onset amplitude (lead V6) (p = 3.1 × 10-6), P'-wave amplitude (lead V2) (p = 2.1 × 10-5), and P-wave duration (lead V2) (p = 2.4 × 10-3). These variables remained significant in multivariate analysis alongside global ECG variables (e.g., heart rate, QRS duration, and LVH). Systematic screening and utilizing the full prognostic potential of the 12‑lead ECG reveal several key elements of the electrical properties of the heart that associate with SCD.
Cardiac resynchronization therapy (CRT) with biventricular (BiV) pacing is non-physiological, and a third of patients do not respond. This study aimed to compare conduction system pacing (CSP) with BiV. Systematic searching of databases was conducted to include RCTs and comparative propensity-matched studies. CSP includes left bundle branch pacing (LBBP), his bundle pacing (HBP), and HOT/ LOT CRT (optimized HBP/ LBBP). Frequentist and Bayesian meta-analyses were performed. Twenty-eight studies (13 RCTs) with 5524 patients were included. CSP was associated with better CRT response (OR 1.69, CI: 1.20-2.39; p = 0.0027) and better clinical response (OR 1.83, CI: 1.12-2.99; p = 0.01). CSP was associated with lower odds of composite outcomes (OR 0.51, CI: 0.30-0.88, p = 0.01), HF hospitalization (OR 0.58, CI: 0.35-0.96; p = 0.0347), and all-cause mortality (OR 0.67, CI: 0.46-0.97, p = 0.0340). CSP was also associated with significantly higher improvement in QRS duration, LVEF, LVESD, NT-pro BNP, NYHA, and 6MWD (all p < 0.05). Bayesian meta-analysis consistently favoured CSP across all clinical outcomes, with probability of meaningful benefit exceeding 90% for CRT response, super-response, composite outcome, and HF hospitalization. However, RCT-only analysis yielded inconsistent results across most outcomes, with only clinical response remaining statistically significant. In subgroup analyses, LBBP appears to have the most benefit across CRT response and HF hospitalization outcomes. CSP may offer potential advantages over BiV pacing in patients indicated for CRT; however, confirmation in larger randomized clinical trials is required.
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Accurate prediction of fluid responsiveness is essential in managing circulatory shock. While passive leg raising (PLR) is recommended in international guidelines, its diagnostic validity depends critically on the monitoring modality used to detect hemodynamic responses. In resource-limited settings, manual blood pressure measurement remains the predominant available technology, yet its adequacy for PLR interpretation has not been rigorously evaluated in an adequately powered study with an independent reference standard. To compare the diagnostic accuracy of manual pulse pressure change (ΔPP%) versus continuous flow monitoring (USCOM-1 A, ΔSV%) for predicting fluid responsiveness during PLR in intensive care unit (ICU) patients with undifferentiated shock, using echocardiographic cardiac output assessment as an independent reference standard. Prospective single-center diagnostic accuracy study enrolling consecutive ICU patients with undifferentiated shock at Sina Educational and Medical Center, Tehran, Iran (2020-2021). A standardized PLR protocol was performed with simultaneous blinded measurements by three independent operators: manual blood pressure via calibrated sphygmomanometer, continuous flow monitoring via USCOM-1 A, and echocardiographic velocity-time integral (VTI) measurement as the reference standard. Fluid responsiveness was defined as ≥ 15% cardiac output increase following 500 mL crystalloid challenge. Primary outcome was area under the receiver operating characteristic curve (AUC). The study followed Standards for Reporting Diagnostic Accuracy Studies (STARD) 2015 guidelines (Ethics approval: IR.SBMU.PHARMACY.REC.1399.316). Of 124 patients analyzed (mean age 58.1 ± 19.8 years, 65.3% female), 58 (46.8%) were fluid responders. Continuous flow monitoring demonstrated acceptable diagnostic accuracy (AUC 0.712, 95% confidence interval [CI] 0.622-0.802; sensitivity 81.0%; specificity 61.8%; negative predictive value [NPV] 79.2%). Manual pulse pressure demonstrated significantly inferior discrimination (AUC 0.601, 95%CI 0.502-0.700; DeLong test P = 0.029) with critically low sensitivity (32.8%) and clinically inadequate NPV (57.8%). Bootstrap-corrected performance estimates confirmed the robustness of findings (USCOM AUC 0.708; Manual pulse pressure [PP] AUC 0.596). Mean pulse pressure remained essentially unchanged during PLR (+ 0.4 ± 4.6 mmHg, P = 0.287) despite significant proportional increases in both systolic (+ 3.7%) and diastolic (+ 5.6%) pressures, and despite echocardiographically confirmed stroke volume augmentation (left ventricular outflow tract [LVOT] VTI + 15.9%). The correlation between ΔPP% and ΔSV% was weak (r = 0.39, R²=0.15). Baseline method comparison between