The selection of the optimal antithrombotic regimen in patients with atrial fibrillation and acute coronary syndrome remains challenging. Previous trials have demonstrated that dual antithrombotic therapy (DAT), consisting of direct oral anticoagulants (DOACs) plus a P2Y12 inhibitor, reduces bleeding compared to a triple-therapy regimen using vitamin K antagonists. However, subsequent meta-analyses have suggested an increased risk of ischemic events with DAT, particularly within the first month of treatment. Clopidogrel has been the predominant P2Y12 inhibitor used across these studies, despite the risk of high on-treatment platelet reactivity when using this drug. In this study, we conducted an open-label, randomized controlled trial (EPIDAURUS) in patients with atrial fibrillation and acute coronary syndrome, designed to assess the efficacy and safety of a 1-month regimen of DOAC plus potent P2Y12 inhibitor (prasugrel or ticagrelor) compared to DOAC plus clopidogrel and in-hospital aspirin. The primary outcomes of the trial were an efficacy endpoint, recurrent ischemic events and safety endpoints, including death and major bleeding, which were evaluated 6 weeks after randomization using separate win-loss ratio analyses. The study was prematurely terminated after enrollment of 602 patients (154 female) of an expected 1,474 patients, owing to safety concerns raised by the Data and Safety Monitoring Board. Exploratory analyses of secondary safety endpoints, including bleeding type ≥2 and ≥3 according to the Bleeding Academic Research Consortium scale, revealed that, compared to clopidogrel and in-hospital aspirin, treatment with a potent P2Y12 inhibitor was associated with higher bleeding rates without a clear reduction in the risk of ischemic complications. These findings do not support the routine use of potent P2Y12 inhibitors in combination with DOACs in this patient population. ClinicalTrials.gov identifier: NCT04981041 .

27 July, 2026. This preprint has been retracted at the request of the authors due to a conflict with the European Society of Cardiology conference embargo policy. The retraction is unrelated to the scientific content of the manuscript.

Targeting ACKR3/CXCR7 regulates enzymatic generation of pro-thrombotic, while favoring anti-thrombotic lipids that inhibit platelets through AC-cAMP-PKA pathway in coordination with prostacyclin-IP receptor. This investigation validated the impact of CXCR7 in modulating non-enzymatic lipid (per)oxidation, platelet response to lipoproteins-(LDL, oxLDL), mitochondrial metabolism and procoagulatory functions. Pharmacological CXCR7-agonist-(VUF11207) preserved mitochondrial membrane integrity-(Δψm), counteracted activation-induced mitochondrial superoxide generation-(MitoSOXRed), and nonenzymatic lipid (per)oxidation. Additionally, CXCR7-agonist regulated lipoprotein-induced platelet adhesion on thrombogenic matrices, degranulation, αIIbβIII-integrin activation, aggregation and thrombotic response, by reducing lipoprotein uptake through scavenger receptors-(CD36, ApoER2). CXCR7-ligation triggered activation of metabolic energy sensor Adenosine MonoPhosphate-dependent Kinase-(AMPKSer-172), prompted AMPK-mediated inhibitory phosphorylation of Acetyl-CoA-Carboxylase-(ACC)Ser-79, to foster lipolysis over lipogenesis. Consequently AMPKSer-172-ACCSer-79 pathway increased anticoagulatory FXa-inhibitory long-chain acylcarnitine-(LC-CARs)-(16:0, 18:1, 18:2) generation in platelets from healthy subjects and CAD patients. Increased intraplatelet LC-CARs was not due to dysregulated mitochondrial respiration; since CXCR7-agonist improved maximal respiration, spare respiratory capacity, and ATP-linked respiration in thrombin-activated platelets, suggesting sustained mitochondrial metabolism. Exerting a two-pronged effect on procoagulant function, CXCR7-agonist downregulated phosphatidylserine exposure on activated platelets, reducing FX/FXa binding, while platelet-derived anticoagulatory-LC-CARs regulated thrombin generation. CXCR7-agonist administration reduced thrombus formation, platelet degranulation, αIIbβIII-integrin activation, procoagulant activity, circulatory platelet-leukocyte aggregates in murine venous thrombosis model; besides, decreased plasma procoagulant lipids-(platelet COX-1, 12-LOX, and leukocyte 5/15-LOX-derived) and thrombo-inflammatory mediators-(IL-1β, IL-6, IFN-γ, TNF-α, MCP-1), and increased plasma LC-CAR levels. Therefore, pharmacological targeting of CXCR7 could regulate (non)enzymatic lipid processing, and promote anticoagulatory LC-CAR generation to check platelet-directed thrombotic propensity, and hypercoagulation, moreover, replenish reduced levels of circulatory anticoagulant-LC-CARs in STEMI and venous thromboembolism-(VTE) patients.

