Daily Cardiology Research Analysis
Analyzed 59 papers and selected 3 impactful papers.
Summary
Analyzed 59 papers and selected 3 impactful articles.
Selected Articles
1. Effect of a clinical decision support system on stroke care quality and outcomes in patients with acute ischaemic stroke (GOLDEN BRIDGE II): cluster randomised clinical trial.
In 77 Chinese hospitals enrolling 21,603 acute ischaemic stroke patients, a cluster randomized CDSS intervention reduced 3‑month new vascular events versus usual care (adjusted HR 0.74). CDSS improved adherence to evidence-based performance measures and reduced longer-term vascular events without excess bleeding.
Impact: Demonstrates that AI-enabled CDSS improves hard clinical outcomes and care quality at scale, supporting implementation in acute stroke systems of care.
Clinical Implications: Health systems should consider integrating validated CDSS to standardize imaging interpretation, etiologic classification, and evidence-based therapies in acute stroke pathways to reduce recurrent vascular events.
Key Findings
- CDSS reduced 3‑month new vascular events versus usual care (adjusted HR 0.74, 95% CI 0.58–0.93; P=0.01).
- Composite evidence-based care performance was higher with CDSS (improved composite and all‑or‑none measures).
- Reductions in vascular events persisted at 6 and 12 months; no signal for increased moderate/severe bleeding.
Methodological Strengths
- Large multicentre cluster randomized design with prospective registration (NCT04524624).
- Hard clinical endpoints and comprehensive quality-of-care metrics across 77 hospitals.
Limitations
- Cluster design may allow residual cluster-level confounding or contamination.
- Generalizability outside the Chinese hospital network and integration with diverse EHRs remains to be tested.
Future Directions: Evaluate cost-effectiveness, workflow integration, and model transparency; validate in other health systems and explore extension to secondary prevention clinics.
OBJECTIVE: To evaluate the efficacy of a clinical decision support system (CDSS) on stroke care quality and clinical outcomes among patients with acute ischaemic stroke. DESIGN: Multicentre, cluster randomised clinical trial. SETTING: 77 hospitals across China. PARTICIPANTS: 77 hospitals (38 randomised to intervention group, 39 to control group) enrolled 21 603 patients with acute ischaemic stroke admitted to hospital within seven days after symptom onset. INTERVENTIONS: Hospitals in the intervention group received stroke CDSS support including artificial intelligence assisted imaging analysis, classification of stroke causes, and evidence based treatment recommendations. Hospitals in the control group provided usual care. MAIN OUTCOMES MEASURES: The primary outcome was a new vascular event (composite of ischaemic stroke, haemorrhagic stroke, myocardial infarction, and vascular death) within three months after initial symptom onset. Secondary outcomes included the composite measure and all-or-none measure of evidence based performance measures for acute ischaemic stroke care quality, a new vascular event at six and 12 months, and disability (modified Rankin Scale score 3-6) and all cause mortality at three, six, and 12 months.
2. Myocardial T2 mapping using wideband T2 preparation gradient echo readout for patients with implantable cardiac devices at 1.5T.
A wideband T2‑prepared GRE sequence with patch-based denoising substantially reduced device-related artefacts and restored accurate myocardial T2 values. In subjects with ICDs, conventional GRE underestimated global T2 by 16% and increased segmental variability, whereas wideband GRE preserved edema detection comparable to bSSFP (relative T2 elevation ~44%).
Impact: Solves a pervasive barrier to inflammatory edema imaging in the growing population with pacemakers/ICDs, enabling broader clinical use of T2 mapping.
Clinical Implications: Centers can adopt wideband T2-prepared GRE protocols for device patients to reliably assess myocardial edema/inflammation, informing myocarditis, infarct-related edema, and therapy monitoring.
Key Findings
- With implantable devices, conventional GRE underestimated global T2 by 16% (P<0.001) and increased segmental coefficient of variation up to 30%, while wideband GRE provided accurate T2 values (P=0.56 vs reference).
- Edema detection was preserved with wideband GRE, showing relative T2 elevations of ~44% comparable to bSSFP.
- Patch-based denoising improved precision (P=0.006) without biasing mean T2 (P=0.999); results were consistent across phantom, volunteers, patients, and animal validation.
Methodological Strengths
- Multimodal validation spanning phantom, healthy volunteers, device and non-device patients, and an animal model with histology.