USCOM-derived and echocardiography-derived cardiac output showed low paired bias, although the percentage error exceeded the conventional interchangeability threshold, supporting interpretation of USCOM as a directional flow-monitoring index rather than a fully interchangeable substitute for echocardiography. In this single-center study, manual pulse pressure demonstrated insufficient sensitivity (32.8%) and inadequate NPV (57.8%) for reliable fluid responsiveness prediction during PLR. Our findings suggest it should be interpreted with considerable caution, particularly when the test result is negative. Continuous flow monitoring provides superior and clinically acceptable diagnostic accuracy when available, although USCOM should be interpreted as a directional flow-monitoring index rather than a fully interchangeable substitute for echocardiographic cardiac output measurement. The proportional pressure increase phenomenon provides a mechanistic explanation for this diagnostic limitation. These findings require multicenter validation before definitive practice recommendations can be issued.
Paediatric obstructive hypertrophic cardiomyopathy (oHCM) is a rare inherited cardiac disease that may present from childhood through adolescence and is associated with substantial long-term morbidity and mortality. Its management is based largely on observational studies and clinical experience and currently focusses on symptom improvement through medical therapy and, when indicated, septal reduction therapy to alleviate left ventricular outflow tract (LVOT) obstruction. In adult oHCM, mavacamten has established cardiac myosin inhibition as an effective strategy to reduce LVOT obstruction, but paediatric trial evidence has been lacking. The SCOUT-HCM trial is the first randomised placebo-controlled trial in adolescents to investigate the efficacy and safety of mavacamten for symptomatic oHCM. Among 44 adolescents (mean age 14.7 ± 1.7 years) mavacamten significantly reduced Valsalva-provoked LVOT gradients at 28 weeks, confirming short-term physiological efficacy. Secondary and exploratory findings, including NYHA functional class, cardiac structure and biomarkers, showed a trend to improvement, without a signal of left ventricular systolic dysfunction. The positive results of SCOUT-HCM, align with larger and longer adult oHCM trials and are likely to influence clinical practice, supporting a cautious integration of mavacamten in adolescent oHCM management. Longer follow-up and broader paediatric studies should determine durability of benefit, validated patient-reported outcomes, exercise capacity, arrhythmia burden, long-term safety and the need for septal reduction therapy in paediatric oHCM.
Echocardiography is the primary imaging modality for cardiac disease diagnosis. However, sound speed variations across heterogeneous tissue layers induce acoustic reverberation, leading to near-field haze which severely obscures cardiac structures and impairs diagnostic accuracy. Existing dehazing methods for echocardiographic sequences mainly rely on simplified haze distribution assumptions or basic dehazing architectures, resulting in suboptimal haze removal efficacy and computational efficiency. In this paper, we propose EchoWDiff, a real-time echocardiography dehazing framework that leverages a tailored wavelet-inspired Diffusion model with near-field constraint to reconstruct clean cardiac anatomy. First, with unpaired echocardiography sequences, an adversarial pairing module is introduced to learn the complex nonlinear mapping from clean images to hazy ones, thus generating realistic and physically-plausible clean-hazy pairs for diffusion training. Then, we devised a novel wavelet-inspired diffusion model that enables high-fidelity reconstruction of cardiac structures and fine texture details. This approach uniquely integrates multi-scale frequency analysis at both image and feature levels, allowing precise preservation of subtle anatomical boundaries and textural variations while reducing spatial dimensionality by four-fold, significantly enhancing computational efficiency without sacrificing reconstruction quality. Finally, a near-field haze contrastive perceptual loss is designed to guide the dehazing model to focus on near-field haze features through contrastive learning, ensuring more comprehensive and physiologically accurate haze removal. Extensive experiments on three multi-center clinical datasets from high- and low-end imaging machines validate the superiority of EchoWDiff, achieving improvements of up to 20.23 (FID) and 0.21 (gCNR) in echocardiography dehazing, and up to 0.10 (Dice) and 0.89 (ASD) in near-field left ventricle segmentation. It also boosts the processing speed by 27 FPS, demonstrating promising clinical applicability. The code repository is released on https://github.com/gaoxue0608/EchoWDiff.
