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Journal articleVerheye S, Hoef TPVD, de Silva R, et al., 2025,
Coronary sinus narrowing for the treatment of refractory angina: one-year results of the REDUCER-I study
, EUROINTERVENTION, Vol: 21, Pages: e879-e881, ISSN: 1774-024X -
Journal articleGutmann C, Barwari T, Schulte C, et al., 2025,
Platelets and inflammation-insights from platelet non-coding RNA content and release in the Bruneck study and the PACMAN-AMI trial
, CARDIOVASCULAR RESEARCH, Vol: 121, Pages: 1392-1406, ISSN: 0008-6363- Cite
- Citations: 1
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Journal articleKeles M, Lawrie A, 2025,
Assessing pulmonary artery stiffening with ultrasonography: a step forward for the assessment of pulmonary hypertension due to left heart disease?
, CARDIOVASCULAR RESEARCH, Vol: 121, Pages: 1314-1315, ISSN: 0008-6363 -
Journal articleLi Kam Wa ME, Ezad SM, Modi B, et al., 2025,
Randomized comparison of fractional flow reserve and instantaneous wave free ratio in serial disease
, JACC: Cardiovascular Interventions, Vol: 18, Pages: 1617-1627, ISSN: 1936-8798BackgroundFractional flow reserve (FFR) and the instantaneous wave-free ratio (iFR) identify arteries that benefit from percutaneous coronary intervention (PCI). FFR or iFR gradients on pullback are often used to predict the physiological result (FFRΔ or iFRΔ), but this approach is unvalidated.ObjectivesThe aim of this study was to compare the accuracy of FFRΔ, iFRΔ and FFRcalc (a mathematical solution incorporating interaction between lesions) for predicting post-PCI physiology in serial or diffuse disease.MethodsPatients with a focal target lesion and either a second focal lesion or a diffusely diseased segment in the same vessel were randomized to FFR- vs iFR-guided PCI (ISRCTN18106869). FFR and iFR pullbacks were performed, with operators blinded to one modality. Following target lesion PCI, FFR and iFR were remeasured. The primary outcome was the error in predicted post-PCI physiology compared with actual values.ResultsA total of 87 patients were randomized to FFR (n = 45) or iFR (n = 42). Median FFR and iFR were 0.70 (Q1-Q3: 0.62 to 0.78) and 0.81 (Q1-Q3: 0.68 to 0.90) at baseline and 0.82 (Q1-Q3: 0.74 to 0.87) and 0.89 (Q1-Q3: 0.83 to 0.93) after target lesion PCI. The predictive errors were 12% (6% to 17%) for FFRΔ, 4% (0% to 9%; P < 0.001) for iFRΔ, and −5% (−18% to 8%; P = 0.427) for FFRcalc. Significant residual disease was missed in 36% of cases with FFRΔ, 34% with iFRΔ, and 14% with FFRcalc.ConclusionsFFR and iFR pullback gradients overestimate the benefit of target lesion PCI and can miss residual ischemia in one-third of patients. FFR or iFR should be routinely repeated post-PCI in serial disease.
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Journal articleDurrington C, Battersby C, Holt L, et al., 2025,
NT-proBNP and BNP Testing in Pulmonary Arterial Hypertension: Point-of-Care and Remote Monitoring
, RESPIROLOGY, ISSN: 1323-7799 -
Journal articleMacanovic P, Cheng K, Ramasamy A, et al., 2025,
Persistent angina with non-obstructive coronary artery disease: unmasking coronary microvascular dysfunction post-oncotherapy
, JACC: Case Reports, Vol: 30, ISSN: 2666-0849BackgroundCoronary microvascular dysfunction (CMD) is frequently the cause of patients presenting with angina and non-obstructed coronary arteries (ANOCA) and may have increased prevalence in cancer survivors. Case SummaryWe report a case of refractory angina in a survivor of Hodgkin lymphoma, previously treated with radiotherapy and chemotherapy. After demonstrating unobstructed epicardial arteries, advanced diagnostics including quantitative stress perfusion cardiac MRI and invasive coronary physiology testing, revealed CMD as a likely sequela of oncotherapy and informed initiation of mechanism-specific treatment. DiscussionCMD may represent an under-recognized cardiotoxicity of oncotherapy. This case highlights the value of formal, multimodal coronary microvascular function assessment to identify CMD and implement stratified management. Future systematic evaluation investigating the relationship and underlying mechanisms of oncotherapy in CMD is warranted.Take Home messagesIn cancer survivors presenting with ANOCA, clinicians should have a high index of suspicion for CMD and consider systematic evaluation to guide stratified treatment.