Platelet lipidomics offers a window into the thromboinflammatory responses to acute coronary syndromes (ACS) and chronic coronary syndromes (CCS), yet differences between the platelet lipidomes of these two coronary artery disease subtypes remain poorly characterized. In this pilot study, untargeted platelet lipidomics and miRNA transcriptomics were performed on platelets isolated from 19 ACS and 57 CCS patients undergoing coronary angiography, integrated with routine clinical and hematological traits in statistical network analyses and cross-validated machine learning models. Platelet lipidomics identified 81 lipid features significantly altered between ACS and CCS (FDR q < 0.05), predominantly involving phosphatidylcholines, lysophosphatidylcholines, and ceramides. Cer 18:2;O2/24:0 showed the strongest inverse association with ACS of any identifiable lipid (q = 0.0394, OR = 0.297, 95% CI [0.171, 0.515]), while increased Cer 18:0;O2/22:1 (q = 0.088, OR = 3.072, 95% CI [1.607, 5.878]) and Cer 18:0;O2/18:0 (q = 0.088, OR = 2.791, 95% CI [1.515, 5.145]) demonstrate nominally significant promotive effects on ACS. Differential correlation analysis further identified oxidized phospholipid species as connectivity hubs in ACS-specific lipid networks, a pattern not detectable by differential abundance approaches alone. Although untargeted lipidomics did not meaningfully outperform a routine clinical trait benchmark in ACS classification, phosphatidylcholine-trained models achieved modest gains in AUROC, and the prominent ceramide signal—platelet-specific and mechanistically distinct from plasma ceramide risk scores—supports a targeted validation strategy centered on a ceramide-enriched platelet lipid panel in prospective, adequately powered cohorts.

Background/Objectives: Myocardial injury is linked to poor outcomes in respiratory infections. This study evaluated the prognostic value of high-sensitivity troponin I (hsTnI) in predicting 30-day outcomes in patients hospitalized with seasonal influenza. Methods: In this single-center retrospective study, 277 adults with laboratory-confirmed influenza were analyzed. Myocardial injury was defined by elevated hsTnI. The primary composite endpoint included 30-day mortality, intensive care unit (ICU) admission, and mechanical ventilation. Results: Patients with myocardial injury had significantly higher event rates for the composite endpoint than those without (p < 0.0001). Dynamic hsTnI elevations, reflecting acute myocardial injury, were also associated with worse outcomes (p = 0.026). Machine learning models incorporating hsTnI and laboratory data achieved excellent predictive performance (AUC = 0.99) and improved risk classification compared with conventional scores (p < 0.0001). Conclusions: Among hospitalized influenza patients, myocardial injury identified by hsTnI strongly predicted short-term adverse outcomes. Routine hsTnI assessment enhances risk stratification beyond standard clinical scores and may facilitate early identification and management of high-risk patients.