Current therapies cannot simultaneously address the interconnected metabolic, cardiac, and renal damage in Cardiovascular-Kidney-Metabolic (CKM) syndrome. This study investigated ACF210, a novel long-acting dual agonist targeting both GLP-1 and APJ receptors, as a potential treatment for type 2 diabetes (T2D)-induced CKM syndrome. ACF210 was synthesized by fusing the human IgG4 Fc fragment to the C-terminus of GLP-1 and the N-terminus of Elabela-21 (ELA). In vitro receptor activation assays confirmed that ACF210 effectively activated the GLP-1 and APJ receptor signaling simultaneously. db/db leptin receptor-deficient mice and high-fat diet/streptozotocin-induced T2D were treated with dulaglutide, Fc-ELA, or ACF210 for 12 weeks. We assessed tissue morphology, organ function, and serum biomarkers. Compared to the diabetic control mice, ACF210 significantly improved blood glucose control and pancreatic β-cell function. Crucially, ACF210 demonstrated superior multi-organ protective effects over other treatments. Specifically, ACF210 reduced hepatic steatosis and provided comprehensive cardiac protection by lessening mitochondrial damage and fibrosis, enhancing diastolic function, reducing heart failure biomarkers such as NT-proBNP, and promoting microangiogenesis. In the kidneys, ACF210 alleviated podocyte damage and thickening of the glomerular basement membrane, while improving renal function as indicated by reduced levels of urinary albumin-to-creatinine ratio (UACR) and serum cystatin C. In conclusion, ACF210 not only effectively alleviates dysglycemia by potentially enhancing β-cell function but also significantly protects against diabetes-associated hepatic, cardiac, and renal damage, supporting its further exploration for the clinical management of CKM syndrome.
Doxorubicin (DOX)-based chemotherapy has improved survival outcomes in breast cancer patients but is often limited by doxorubicin-induced cardiotoxicity (DIC). Currently, no validated biomarkers can predict early DIC. Identifying novel biomarkers is essential for detecting patients at higher risk and enable timely interventions before irreversible cardiac injury occurs. Twenty-seven breast cancer patients treated with DOX-containing chemotherapy were stratified by change in left ventricular ejection fraction (LVEF): 19 patients who maintained normal cardiac function (normal, decline < 10%) and 8 who developed cardiotoxicity (abnormal, decline > 10%). Plasma samples were collected at baseline and after chemotherapy for untargeted metabolomic profiling. Both baseline and pre-post designs were employed to capture static and dynamic metabolic alterations associated with DIC. Stepwise logistic regression was used to filter non-informative metabolites, and predictive performance was further validated using Random Forest modeling. A well-marked separation of plasma metabolomic profiles was observed between normal and abnormal cardiotoxicity groups at baseline (T0). Statistical analysis identified 100 significant metabolites at baseline (T0) and 78 metabolites after the first cycle of chemotherapy (T0-T1), with 10 metabolites common to both time-points: 3-phosphoglycerate, 2-hydroxyphenylacetate, inosine, taurine, suberate (C8-DC), sebacate (C10-DC), sphingadienine, oxindolylalanine. Machine learning models identified key metabolites (e.g., sebacate [C10-DC], 2-hydroxyhippurate, orotate, picolinate, and suberate [C8-DC]) as candidate predictors of cardiotoxicity, achieving moderate discriminatory performance in cross-validation, with higher specificity than sensitivity, indicating limited detection of abnormal cases. Metabolomic profiling shows potential for early detection of DIC in breast cancer patients, supporting personalized interventions to prevent irreversible cardiac damage.