- Direct head-to-head comparison with conventional GRE and bSSFP, with quantitative precision analyses.
Limitations
- Sample size of device-implanted patients was modest and single-field strength (1.5T).
- Single-sequence, initial study; multicenter reproducibility and vendor-agnostic implementation need evaluation.
Future Directions: Prospective multicenter diagnostic accuracy and outcomes studies; extension to 3T and 3D acquisitions; standardization across vendors and integration into clinical pathways.
BACKGROUND: Myocardial T2 mapping enables non-invasive assessment of inflammation and oedema. However, in patients with implantable cardiac devices, such as pacemakers or defibrillators (ICDs), off-resonance effects often cause severe image artefacts and inaccurate T2 values. PURPOSE: The aim of this study was to develop and evaluate a wideband T2-prepared gradient-echo (GRE) myocardial T2 mapping sequence combined with an advanced patch-based denoising approach, designed to reduce artefacts and improve image quality in device-implanted patients at 1.5T. METHODS: A T2 preparation with wideband adiabatic refocusing pulses (5.0kHz bandwidth) was integrated into a breath-held 2D GRE T2 mapping sequence (TE = 0/27/55 ms). Patch-based denoising was applied after image reconstruction. The sequence was tested in a phantom, eight healthy volunteers with and without ICDs placed on their chests, thirteen patients without devices, seven patients with ICDs or pacemakers, and one sheep scanned before and after induced myocardial infarction with and without external ICD. The proposed sequence was compared against reference conventional GRE and balanced steady-state free-precession (bSSFP) T2 mapping.
3. USP25 regulates atherosclerosis by restricting RIPK1-mediated inflammatory responses.
USP25 expression is reduced in human atherosclerotic plaques and is predominantly localized to macrophages. Genetic ablation of macrophage USP25 in ApoE−/− mice exacerbated atherosclerosis, mechanistically via restriction of RIPK1-mediated inflammatory signaling, positioning USP25 as a protective regulator and potential therapeutic target.
Impact: Identifies a deubiquitinating enzyme as a gatekeeper of macrophage inflammatory signaling in atherosclerosis, highlighting a druggable axis (USP25–RIPK1) for intervention.
Clinical Implications: Translational efforts to modulate USP25 activity or downstream RIPK1 signaling could yield anti-inflammatory therapies for atherosclerosis, complementing lipid-lowering regimens.
Key Findings
- USP25 was significantly downregulated in human atherosclerotic lesions and was predominantly expressed in macrophages.
- Macrophage-specific USP25 ablation significantly exacerbated atherosclerosis in ApoE−/− mouse models.
- Mechanistically, USP25 restricted RIPK1-mediated inflammatory responses, identifying a protective role and therapeutic axis.
Methodological Strengths
- Human tissue profiling integrated with macrophage-targeted genetic mouse models.
- Mechanistic linkage to RIPK1 signaling provides a concrete pathway target.
Limitations
- Preclinical models; causal relevance and safety of targeting USP25 in humans remain untested.
- Extent of effect across diverse plaque phenotypes and comorbidities is not delineated in the abstract.
Future Directions: Develop selective USP25 modulators and test efficacy/safety in large-animal models; assess USP25–RIPK1 axis in human macrophages and clinical specimens longitudinally.
BACKGROUND: Atherosclerosis is a common vascular disease that poses a serious threat to global health. However, the mechanism underlying the pathogenesis and progression of atherosclerosis remains elusive. METHODS: We analysed the expression of deubiquitinating enzymes in human atherosclerotic lesions and found that USP25 was significantly downregulated. The role of USP25 in atherosclerosis was validated in mouse models with an ApoE FINDINGS: USP25 was predominantly expressed in macrophages in atherosclerotic lesions, and ablation of macrophagic USP25 significantly exacerbated atherosclerosis in ApoE INTERPRETATION: This study elucidated the function and molecular mechanism of USP25 in atherosclerosis, identifying USP25 as a beneficial regulator for this disease. FUNDING: This work was supported by the Natural Science Foundation of Zhejiang Province (LZ24H090003 to X.W. and LTGY23H090001 to W.W.), the National Natural Science Foundation of China (82150710557 and 82293642 to W.S.; 81971143 to X.W., and 82271347 to G.W.), and Wenzhou Municipal Science and Technology Bureau (Y2021094 to J.H.).