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Journal articleJose A, Yogeswaran A, Fuenderich M, et al., 2025,
Survival outcomes and impact of targeted PAH therapy in portopulmonary hypertension in the PVRI GoDeep meta-registry
, Pulmonary Circulation, Vol: 15, ISSN: 2045-8932Portopulmonary hypertension (PoPH), a type of pulmonary arterial hypertension (PAH) in patients with liver disease, is associated with high morbidity and mortality. The relationship between cardiopulmonary hemodynamics, PAH therapy, and survival in PoPH remains unclear. We performed a retrospective cohort study of PoPH patients from the international pulmonary hypertension (PH) meta-registry, PVRI GoDeep. PAH was defined by a mean pulmonary arterial pressure > 20 mmHg, pulmonary arterial wedge pressure ≤ 15 mmHg, and a pulmonary vascular resistance (PVR) > 2 Wood Units. PoPH diagnoses were assigned by each center's PH specialist based on international guidelines at the time of enrollment. 246 incident PoPH patients met eligibility criteria and were included in the analysis, equally split between males (51%) and females (49%), with a median age of 54 years. When compared to both patients with IPAH and those with other subtypes of PAH (not classified as PoPH or IPAH), those with PoPH had significantly lower 5-year survival rates (46% vs. 68% vs. 65%, log-rank p < 0.001). Amongst the PoPH patients, however, there was no significant difference in 5-year survival when dichotomized by disease severity, either by a PVR of 5 Wood Units or a CI of 2.5 L/min/m2. Treatment of the PoPH patients with PAH-targeted therapies was associated with significantly higher 5-year survival rates compared to those not receiving such treatments, as shown by Kaplan–Meier analysis. This survival benefit was observed for PDE5i (50% vs. 34%, log-rank p = 0.029), ERA (58% vs. 34%, log-rank p < 0.001), and the combination of PDE5i and/or ERA (51% vs. 22%, log-rank p < 0.001), as well as any PAH-targeting treatment (50% vs. 26%, log-rank p = 0.007). Corresponding survival advantage was noted when including only PoPH patients with MELD Score ≥ 13. P
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Journal articleHarmadha PSW, Wang D, Masood M, 2025,
Comparative study of coronary artery disease prediction: conventional QRISK3 vs. enhanced machine learning models combined with particle swarm optimisation algorithm
, Open Heart, Vol: 12, ISSN: 2053-3624Background Coronary artery disease (CAD) is one of the biggest causes of mortality worldwide. Risk stratification for early detection is essential for the primary prevention of CAD. QRISK3 is known to overestimate future CAD risk in some populations, resulting in unnecessary preventive treatment that reduces the cost-effectiveness and safety. Combining machine learning with a metaheuristic optimisation approach using the Particle Swarm Optimization algorithm may outperform QRISK3 in predicting CAD. It may improve performance by selecting the best-performing subset of features related to clinical outcomes.Methods This study uses the UK Biobank dataset consisting of 348 015 participants aged 24–84 years with no prior diagnosis of CAD. The performance of both QRISK3 and machine learning models was evaluated separately using receiver operating characteristic analysis. Several machine learning models were assessed: Logistic Regression, Decision Tree, Random Forest, Naïve Bayes and Gradient Boosting. The dataset was split into training and test sets with a ratio of 4:1 for the machine learning models. Each model has been developed by adding a Particle Swarm Optimization algorithm to enhance the model’s classification accuracy.Results Out of 348 015 participants, 23 136 individuals (6.64%) were diagnosed with CAD within 10 years following their first visit, while 324 879 individuals (93.4%) did not develop CAD. The area under the curve (AUC) value of the QRISK3 prediction was 0.6113, while the gradient boosting model using Particle Swarm Optimization achieved a better performance AUC of 0.7258.Conclusions This study shows hybrid machine learning models optimised with the Particle Swarm Optimization algorithm can better predict CAD than QRISK3. The application of such machine learning models can effectively identify high-risk CAD patients, allowing for more personalised preventative strategies and supporting policymakers in imple
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Journal articleHarbaum L, Klose H, Wilkins MR, 2025,
From Blood to Vessel: Lipid Ratios in Pulmonary Hypertension
, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 211, Pages: 1124-1126, ISSN: 1073-449X -
Journal articleSmith A, Elliott P, Mayr M, et al., 2025,
Proteomic risk scores for predicting common diseases using linear and neural network models in the UK biobank