Atherosclerosis is the underlying cause of myocardial infarction and ischemic stroke. It is a lipid-triggered and cytokine/chemokine-driven arterial inflammatory condition. We identify D-dopachrome tautomerase/macrophage migration-inhibitory factor-2 (MIF-2), a paralog of the cytokine MIF, as an atypical chemokine promoting both atherosclerosis and hepatic lipid accumulation. In hyperlipidemic Apoe-/- mice, Mif-2-deficiency and pharmacological MIF-2-blockade protect against lesion formation and vascular inflammation in early and advanced atherogenesis. MIF-2 promotes leukocyte migration, endothelial arrest, and foam-cell formation, and we identify CXCR4 as a receptor for MIF-2. Mif-2-deficiency in Apoe-/- mice leads to decreased plasma lipid levels and suppressed hepatic lipid accumulation, characterized by reductions in lipogenesis-related pathways, tri-/diacylglycerides, and cholesterol-esters, as revealed by hepatic transcriptomics/lipidomics. Hepatocyte cultures and FLIM-FRET-microscopy suggest that MIF-2 activates SREBP-driven lipogenic genes, mechanistically involving MIF-2-inducible CD74/CXCR4 complexes and PI3K/AKT but not AMPK signaling. MIF-2 is upregulated in unstable carotid plaques from atherosclerotic patients and its plasma concentration correlates with disease severity in patients with coronary artery disease. These findings establish MIF-2 as an atypical chemokine linking vascular inflammation to metabolic dysfunction in atherosclerosis.

Patients with coronary artery disease (CAD) are at increased risk of developing ischemic events and contemporary antiplatelet therapy often leads to bleeding events following percutaneous coronary intervention (PCI). Glycoprotein VI (GPVI) is the key receptor of collagen-dependent thrombus formation and crucial for platelet homeostasis. We analysed the influence of GPVI inhibition with revacept in a randomized double-blinded trial enrolling 334 patients with CAD undergoing elective PCI. Ex vivo platelet function analyses were assessed alongside plasma chemokine concentrations. We then elucidate changes of GPVI-dependent chemokine concentrations in patients with bleeding events during the 30-day clinical follow-up. Changes in platelet function occur in patients with revacept treatment and are associated with a characteristic alteration of circulating chemokine concentrations. Further, patients with adverse bleeding events share a distinct fingerprint of chemokines that is associated with modulation of in vitro platelet functions. In addition, assessment of GPVI-associated changes in chemokine signalling and platelet functions demonstrated an increased diagnostic value in patients with CAD and might improve early risk discrimination for bleeding events. The composition of platelet-derived chemokines correlated with platelet functions following antiplatelet treatment. Thus, assessment of chemokines may offer the perspective to identify patients at increased risk for bleeding events. Likewise, modulation of platelet chemokines in patients with revacept treatment contributes to the efficacy of antiplatelet treatment and might attenuate pathophysiological cascades leading to haemorrhagic diathesis in patients with CAD. Study design and rationale: patients with coronary artery disease (CAD) undergoing elective percutaneous coronary intervention (PCI) and the impact of treatment with soluble GPVI inhibitor revacept. Changes in ex vivo platelet function and plasma chemokine concentrations were associated with an increased bleeding risk during the clinical follow-up. Further, GPVI-associated changes in chemokine signalling might attenuate pathophysiological cascades leading to haemorrhagic diathesis and improve early risk discrimination for bleeding events

Arterial spin labeling MRI detected substantial improvement in lung perfusion after treatment and identified residual perfusion defects associated with persistent dyspnea in participants with pulmonary embolism.

Background: Thromboangiitis obliterans (TAO) is a rare but threatening disease associated with significant morbidity and mortality. The pathophysiology is poorly understood, the diagnosis is often obscure and causal treatment options are limited. In the current study, we aimed to identify distinct TAO patient clusters that differed in clinical presentation and prognosis. Patients and methods: We retrospectively analysed a cohort of 48 patients with the working diagnosis TAO who were assessed for clinical presentation at hospital admission. We applied hierarchical clustering to divide patients into clinically meaningful subgroups. Results: Patients were followed-up for a median of 95 months. We found that cluster analyses including a variety of demographic and diagnostic parameters were valuable to identify patient subgroups with similar clinical presentation, but with different clinical course of the disease, including the individual risk for mortality and major amputation. Patients treated with statins showed a significantly better survival, which may allow us to hypothesize that a conventional secondary prevention strategy, which is recommended for atherosclerotic artery diseases, may be of benefit also in patients that present with TAO. Conclusions: The current data may help to develop strategies to identify high-risk TAO patients. Furthermore, statins may serve as a readily available therapeutic option to this rare but serious disease.