To evaluate the relationship between cardiopulmonary bypass (CPB) duration, change in thoracic fluid content (ΔTFC) measured using electrical cardiometry, and postoperative oxygenation in infants undergoing ventricular septal defect (VSD) closure. Prospective observational study. Single tertiary academic cardiac center. Thirty infants (1-12 months) undergoing elective VSD closure with CPB. Thoracic fluid content was measured using an electrical cardiometry (ICON monitor) before CPB and after separation from CPB. Arterial blood gases and ventilatory parameters were recorded at corresponding time points. CPB duration was positively correlated with ΔTFC (r = 0.50, p = 0.0045) and negatively correlated with a change in PaO2/FIO2 ratio (ΔP/F; r = -0.60, p = 0.0005) and dynamic compliance (r = -0.48, p = 0.007). Receiver operating characteristic analysis demonstrated excellent discrimination for postoperative oxygenation impairment (P/F <300) for both ΔTFC (area under the curve [AUC] = 0.91) and CPB duration (AUC 0.92). The optimal thresholds obtained were ΔTFC ≥13 kΩ-1 and CPB ≥84 minutes. In the multivariate linear regression adjusted for IL-6, prime volume/kg, transfusion/kg, and conventional ultrafiltration, ΔTFC independently predicted the postoperative P/F ratio (β = -5.68; p = 0.013), whereas CPB duration was not independently associated. Prolonged CPB is associated with greater thoracic fluid accumulation and impaired oxygenation in infants undergoing VSD closure. However, the relationship between CPB duration, ΔTFC, and pulmonary dysfunction appeared multifactorial and was influenced by perioperative inflammatory and fluid-related variables. Perioperative ΔTFC monitoring may provide a useful noninvasive adjunct for assessing postoperative pulmonary status after pediatric cardiac surgery.
Tisdale risk score has been validated for predicting drug-induced QTc prolongation (QTP) in cardiac care. This study aims to determine whether it can guide prescribing and monitoring of QTc-prolonging medications in primary care. A retrospective chart audit using Tisdale Risk Score was conducted. Data from 486 primary care patients from two Family Medicine Clinics, prescribed medications with known or possible risk of Torsades de Pointes (TdP) were reviewed. Eighty-five patients with pre- and post-pharmacotherapy ECGs comprised the cases. A control group of 184 patients not on QTc-prolonging medications was assessed. Patients were categorized as low, moderate, or high risk for QTP. Psychotropics were the most frequently prescribed QTc-prolonging medications. Baseline QTc did not differ significantly between cases (428 ms) and controls (426 ms). Among cases, most were stratified as low risk (69.4%), with fewer in moderate (25.9%) and high-risk (4.7%) categories. Comparatively, 99.5% of control patients were at low risk. QTc prolongation occurred in 5/85 (5.9%) post-pharmacotherapy, with none in the high-risk category. Odds ratio for QTP in moderate-risk patients versus low-risk was 0.71 (95% CI: 0.07-6.98). Most primary care patients were at low risk for drug-induced QTc prolongation. QTP events were low with none in the high-risk category, which limited evaluation of association between risk categories and QTc prolongation. The study highlights commonly prescribed QTc-prolonging medications in family medicine and their variable QTc effects, emphasizing the need for an outpatient-tailored risk assessment tool.
An isolated increase in tricuspid regurgitation velocity (TRV) during exercise stress echocardiography is frequently observed in patients with dyspnea, even in the absence of E/e' elevation. However, the pathophysiological and prognostic significance of this finding, particularly in patients without risk factors for pulmonary hypertension (PH), remains uncertain. Patients who underwent bicycle exercise stress echocardiography with simultaneous expired gas analysis for the evaluation of exertional dyspnea were retrospectively identified. After excluding patients with risk factors for PH, participants were categorized into three groups: controls (exercise TRV ≤ 3.2 m/s and exercise E/e' <15; n = 360), isolated exercise-induced increase in TRV (isolated Ei-TRV, exercise TRV > 3.2 m/s and exercise E/e' <15; n = 83), and heart failure with preserved ejection fraction (HFpEF, exercise E/e' ≥15; n = 211). Peak oxygen consumption was comparable between isolated Ei-TRV and controls, but significantly reduced in HFpEF. Over a median follow-up of 595 days, HFpEF patients had a two-fold higher risk of all-cause death and worsening HF events compared with controls whereas outcomes in isolated Ei-TRV did not significantly differ from controls. Nearly all patients with isolated Ei-TRV exhibited an abnormally elevated mean pulmonary artery pressure/cardiac output slope (mPAP/CO > 3 mmHg/L/min), and those with slopes > 5.2 mmHg/L/min had reduced peak oxygen consumption compared with those with slope ≤ 5.2 mmHg/L/min. In dyspneic patients without apparent risks for PH, isolated Ei-TRV was associated with preserved exercise capacity, without increased adverse outcomes compared with controls. Assessment of mPAP/CO slope may help refine risk stratification compared to exercise TRV alone in this population.