, Scientific Reports, Vol: 15, ISSN: 2045-2322Plasma proteomics provides a unique opportunity to enhance disease prediction by capturing protein expression patterns linked to diverse pathological processes. Leveraging data from 2,923 proteins measured in 53,030 UK Biobank participants, we developed proteomic risk scores for 27 common outcomes over 5- and 15-year follow-up periods using two approaches: a linear ElasticNet regression model and a deep learning neural network (NN) model. Using Cox regression, we assessed the discrimination of proteomic risk scores either in isolation or as incremental improvements over clinical risk factors. We also studied the shared and unique protein predictors across conditions. Proteomic risk scores demonstrated strong discrimination for most outcomes, with a C-index >0.80 for 12 diseases. NN models outperformed linear models for 11 outcomes, particularly for diseases such as Parkinson’s disease (C-index 0.84) and pulmonary embolism (C-index 0.83), where nonlinear relationships contributed significantly to prediction. Across all outcomes, the addition of proteomic scores to clinical models improved predictive accuracy (ΔC-index 0.03), with the greatest gains observed in 9 diseases (ΔC-index>0.1), including end-stage renal disease, pulmonary embolism, and Parkinson’s disease. Analysis of protein contributions revealed shared predictors across multiple diseases, such as growth differentiation factor 15 (GDF15), as well as unique predictors like PAEP for endometriosis. While NN models may capture complex relationships, linear models provided value through simplicity and interpretability. These findings underscore the importance of tailoring predictive approaches to specific diseases and demonstrate the pivotal potential of proteomics in advancing risk stratification and early detection.
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Journal articleHartley A, Rostamian S, Kaura A, et al., 2025,
The relationship of baseline high-sensitivity C-reactive protein with incident cardiovascular events and all-cause mortality over 20 years
, EBioMedicine, Vol: 117, ISSN: 2352-3964Background:The prediction of future cardiovascular events in those with risk factors is important for the appropriate optimisation of preventative therapies for those at greatest risk. The value of high sensitivity C-reactive Protein (hsCRP) has been questioned in this regard. The objectives of this post-hoc analysis of a randomised controlled trial were to investigate the usefulness of baseline serum hsCRP for predicting very long-term cardiovascular events in patients with hypertension in the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) Legacy Study.Methods:The ASCOT Legacy Study reports events up to 20 years of follow-up of the UK participants in the Lipid Lowering Arm of the original ASCOT trial. We examined outcomes related to serum hsCRP levels measured using a commercial ELISA, in tertiles or continuously, adjusting for classical cardiovascular risk factors as well as treatment allocation within ASCOT. The primary outcome was non-fatal myocardial infarction (MI) and fatal coronary heart disease (CHD); whilst secondary outcomes were all-cause mortality, total coronary events and procedures, total cardiovascular events and stroke.Findings:After excluding 3286 participants without hsCRP data, 5294 participants were included in the final cohort. The highest tertile of hsCRP was associated with the following outcomes compared to the lowest tertile: non-fatal myocardial infarction (MI) and fatal CHD (HR 1.32 [1.05–1.67]); total coronary events and procedures (HR 1.27 [1.09–1.47]); total cardiovascular events (HR 1.22 [1.08–1.37]); and all-cause mortality (HR 1.25 [1.10–1.42]). However, there was insufficient evidence regarding the association between hsCRP levels and stroke events. Addition of hsCRP in tertiles resulted in an improved net reclassification index for the prediction of non-fatal MI and fatal CHD at 20 years (9.68%, p < 0.0001).Interpretation:Higher baseline serum hsCRP levels can independently predict cardiovascular eve
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Journal articlePalm KCA, Yin X, Baig F, et al., 2025,
Proteomic profiling reveals a higher presence of glycolytic enzymes in human atherosclerotic lesions with unfavourable histological characteristics
, CARDIOVASCULAR RESEARCH, Vol: 121, Pages: 1187-1203, ISSN: 0008-6363- Cite
- Citations: 1
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Journal articleSitbon O, Boucly A, Weatherald J, et al., 2025,
Drugs targeting novel pathways in pulmonary arterial hypertension
, EUROPEAN RESPIRATORY JOURNAL, Vol: 66, ISSN: 0903-1936- Cite
- Citations: 1
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Journal articleYin X, Mayr M, 2025,
Cardiac regeneration beyond stem cells: harnessing sarcomere dynamics and endogenous repair mechanisms
, CARDIOVASCULAR RESEARCH, Vol: 121, Pages: 1146-1148, ISSN: 0008-6363 -
Journal articleLennicke C, Bjedov I, Grönke S, et al., 2025,
Enhancing autophagy by redox regulation extends lifespan in Drosophila
, Nature Communications, Vol: 16, ISSN: 2041-1723Dysregulation of redox homeostasis is implicated in the ageing process and the pathology of age-related diseases. To study redox signalling by H2O2 in vivo, we established a redox-shifted model by manipulating levels of the H2O2-degrading enzyme catalase in Drosophila. Here we report that ubiquitous over-expression of catalase robustly extends lifespan in females. As anticipated, these flies are strongly resistant to a range of oxidative stress challenges, but interestingly are sensitive to starvation, which could not be explained by differences in levels of energy reserves. This led us to explore the contribution of autophagy, which is an important mechanism for organismal survival in response to starvation. We show that autophagy is essential for the increased lifespan upon catalase up-regulation, as the survival benefits are completely abolished upon global autophagy knock-down. Furthermore, using a specific redox-inactive knock-in mutant, we highlight the in vivo role of a key regulatory cysteine residue in Atg4a, which is required for the lifespan extension in our catalase model. Altogether, these findings confirm the redox regulation of autophagy in vivo as an important modulator of longevity.