BACKGROUND:Transcatheter edge-to-edge repair (TEER) has been shown to be an effective treatment option for patients experiencing cardiogenic shock (CS) with concomitant high-grade mitral valve regurgitation. However, haemodynamic changes following M-TEER have not been thoroughly investigated. Afterload mismatch, leading to the deterioration of haemodynamics subsequent to mitral regurgitation correction, could potentially occur and adversely impact prognosis. Our objective was to analyse the effect of TEER on haemodynamic and echocardiographic parameters in patients with CS. METHODS AND RESULTS:We conducted a retrospective study of patients undergoing TEER for mitral valve regurgitation in the setting of CS. Haemodynamic and echocardiographic parameters before and after TEER were systematically analysed. A total of 25 patients underwent TEER in the context of CS. All patients were successfully treated with at least of one grade reduction in mitral regurgitation. The median left atrial mean pressure decreased from 23 mmHg (IQR 17-30) to 16 mmHg (IQR 11-20, P < 0.01), and the V-wave decreased from 36 mmHg (IQR 27-44) to 21 mmHg (IQR 14-25, P < 0.01) following the procedure. The stroke volume index and cardiac index increased from 25 mL/m2 (IQR 18-29) to 34 mL/m2 (IQR 25-44, P < 0.01) and from 1.90 L/min/m2 (IQR 1.41-2.30) to 2.50 L/min/m2 (IQR 1.99-2.86, P < 0.01), respectively. We did not observe any worsening of the ejection fraction after the procedure. Ten patients (40%) died during their hospital stay. CONCLUSIONS:Our study demonstrates that TEER leads to favourable haemodynamic changes in patients with CS. We observed a significant reduction in left atrial pressure, V-wave, and an elevation in cardiac index. Importantly, we did not observe any deterioration in left ventricular function following the procedure. This supports the concept of haemodynamic stabilization with TEER in patients with CS and high-grade mitral regurgitation.

Purpose:Patients with metabolic syndrome and coronary artery disease (CAD) are at increased risk of metabolic dysfunction-associated steatotic liver disease (MASLD), which can progress to steatohepatitis, cirrhosis, and hepatocellular carcinoma. MASLD is the most common liver disease and a significant contributor to cardiovascular morbidity. Enhanced platelet aggregation is linked to steatohepatitis, and antiplatelet therapy has been suggested as a potential treatment. Patients and Methods:In a prospective study of 51 patients with type 2 diabetes mellitus and/or obesity (BMI≥30), we evaluated the impact of antiplatelet therapy on hepatic fat content, liver volume, and iron deposition using magnetic resonance imaging (MRI) at baseline and six months. Ex vivo platelet function testing and plasma levels of proinflammatory chemotactic cytokines were measured to characterize thromboinflammatory mechanisms underlying MASLD. Results:Increased platelet reactivity correlated with greater hepatic fat, iron deposition, and liver volume. Antiplatelet therapy was associated with reductions in hepatic volume and iron accumulation. Progression of steatosis was linked to dyslipidemia, platelet hyperreactivity, and elevated plasma levels of profibrotic, inflammatory, and apoptotic chemokines/cytokines. A distinct systemic cytokine profile corresponded with morphological features of progressive MASLD. Conclusion:Reduced platelet aggregation is associated with attenuation of MASLD features. Antiplatelet therapy correlates with decreased pro-inflammatory and pro-fibrotic chemokine signaling linked to the morphological characteristics of MASLD. Assessment of platelet reactivity and specific chemokines may enhance understanding of MASLD pathophysiology and support the development of novel therapeutic strategies.

