Reviews in cardiovascular medicine最新文献

{"title":"The Role of Soluble Suppression of Tumorigenicity-2 and Galectin-3 in Heart Failure With Preserved Ejection Fraction: A Scoping Review of the Literature.","authors":"Konstantina Ntalekou, Panagiotis Iliakis, Nikitas Katsillis, Nikolaos Patsourakos, Dimitrios Tsiachris, Dimitrios Farmakis, Polykarpos Christos Patsalis, Christina Chrysohoou, Konstantinos Tsioufis","doi":"10.31083/RCM51830","DOIUrl":"https://doi.org/10.31083/RCM51830","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) represents a heterogeneous clinical syndrome characterized by complex pathophysiological mechanisms and substantial diagnostic and prognostic challenges. Recently, circulating biomarkers have emerged as potential tools for improving risk stratification and disease characterization in this population. Among these biomarkers, soluble suppression of tumorigenicity-2 (sST2) and galectin-3 (Gal-3) have gained particular attention due to their association with myocardial fibrosis, inflammation, and adverse cardiac remodeling. This scoping review aimed to evaluate the current evidence on the diagnostic and prognostic roles of sST2 and Gal-3 in patients with HFpEF. A literature search was conducted in PubMed and ScienceDirect to identify studies investigating the clinical significance of these biomarkers in HFpEF. Titles and abstracts were screened, and eligible studies were assessed through full-text review according to predefined inclusion criteria. Ultimately, 11 studies were included in the qualitative synthesis. Evidence from the available literature suggests that both sST2 and Gal-3 are associated with markers of myocardial fibrosis, inflammation, and disease severity in HFpEF. Elevated circulating levels of these biomarkers have been linked to poorer clinical outcomes, including an increased risk of hospitalization and mortality. However, variability across studies in study populations, biomarker thresholds, and methodological approaches limits the direct translation of these findings into routine clinical practice. Overall, sST2 and Gal-3 appear to hold promise as complementary biomarkers for risk stratification in HFpEF. Nonetheless, further large-scale prospective studies are needed to clarify the clinical utility of these biomarkers and determine the subsequent integration into multimarker strategies for the management of patients with HFpEF.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"51830"},"PeriodicalIF":2.2,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Initiation of Sodium-Glucose Cotransporter 2 Inhibitors in Acute Decompensated Heart Failure: Efficacy, Safety, and Implementation in Stabilized Patients.","authors":"Alfredo Mauriello, Adriana Correra, Anna Chiara Maratea, Valeria Cetoretta, Francesco Giallauria, Giovanni Esposito, Alfonso Desiderio, Francesco Sabatella, Renato Gioia, Gemma Marrazzo, Biagio Liccardo, Vincenzo Russo, Paolo Trambaiolo, Antonello D'Andrea","doi":"10.31083/RCM53604","DOIUrl":"https://doi.org/10.31083/RCM53604","url":null,"abstract":"<p><p>Sodium-glucose cotransporter 2 (SGLT2) inhibitors have fundamentally reshaped the pharmacological management of chronic heart failure (HF). However, the role of these inhibitors during the vulnerable phase of acute decompensated heart failure (ADHF) has historically been limited by concerns regarding hemodynamic stability and renal function. Recent clinical evidence suggests that the intensive care unit (ICU) and coronary care unit (CCU) may be optimal settings for initiating these disease-modifying therapies. This narrative review aims to evaluate the safety, efficacy, and clinical impact of early in-hospital initiation of SGLT2 inhibitors in patients admitted for ADHF, focusing on hemodynamic recovery, decongestion, and prevention of early readmission. Early initiation of SGLT2 inhibitors is associated with significant clinical benefits, including rapid decongestion, shorter length of hospital stay, and a reduction in the 30-day composite endpoint of death or worsening HF. Furthermore, SGLT2 