Transfusion-related acute lung injury (TRALI) and anaphylactic shock are rare but life-threatening transfusion-related complications. Differentiating between these conditions during general anesthesia is difficult because subjective symptoms cannot be assessed and intraoperative diagnostic evaluation is limited. A 40-year-old woman undergoing surgery for ovarian cancer under general anesthesia developed acute hypoxemia during transfusion. After completion of the transfusion, she developed sudden hypotension, tachycardia, and generalized erythema, which responded promptly to adrenaline administration. Respiratory failure persisted, and frothy sputum appeared in the endotracheal tube. Postoperative chest radiography showed bilateral pulmonary infiltrates, while echocardiography revealed preserved cardiac function. Anti-human leukocyte antigen (HLA) class I and II antibodies were detected in the transfused fresh frozen plasma, and serum tryptase levels were elevated postoperatively. This case demonstrated overlapping clinical features of TRALI and anaphylactic shock during general anesthesia. Although donor anti-HLA antibodies supported the possibility of TRALI, severe anaphylaxis alone could not be completely excluded as an explanation for the pulmonary edema.
Standing sedation is frequently required in donkeys for minor surgical and diagnostic procedures, yet information on the cardiac safety of α2-adrenoceptor agonists and opioid combinations in this species is limited. This study evaluated the echocardiographic effects of intravenous medetomidine, butorphanol, and their combination in clinically healthy donkeys. Sixty donkeys were randomly assigned to four groups (n = 15/group) to receive intravenous saline (control group, CG), medetomidine group (10 µg/kg, MG), butorphanol group (50 µg/kg, BG), or medetomidine-butorphanol group (10 µg/kg + 50 µg/kg, MBG). Butorphanol was administered 5 min after medetomidine in the MBG. M-mode echocardiography was performed from a right parasternal short-axis view at baseline and at 5, 15, 30, 45, 60, 90, and 120 min after treatment. Left ventricular internal diameter (LVID), interventricular septal thickness (IVST), and left ventricular posterior wall thickness (LVPW) were measured at end-diastole (d) and end-systole (s). Left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), stroke volume (SV), ejection fraction (EF%), and fractional shortening (FS%) were calculated. Data were analyzed using a repeated-measures general linear model. Medetomidine alone was associated with significant reductions in EF% and FS%, together with significant changes in LVIDs and LVIDd. SV was also significantly lower in the medetomidine group than in the control group during the main post-treatment period; however, SV and the calculated LV volumes were interpreted cautiously because they are load-dependent variables derived from linear M-mode measurements. These changes were accompanied by an increase in LVIDs and a reduction in IVSs, indicating transient depression of conventional left ventricular systolic indices and altered loading conditions. Butorphanol alone produced only minor, parameter-specific changes in LVID, IVST, and most echocardiographic indices, with no consistent clinically relevant deterioration compared with baseline or the CG. In contrast, the MBG showed marked changes in ventricular dimensions and calculated indices from 15 to 60 min; however, these findings were interpreted cautiously because the calculated systolic indices are load-dependent. Intravenous medetomidine, butorphanol, and their combination exert distinct and protocol-dependent effects on left ventricular dimensions and systolic function in donkeys. Medetomidine alone substantially and transiently depresses systolic performance, whereas butorphanol alone is comparatively cardiovascular-sparing. The medetomidine-butorphanol combination may be considered for standing sedation in clinically healthy donkeys; however, its echocardiographic effects should be interpreted cautiously as load-dependent changes, and cardiovascular monitoring remains advisable.