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Journal articleYin X, Beele A, Theofilatos K, et al., 2025,
A Comparative Proteomics Study of Autopsy and Fresh-Frozen Coronary Artery Samples
, JOURNAL OF PROTEOME RESEARCH, Vol: 24, Pages: 3154-3159, ISSN: 1535-3893 -
Journal articleArmour C, Gopalan D, Statton B, et al., 2025,
Patient-specific modelling of pulmonary arterial hypertension: wall shear stress correlates with disease severity
, Frontiers in Bioengineering and Biotechnology, Vol: 13, ISSN: 2296-4185Introduction: Pulmonary arterial hypertension (PAH) requires an invasive right heart catheter (RHC) procedure for diagnosis. Patients can present with initial symptoms and interact with healthcare institutes for up to 3 years before referral for diagnosis. Thus, there is a great need to develop non-invasive tools, to better screen patients and improve early diagnosis rates.Methods: seven patients diagnosed and treated for PAH were included in this study. Patient-specific computational fluid dynamics (CFD) models were built for all patients, with all model parameters tuned using non-invasive imaging data, including CT, cardiac MR, echocardiogram, and 4D-flow MRI scans–crucially, a 3D inlet velocity profile was derived from 4D-flow MRI.Results: CFD models were quantitatively and qualitatively well matched with in-vivo 4D-flow hemodynamics. A linear correlation of R2 = 0.84 was found between CFD derived time-averaged wall shear stress (TAWSS) and RHC measured mean pulmonary pressure (key diagnostic value): low TAWSS correlated with high pressure.Conclusion: This study highlights TAWSS as a potential computational biomarker for PAH. The clinical use of TAWSS to diagnose and stratify PAH patients has the potential to greatly improve patient outcomes. Further work is ongoing to validate these findings in larger cohorts.
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Journal articleCheng K, Alpendurada F, Bucciarelli-Ducci C, et al., 2025,
Segmental redistribution of myocardial blood flow after coronary sinus reducer implantation demonstrated by quantitative perfusion cardiovascular magnetic resonance
, Journal of Cardiovascular Magnetic Resonance, Vol: 27, ISSN: 1097-6647BackgroundThe coronary sinus reducer (CSR) is a novel percutaneous treatment for patients with refractory angina. Increasing evidence supports its clinical efficacy in patients with advanced epicardial coronary artery disease. However, its mechanism of action and its effects on myocardial perfusion remain undefined. Using quantitative stress perfusion cardiovascular magnetic resonance (CMR), this study assessed changes in myocardial perfusion in patients with refractory angina undergoing CSR implantation.MethodsThis single-center retrospective observational cohort study included 16 patients. Rest and adenosine stress perfusion CMR was performed before and at median 5 months after CSR implantation. Perfusion images were acquired using a dual-sequence quantitative protocol with automated generation of myocardial blood flow (MBF; mL/min/g). In addition to visual assessment of ischemic segments, changes in absolute MBF across myocardial segments and between myocardial layers were analyzed.ResultsA high proportion of myocardial segments had visually adjudicated ischemia at baseline (208 out of 254: 81.9%), which significantly reduced after CSR implantation (175 out of 254: 68.9%; P = 0.001). There were no changes in global MBF or strain values. Changes in myocardial perfusion reserve (MPR) correlated with baseline MPR with more ischemic segments at baseline improving to a greater extent at follow-up. Similar patterns were observed in both the left and right coronary artery territories. Changes in endocardial/epicardial MBF ratio at stress were similarly dependent on baseline values.ConclusionIn patients with refractory angina undergoing CSR implantation, quantitative stress perfusion CMR demonstrated redistribution of myocardial perfusion across segments, from less ischemic to more ischemic myocardium, and across myocardial layers with greatest improvements in endocardial perfusion observed in the most ischemic myocardium. Further studies are needed to validate the diffe
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Journal articleErrington N, Zhou L, Rhodes CJ, et al., 2025,