Surgical total hip arthroplasty (THA) is associated with high risk of venous thromboembolism (VTE), but the appropriate duration of postoperative anticoagulation remains controversial. “Enhanced Recovery and Abbreviated Length of Anticoagulation for Thromboprophylaxis After Primary Hip Arthroplasty” (ENABLE-Hip) is a multicenter investigator-initiated and academically sponsored randomized double-blind active-control non-inferiority trial. Patients will be mobilized early after surgery, following a standardized enhanced recovery protocol. After an initial open-label prophylactic anticoagulation as per local standard of care until day 2 after surgery, treatment with rivaroxaban (10 mg once daily) will be started on day 3 and continued until day 10. Subsequently, patients will be switched to placebo in the experimental arm, or continue on active drug in the control arm, until a total of 35 days. The primary endpoint is acute symptomatic or fatal VTE within 3 months. A sample size of 2,932 patients will provide ≥ 80% power to reject the null hypothesis that δ ≥ 0.01 (δ = difference between the two arms in symptomatic VTE probability) at a significance level α = 0.05. An interim analysis will be performed after 3-month follow-up of the first 1,760 randomized patients at a significance level α = 0.50, leading to stop for futility if significance is not obtained, or if recalculation yields a sample size of > 3,200 patients. ENABLE-Hip will be the first major randomized trial to test an overall reduction in the duration of post-THA thromboprophylaxis and will inform future guideline recommendations concerning this continuously growing patient population. Trial registration: ClinicalTrials.gov Identifier: NCT06611319 Graphical Abstract Flow diagram of the ENABLE-Hip trial (ClinicalTrials.gov Identifier: NCT06611319). ERAS: enhanced recovery after surgery; o.d .: omni die (once daily).

Closure of a patent foramen ovale (PFO) is an effective strategy in the prevention of recurrent stroke after cryptogenic stroke. Residual shunt (RS) is a common issue following PFO closure and may affect safety and efficacy. Transesophageal echocardiography (TEE) is the key diagnostic tool, but standardized assessment of morphological parameters to prevent RS remains challenging. In this study, we investigate the diagnostic value of different anatomical parameters assessed by TEE to predict RS after PFO closure. We consecutively enrolled five-hundred and twenty-seven (n = 527) patients undergoing PFO closure. We performed pre-interventional TEE, and after PFO closure, we then screened for RS by TEE at 6-month follow-up. Pre-interventional TEE measures of PFO morphology revealed significant differences in patients with RS in comparison to those with closed PFO. Incidence of RS was significantly more frequent in patients with atrial septum aneurysm (p = 0.022) and increasing PFO size (p = 0.025). In patients with RS, we found significantly increased length (p = 0.005) of septum primum and PFO tunnel (p = 0.036) as well as excursion (p = 0.005) of septum primum. By training machine learning models on TEE parameters, stratification of PFO morphology resulted in high diagnostic accuracy to predict RS after PFO closure. Our study elucidates that a baseline characterization of PFO morphology using TEE improves diagnostic precision to identify patients with RS after PFO closure. A standardized approach might thus enhance the efficacy and safety of transcatheter PFO closure. Prediction of complete closure might reduce complications and allow for a more refined patient selection and treatment. Prediction of peri-device leak in patients PFO and paradoxical embolism undergoing percutaneous PFO closure. Workflow of this study investigating the association of morphological determinants with an increased incidence of residual shunting assessed through transesophageal echocardiography.

Coronary artery disease (CAD) often leads to adverse events resulting in significant disease burdens. Underlying risk factors often remain inapparent prior to disease incidence and the cardiovascular (CV) risk is not exclusively explained by traditional risk factors. Platelets inherently promote atheroprogression and enhanced platelet functions and distinct platelet lipid species are associated with disease severity in patients with CAD. Lipidomics data were acquired using mass spectrometry and processed alongside clinical data applying machine learning to model estimates of an increased CV risk in a consecutive CAD cohort (n = 595). By training machine learning models on CV risk measurements, stratification of CAD patients resulted in a phenotyping of risk groups. We found that distinct platelet lipids are associated with an increased CV or bleeding risk and independently predict adverse events. Notably, the addition of platelet lipids to conventional risk factors resulted in an increased diagnostic accuracy of patients with adverse CV events. Thus, patients with aberrant platelet lipid signatures and platelet functions are at elevated risk to develop adverse CV events. Machine learning combining platelet lipidome data and common clinical parameters demonstrated an increased diagnostic value in patients with CAD and might improve early risk discrimination and classification for CV events.

