Daily Cardiology Research Analysis
Analyzed 59 papers and selected 3 impactful papers.
Summary
A large multicenter cluster randomized trial showed that an AI-enabled clinical decision support system reduced new vascular events after acute ischemic stroke while improving care quality. Methodologically, a new wideband T2-prepared GRE sequence enabled accurate myocardial T2 mapping in patients with cardiac devices, and basic research identified USP25 as a macrophage regulator restraining RIPK1-driven inflammation in atherosclerosis, highlighting a druggable pathway.
Research Themes
- AI-enabled decision support improving vascular outcomes
- Advanced CMR methods overcoming device-related artifacts
- Inflammation-ubiquitin signaling as therapeutic targets in atherosclerosis
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 a multicenter cluster randomized trial across 77 hospitals enrolling 21,603 acute ischaemic stroke patients, an AI-enabled CDSS reduced 3‑month new vascular events (adjusted HR 0.74) and improved evidence-based care performance. Benefits persisted in cluster-level analyses and extended to longer-term vascular outcomes without excess bleeding.
Impact: This is a large pragmatic RCT demonstrating that AI-driven decision support can meaningfully reduce vascular events after stroke while improving adherence to guideline-based care.
Clinical Implications: Health systems can consider deploying validated CDSS platforms to standardize imaging interpretation, etiologic classification, and treatment recommendations for acute stroke to reduce recurrent vascular events.
Key Findings
- AI-enabled CDSS reduced 3-month composite new vascular events (adjusted HR 0.74; 95% CI 0.58–0.93).
- Improved adherence to evidence-based performance measures for stroke care in the intervention group.
- Favorable effects persisted in cluster-level analyses and extended to 6- and 12-month vascular outcomes without increased bleeding.
Methodological Strengths
- Multicenter cluster randomized design with over 21,000 participants enhancing generalizability.
- Predefined outcomes and clinically meaningful composite endpoint with time-to-event analysis.
Limitations
- Conducted in China; external generalizability to other health systems and resource settings requires validation.
- Cluster design may be subject to contamination or variable implementation fidelity across hospitals.
Future Directions: Evaluate CDSS scalability, integration with electronic health records, and cost-effectiveness across diverse health systems; assess subgroup effects and implementation strategies.
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. Safety outcomes were moderate or severe bleeding events and all bleeding events at three, six, and 12 months. RESULTS: 11 054 patients in the intervention group and 10 549 patients in the control group were enrolled from January 2021 to June 2023. New vascular events at three months occurred in 2.9% (320/11 054) in the intervention group compared with 3.9% (416/10 549) in the control group (adjusted hazard ratio 0.74, 95% confidence interval (CI) 0.58 to 0.93, P=0.01). The CDSS intervention effect remained significant in the cluster level analysis (-0.01, -0.02 to -0.004, P=0.003). Patients in the intervention group were more likely to have a higher composite measure (91.4% (77 049/84 276)
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 mitigated device-related off-resonance artifacts, restoring accurate myocardial T2 values and preserving edema detection in patients with cardiac implants. Performance matched conventional methods in non-device subjects and bSSFP for edema detection, with improved precision and no bias.
Impact: This methodological advance overcomes a major diagnostic blind spot in CMR for patients with pacemakers/ICDs, enabling reliable tissue characterization where it was previously limited.
Clinical Implications: Clinicians can consider wideband GRE T2 mapping for inflammatory/edematous myocardial diseases in device patients, improving diagnostic confidence when bSSFP or conventional GRE are artifact-prone.
Key Findings
- Conventional GRE T2 mapping underestimated global T2 by 16% and increased segmental COV up to 30% in ICD settings.
- Wideband GRE T2 mapping yielded accurate T2 values and preserved edema detection (relative T2 elevation ~44%), comparable to bSSFP.
- Patch-based denoising improved precision (P=0.006) without biasing mean T2 values (P=0.999).
Methodological Strengths
- Comprehensive validation across phantom, healthy volunteers, patients with and without devices, and an animal model with histology.
- Technical innovation using wideband adiabatic refocusing pulses and advanced denoising to address off-resonance artifacts.
Limitations
- Small sample size of patients with implanted devices (n=7) and single-center initial evaluation.
- Breath-held 2D acquisition; performance in arrhythmia or free-breathing 3D settings remains to be studied.
Future Directions: Multicenter studies to assess diagnostic and prognostic impact in myocarditis, sarcoidosis, and ischemic injury among device patients; integration with quantitative mapping protocols.
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. Patch-based denoising was optimized in patients without devices and impact on T2 precision and accuracy was assessed. Phantom studies included Bland-Altman and correlation analyses between the sequences. In-vivo performance was assessed through global and segmental T2 quantification, coefficient of variation (COV), artefact scoring, and oedema detection. ANOVA with Bonferroni correction and pairwise testing were used for statistical comparisons. RESULTS: In subjects without devices, wideband and conventional GRE T2 mapping yielded comparable T2 values (P=0.60). With ICDs, conventional GRE T2 mapping underestimated global T2 by 16% (P<0.001) and increased segmental COV up to 30%. In contrast, wideband GRE T2 mapping provided accurate T2 values (P=0.56) and preserved oedema detection, showing relative T2 elevations of 44% comparable to bSSFP. Patch-based denoising significantly improved precision (P=0.006) without biasing mean values (P=0.999). Results were consistent across phantom, volunteer, patient, and animal experiments, including animal ex-vivo histology confirmation. CONCLUSION: Wideband GRE T2 mapping substantially reduced device-related artefacts, provided accurate T2 values, and allowed oedema detection, offering a clinically feasible solution for patients with cardiac implants in this initial study.
3. USP25 regulates atherosclerosis by restricting RIPK1-mediated inflammatory responses.
USP25 was identified as a macrophage-enriched deubiquitinase that limits RIPK1-driven inflammatory signaling, thereby restraining atherosclerosis progression. Genetic or antibody-based manipulation demonstrated that loss of macrophage USP25 exacerbates disease in ApoE−/− mice, positioning USP25–RIPK1 as a therapeutic axis.
Impact: The study uncovers a mechanistic, druggable node (USP25–RIPK1) linking ubiquitin signaling to inflammatory atherogenesis, offering a path to targeted immunomodulation beyond lipid lowering.
Clinical Implications: Targeting USP25 to augment its activity or inhibiting downstream RIPK1 signaling may complement current therapies for atherosclerosis, particularly in inflammation-dominant plaques; translation will require safety and efficacy studies.
Key Findings
- USP25 expression is downregulated in human atherosclerotic lesions and is predominantly localized in macrophages.
- Macrophage-specific ablation of USP25 exacerbated atherosclerosis in ApoE−/− mice, indicating a protective role.
- USP25 restrains RIPK1-mediated inflammatory responses, mechanistically linking deubiquitination to atherogenesis.
Methodological Strengths
- Integration of human lesion profiling with mechanistic mouse genetics for causal inference.
- Cell-type specific interrogation (macrophage-targeted ablation) pinpointing the effector compartment.
Limitations
- Preclinical models may not fully recapitulate human plaque complexity and comorbidities.
- Therapeutic modulation of USP25/RIPK1 requires careful toxicity assessment given pathway roles in host defense.
Future Directions: Develop small-molecule USP25 activators or selective RIPK1 inhibitors; test efficacy in advanced, comorbidity-rich atherosclerosis models and evaluate biomarkers for patient stratification.
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.).