inhibitors exhibit synergistic effects with loop diuretics, helping to overcome diuretic resistance. Safety profiles remain favorable when patients satisfy basic clinical stability criteria. The traditional wait-and-see approach to initiating SGLT2 inhibitors is being replaced by a proactive early-start strategy. In the cardiac intensive care setting, SGLT2 inhibitors are no longer viewed solely as metabolic agents but also as tools for acute hemodynamic optimization. Further research is required to refine the management of euglycemic ketoacidosis and to determine the optimal timing of initiation in patients requiring mechanical circulatory support.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"53604"},"PeriodicalIF":2.2,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive Value of the Systemic Immune-Inflammation Index for Cardiovascular Events in Patients With Chronic Total Coronary Occlusion.","authors":"Yuhao Zhao, Ping Wang, Shun Zhao, Qin Ma, Ze Zheng, Yuchen Shi, Jinghua Liu","doi":"10.31083/RCM52837","DOIUrl":"https://doi.org/10.31083/RCM52837","url":null,"abstract":"<p><strong>Background: </strong>This large-scale cohort study aimed to evaluate the prognostic role of the systemic immune-inflammation index (SII) in patients with chronic total occlusion (CTO) undergoing percutaneous coronary intervention (PCI).</p><p><strong>Methods: </strong>A total of 3107 patients with CTO lesions who underwent PCI were enrolled in this study. Clinical characteristics were collected, and post-discharge major adverse cardiovascular events (MACEs) were recorded during follow-up, including all-cause mortality, non-fatal myocardial infarction, unplanned revascularization, and heart failure-related readmission. Patients were stratified into three groups according to SII tertiles: the low SII group (SII ≤447.66, n = 1036), the intermediate SII group (447.66 < SII < 679.89, n = 1039), and the high SII group (SII ≥679.89, n = 1032).</p><p><strong>Results: </strong>Over a median follow-up of 2.58 (2.33-2.92) years, 356 (11.5%) MACEs occurred, including 49 (1.6%) all-cause deaths, 105 (3.4%) non-fatal myocardial infarctions, 164 (5.3%) revascularizations, and 38 (1.2%) heart failure rehospitalizations. Multivariable Cox regression analyses demonstrated that elevated SII was independently linked to higher risks of MACEs (hazard ratio [HR] = 1.51, 95% confidence interval [CI]: 1.20-1.90; <i>p</i> = 0.001), all-cause death (HR = 2.06, 95% CI: 1.11-3.84; <i>p</i> = 0.022), non-fatal myocardial infarction (HR = 1.76, 95% CI: 1.15-2.69; <i>p</i> = 0.009), and repeat revascularization (HR = 1.32, 95% CI: 1.01-1.76; <i>p</i> = 0.046) after full adjustment. Kaplan-Meier survival curves showed significantly higher rates of adverse events in patients with elevated SII. Adding SII to traditional risk models improved predictive performance, as reflected by increases in the concordance index (C-index), net reclassification improvement (NRI), and integrated discrimination improvement (IDI).</p><p><strong>Conclusions: </strong>Baseline SII is a reliable and independent predictor of MACEs in patients with CTO after PCI, with superior predictive performance compared with conventional inflammatory markers.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"52837"},"PeriodicalIF":2.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149170076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic Dysfunction-Associated Steatotic Liver Disease and Atrial Fibrillation Recurrence After Catheter Ablation: A Systematic Review and Meta-Analysis.","authors":"Panagiotis Theofilis, Paschalis Karakasis, Panayotis K Vlachakis, Konstantinos Pamporis, Aikaterini Vordoni, Evangelos Oikonomou, Kyriakos Dimitriadis, Gerasimos Siasos, Konstantinos Tsioufis, Dimitris Tousoulis","doi":"10.31083/RCM54276","DOIUrl":"https://doi.org/10.31083/RCM54276","url":null,"abstract":"<p><strong>Background: </strong>Catheter ablation (CA) is an established rhythm-control strategy for atrial fibrillation (AF); however, AF recurrence remains common and is influenced by the underlying cardiometabolic substrate, including metabolic dysfunction-associated steatotic liver disease (MASLD). This study aimed to evaluate the association of MASLD and MASLD-related fibrosis risk with AF recurrence following CA.