BACKGROUND:Transcatheter mitral valve repair is performed in a patient population at risk for thrombotic and bleeding events. The effects on platelet function and reactivity and their association with bleeding events after mitral transcatheter edge-to-edge therapy (M-TEER) have not been systematically examined. OBJECTIVES:We sought to investigate the association of different parameters of platelet function and thrombogenicity with bleeding events post M-TEER. METHODS:In this single-center study, 100 consecutive patients with mitral regurgitation receiving TEER were analyzed. Blood was taken directly from the guide-catheter in the left atrium before and after placing the device. Blood samples were analyzed using impedance aggregometry (Multiplate) and TEG6s. The results were compared pre- and postprocedural. The primary outcome was any bleeding complication according to the Bleeding Academic Research Consortium classification within 6 months. RESULTS:A total of 41 patients experienced bleeding events. TEG analysis showed a significant decrease in ADP aggregation and increase in ADP inhibition. In ROC-analysis, TEG ADP aggregation and inhibition and Multiplate ADP aggregation showed moderate predictive values for bleeding events. The delta-ADP-Test (Multiplate) showed the strongest prediction of bleeding (area under the curve: 0.69). Adding platelet function and TEG markers to a model of clinical bleeding risk factors improved the prediction for bleeding events. CONCLUSION:This study indicates that thrombogenicity might be affected immediately after M-TEER probably due to changes in flow conditions. In particular, platelet aggregation involving the ADP receptor pathway significantly correlated with postprocedural bleeding events. Whether these results could guide peri-interventional antithrombotic therapy and improve peri- and postprocedural outcome requires further investigation.

BACKGROUND: Aortic stenosis (AS) is driven by progressive inflammatory and fibrocalcific processes regulated by circulating inflammatory and valve resident endothelial and interstitial cells. The impact of platelets, platelet-derived mediators, and platelet-monocyte interactions on the acceleration of local valvular inflammation and mineralization is presently unknown. METHODS: We prospectively enrolled 475 consecutive patients with severe symptomatic AS undergoing aortic valve replacement. Clinical workup included repetitive echocardiography, analysis of platelets, monocytes, chemokine profiling, aortic valve tissue samples for immunohistochemistry, and gene expression analysis. RESULTS: The patients were classified as fast-progressive AS by the median ∆Vmax of 0.45 m/s per year determined by echocardiography. Immunohistological aortic valve analysis revealed enhanced cellularity in fast-progressive AS (slow- versus fast-progressive AS; median [interquartile range], 247 [142.3–504] versus 717.5 [360.5–1234]; P <0.001) with less calcification (calcification area, mm 2 : 33.74 [27.82–41.86] versus 20.54 [13.52–33.41]; P <0.001). MIF (macrophage migration inhibitory factor)-associated gene expression was significantly enhanced in fast-progressive AS accompanied by significantly elevated MIF plasma levels (mean±SEM; 6877±379.1 versus 9959±749.1; P <0.001), increased platelet activation, and decreased intracellular MIF expression indicating enhanced MIF release upon platelet activation (CD62P, %: median [interquartile range], 16.8 [11.58–23.8] versus 20.55 [12.48–32.28], P =0.005; MIF, %: 4.85 [1.48–9.75] versus 2.3 [0.78–5.9], P <0.001). Regression analysis confirmed that MIF-associated biomarkers are strongly associated with an accelerated course of AS. CONCLUSIONS: Our findings suggest a key role for platelet-derived MIF and its interplay with circulating and valve resident monocytes/macrophages in local and systemic thromboinflammation during accelerated AS. MIF-based biomarkers predict an accelerated course of AS and represent a novel pharmacological target to attenuate progression of AS.

Aim Data on associations of invasively determined hemodynamic parameters with procedural success and outcomes in patients suffering from mitral regurgitation (MR) undergoing transcatheter edge-to-edge repair of the mitral valve (M-TEER) is limited.Methods and results We enrolled 239 patients with symptomatic MR of grade 2 + , who received M-TEER. All patients underwent extensive pre-interventional invasive hemodynamic measurements via right heart catheterization (mean pulmonary arterial pressure (mPAP), systolic- (PAPsys) and diastolic pulmonary arterial pressure (PAPdia), pulmonary arterial wedge pressure (PAWP), a-wave, v-wave, pulmonary vascular resistance (PVR), transpulmonary pressure gradient (TPG), cardiac index (CI), stroke volume index (SVI)). mPAP and PAWP at baseline were neither associated with procedural success, immediate reduction of MR, nor residual MR after 6 months of follow-up. The composite outcome (All-cause mortality (ACM) and/or heart failure induced rehospitalization (HFH)) and HFH differed significantly after M-TEER when stratified according to mPAP, PAWP, PAPdia, a-wave and v-wave. ACM was not associated with the afore mentioned parameters. Neither PVR, TPG, CI nor SVI were associated with the composite outcome and HFH, respectively. In multivariable analyses, PAWP was independently associated with the composite outcome and HFH. PVR and SVI were not associated with outcomes.Conclusion PAWP at baseline was significantly and independently associated with HFH and might serve as a valuable parameter for identifying patients at high risk for HFH after M-TEER. ACM and procedural success were not affected by pulmonary arterial pressure before M-TEER. We suggest that the post-capillary component of PH serves as the driving force behind the risk of HFH.