Mechanical cardiopulmonary resuscitation (CPR) devices are increasingly used during cardiac arrest to provide consistent chest compressions; however, concerns persist regarding their potential to cause traumatic injuries compared with manual CPR. To compare the cardiothoracic and abdominal injuries caused by mechanical versus manual CPR. A systematic review and meta-analysis was conducted in accordance with PRISMA guidelines. MEDLINE, EMBASE, PubMed, and the Cochrane Library were searched up to October 2025 for randomized controlled trials (RCTs) comparing mechanical with manual CPR in adults. Injury outcomes were grouped into clinically relevant categories and analyzed using Review Manager 5.4 with a random-effects model. Ten RCTs were included. There was no statistically significant difference between mechanical and manual CPR for liver injuries (odds ratio [OR]: 1.59, 95% confidence interval [CI]: 0.47-5.31, Z = 0.75, p = 0.46), rib and sternal fractures (OR 0.99, 95% CI 0.57-1.71; Z = 0.05, p = 0.96), thoracic or pleural injuries (OR: 0.97, 95% CI: 0.80-1.19, Z = 0.28, p = 0.78), or vascular and hemorrhagic complications (OR: 1.02, 95% CI: 0.20-5.13, Z = 0.02, p = 0.98). Subgroup analysis showed no difference for rib fractures or sternal fractures individually. Across all pooled injury categories, mechanical CPR did not demonstrate a significantly different injury profile to manual CPR; however, the low to very low certainty of evidence and absence of any low risk of bias trials mean these findings should be interpreted with caution and do not confirm safety equivalence.
Non-ischemic cardiomyopathy (NICM) includes a wide spectrum of myocardial disorders that result in ventricular dysfunction in the absence of significant coronary artery disease. The currently available treatments are primarily palliative in nature as they are not able to restore damaged cardiomyocytes or reverse structural damage. Stem cell-based regenerative methods show a potential therapeutic solution as instead of providing symptomatic benefits they are aimed at targeting the underlying cause. It has been observed in preclinical studies that the different types of stem cells act through immunomodulation, paracrine signaling, antifibrotic effects, and promoting angiogenesis rather than through direct action on cardiomyocytes. The improvement in left ventricular ejection fraction, functional capacity, and quality of life parameters observed in early-phase clinical trials for NICM show inconsistent results primarily due to heterogeneity in study design, type of stem cells, delivery methods, and patient selection. The main limitations include poor engraftment, heterogeneity of outcomes, and long-term safety concerns, particularly arrhythmogenic potential and tumorigenesis in pluripotent cell-based approaches. The advancements in genetic engineering, extracellular vesicle therapy, and combined cell-gene strategies are expanding the horizons of therapeutic potential of stem cells. This review synthesizes current evidence, highlights translational challenges, and explores emerging directions, including biomaterial-assisted delivery and precision medicine-based patient stratification, which may enable stem cell therapies to become a viable adjunct in managing NICM.
Acute heart failure (AHF) is a major cause of emergency department (ED) visits and is associated with significant morbidity and mortality. In Thailand, real-world data on AHF presentations and outcomes in the ED remain limited, particularly in resource-constrained settings. This study aimed to describe the clinical characteristics, treatment, and outcomes of AHF patients in a tertiary care ED in Northeastern Thailand and identify factors associated with in-hospital mortality. We conducted a retrospective cohort study of adult patients (≥ 18 years) diagnosed with AHF at the ED of Srinagarind Hospital between October 2021 and March 2023. Patients transferred from other hospitals or who were pregnant were excluded. Clinical data were extracted from electronic health records. The primary outcome was in-hospital mortality. Univariable and multivariable logistic regression analyses were performed to identify factors independently associated with in-hospital mortality. Of 902 eligible AHF patients, the median age was 71 years (IQR: 60-80), and 52.0% were male. The in-hospital mortality rate was 6.0%. Non-survivors were more likely to have a history of congestive heart failure, chronic kidney disease, or cerebrovascular accident, and presented with lower diastolic blood pressure and oxygen saturation. They were also more likely to be triaged as Emergency Severity Index (ESI) level 1 and require ICU admission, ventilatory support, and inotropic support. In multivariable analysis, the need for inotropic support was the only variable independently associated with in-hospital mortality (adjusted OR 3.97; 95% CI 1.91-8.40; p < 0.001). In this ED-based cohort, the in-hospital mortality of patients with acute heart failure was comparable to international reports. The need for inotropic support was strongly associated with hospital mortality, likely reflecting severe hemodynamic compromise.