Diagnostic microRNA signatures to support classification of pulmonary hypertension
, Circulation: Genomic and Precision Medicine, Vol: 18, ISSN: 2574-8300BACKGROUND:Patients with pulmonary hypertension (PH) are classified based on disease pathogenesis and hemodynamic drivers. Classification informs treatment. The heart failure biomarker NT-proBNP (N-terminal pro-B-type natriuretic peptide) is used to help inform risk but is not specific to PH or sub-classification groups. There are currently no other biomarkers in clinical use to help guide diagnosis or risk.METHODS:We profiled a retrospective cohort of 1150 patients from 3 expert centers with PH and 334 non-PH symptomatic controls (disease controls) from the United Kingdom to measure circulating levels of 650 microRNAs (miRNAs) in serum. NT-proBNP (ELISA) and 326 well-detected miRNAs (polymerase chain reaction) were prioritized by feature selection using multiple machine learning models. From the selected miRNAs, generalized linear models were used to describe miRNA signatures to differentiate PH and pulmonary arterial hypertension from the disease controls, and pulmonary arterial hypertension, PH due to left heart disease, PH due to lung disease, and chronic thromboembolic pulmonary hypertension from other forms of PH. These signatures were validated on a UK test cohort and independently validated in the prospective CIPHER study (A Prospective, Multicenter, Noninterventional Study for the Identification of Biomarker Signatures for the Early Detection of Pulmonary Hypertension) comprising 349 patients with PH and 93 disease controls.RESULTS:NT-proBNP achieved a balanced accuracy of 0.74 and 0.75 at identifying PH and pulmonary arterial hypertension from disease controls with a threshold of 254 and 362 pg/mL, respectively but was unable to sub-categorize PH subgroups. In the UK cohort, miRNA signatures performed similarly to NT-proBNP in distinguishing PH (area under the curve of 0.7 versus 0.78), and pulmonary arterial hypertension (area under the curve of 0.73 versus 0.79) from disease controls. MicroRNA signatures outperformed NT-proBNP in distinguishing PH classi
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Journal articleAdam F, Quigley K, Leung V, et al., 2025,
Engineered pulmonary artery tissues for measuring contractility, drug testing and disease modelling
, British Journal of Pharmacology, Vol: 182, Pages: 2585-2602, ISSN: 0007-1188Background and PurposeVasoreactivity of pulmonary arteries regulates blood flow through the lungs. Excessive constriction of these vessels contributes to pulmonary arterial hypertension (PAH), a progressive and incurable condition, resulting in right heart failure. The search for new and improved drug treatments is hampered by laboratory models that do not reproduce the vasoactive behaviour of healthy and diseased human arteries.Experimental ApproachWe have developed an innovative technique for producing miniature, three-dimensional arterial structures that allow proxy evaluation of human pulmonary artery contractility. These “engineered pulmonary artery tissues” or “EPATs” are fabricated by suspending human pulmonary artery vascular smooth muscle cells (VSMCs) in fibrin hydrogels between pairs of silicone posts, located on custom-made racks, in 24-well culture plates.Key ResultsEPATs exhibit rapid, robust and reproducible contraction responses to vasoconstrictors (KCl, ET-1, U46619) as well as relaxation responses to clinically approved PAH vasodilatory drugs that target several signalling pathways, such as bosentan, epoprostenol, selexipag and imatinib. EPATs composed of pulmonary artery VSMCs from PAH patients exhibit enhanced contraction to vasoconstrictors and relaxation in response to vasodilators. We also demonstrate the incorporation of endothelial cells into EPATs for the measurement of endothelium-dependent dilatory responses.Conclusion and ImplicationsWe demonstrate the capacity and suitability of EPATs for studying the contractile behaviour of human arterial cells and preclinical drug testing. This novel biomimetic platform has the potential to dramatically improve our understanding and treatment of cardiovascular disease.
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