BACKGROUND:Risk stratification for transcatheter procedures in patients with severe mitral regurgitation is challenging. Deceleration capacity (DC) has already proven to be a reliable risk predictor in patients undergoing transcatheter aortic valve implantation. We hypothesized, that DC provides prognostic value in patients undergoing transcatheter edge-to-edge mitral valve repair (TEER).METHODS:We retrospectively analyzed electrocardiogram signals from 106 patients undergoing TEER at the University Hospital of Tübingen. All patients received continuous heart-rate monitoring to assess DC following the procedure. One-year all-cause mortality was defined as the primary end point.RESULTS:Sixteen patients (15.1%) died within 1 year. The DC in nonsurvivors was significantly reduced compared to survivors (5.1 ± 3.0 vs. 3.0 ± 1.6 ms, p = 0.002). A higher EuroSCORE II and impaired left ventricular function were furthermore associated with poor outcome. In Cox regression analyses, a DC < 4.5 ms was found a strong predictor of 1-year mortality (hazard ratio: 0.10, 95% confidence interval: 0.13-0.79, p = 0.029). Finally, a significant negative correlation was found between DC and residual mitral regurgitation after TEER (r = -0.41, p < 0.001).CONCLUSION:In patients with severe mitral regurgitation undergoing TEER, DC may serve as a new predictor of follow-up mortality.

Background Arterial spin labeling (ASL) MRI can be used to assess organ perfusion but has yet to be implemented for perfusion evaluation of the lung. Purpose To evaluate pseudo-continuous ASL (PCASL) MRI for the detection of acute pulmonary embolism (PE) and its potential as an alternative to CT pulmonary angiography (CTPA). Materials and Methods Between November 2020 and November 2021, 97 patients (median age, 61 years; 48 women) with suspected PE were enrolled in this prospective study. PCASL MRI was performed within a 72-hour period following CTPA under free-breathing conditions and included three orthogonal planes. The pulmonary trunk was labeled during systole, and the image was acquired during diastole of the subsequent cardiac cycle. Additionally, multisection, coronal, balanced, steady-state free-precession imaging was carried out. Two radiologists blindly assessed overall image quality, artifacts, and diagnostic confidence (five-point Likert scale, 5 = best). Patients were categorized as positive or negative for PE, and a lobe-wise assessment in PCASL MRI and CTPA was conducted. Sensitivity and specificity were calculated on a patient level with the final clinical diagnosis serving as the reference standard. Interchangeability between MRI and CTPA was also tested with use of an individual equivalence index (IEI). Results PCASL MRI was performed successfully in all patients with high scores for image quality, artifact, and diagnostic confidence (κ ≥ .74). Of the 97 patients, 38 were positive for PE. PCASL MRI depicted PE correctly in 35 of 38 patients with three false-positive and three false-negative findings, resulting in a sensitivity of 35 of 38 patients (92% [95% CI: 79, 98]) and a specificity of 56 of 59 patients (95% [95% CI: 86, 99]). Interchangeability analysis revealed an IEI of 2.6% (95% CI: 1.2, 3.8). Conclusion Free-breathing pseudo-continuous arterial spin labeling MRI depicted abnormal lung perfusion caused by acute pulmonary embolism and may be useful as a contrast material-free alternative to CT pulmonary angiography for selected patients. German Clinical Trials Register no. DRKS00023599 © RSNA, 2023.