</p><p><strong>Methods: </strong>We conducted a systematic review and random-effects meta-analysis of observational studies reporting AF recurrence after CA, stratified by MASLD status and liver fibrosis risk, as assessed using the fibrosis-4 (FIB-4) index and the non-alcoholic fatty liver disease (NAFLD) fibrosis score (NFS). Eligible studies included adults undergoing CA for AF with recurrence outcomes reported and stratified by MASLD or fibrosis risk categories.</p><p><strong>Results: </strong>A total of 160 records were identified, and seven studies were included in the qualitative synthesis. Six studies, including 2921 patients, contributed to the primary meta-analysis comparing MASLD versus no MASLD. An additional fibrosis-only study contributed to fibrosis-stratified analyses. The meta-analysis of six studies (MASLD: 894; non-MASLD: 2027) demonstrated that MASLD was associated with a significantly higher risk of AF recurrence after CA (risk ratio (RR) 1.77, 95% confidence interval (CI) 1.43-2.18; <i>p</i> < 0.001; <i>I²</i> = 64.1%). In a separate meta-analysis of five studies reporting adjusted estimates, MASLD remained significantly associated with recurrence (hazard ratio (HR) 2.13, 95% CI 1.49-3.04; <i>p</i> < 0.001; <i>I²</i> = 70.5%). In fibrosis-stratified analyses, Intermediate/High FIB-4 (RR 2.03, 95% CI 1.27-3.26; <i>p</i> = 0.003; <i>I²</i> = 71.3%) and Intermediate/High NFS (RR 1.65, 95% CI 1.12-2.43; <i>p</i> = 0.01; <i>I²</i> = 49.9%) were associated with a higher risk of AF recurrence compared with low scores.</p><p><strong>Conclusion: </strong>MASLD is associated with a significantly higher risk of AF recurrence after CA. Fibrosis risk stratification using FIB-4 and NFS also shows a significant association between Intermediate/High fibrosis and increased recurrence rates.</p><p><strong>Prospero registration: </strong>CRD420261335405, https://www.crd.york.ac.uk/PROSPERO/view/CRD420261335405.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"54276"},"PeriodicalIF":2.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutamine Metabolism in Cardiac Hypertrophy.","authors":"Zhi-Guo Hu, Yao Yao, Yan Gong, Yu-Ting Yang","doi":"10.31083/RCM51889","DOIUrl":"https://doi.org/10.31083/RCM51889","url":null,"abstract":"<p><p>Cardiac hypertrophy represents a crucial adaptive response of the heart to various physiological and pathological stimuli, with metabolic reprogramming serving as the core mechanism driving this process. In recent years, the role of glutamine metabolism in cardiac hypertrophy has garnered increasing attention. This review systematically elucidates the similarities and differences in glutamine metabolism between physiological and pathological cardiac hypertrophy, with a focus on the dual role of glutamine metabolism in regulating cardiomyocyte hypertrophy: it has a protective effect by maintaining energy metabolism and reducing oxidative stress, while simultaneously contributing to the hypertrophic process by promoting anabolic metabolism and exacerbating metabolic remodeling. The subsequent analysis delved into the specific mechanisms by which glutamine metabolism regulates cardiomyocyte hypertrophy, focusing on the functions of key metabolic enzymes and transporters that collectively govern glutamine flux and its downstream signaling pathways. Furthermore, we explore the intricate interplay between glutamine metabolism and lipid metabolism, which plays a pivotal role in cardiac energy homeostasis and hypertrophic development. Finally, we discuss the potential of targeting glutamine metabolism as a therapeutic strategy, highlighting the novel therapeutic prospects of glutamine supplementation in cardiac diseases. In summary, as a key component of metabolic reprogramming in cardiomyocyte hypertrophy, glutamine metabolism offers deeper insights into the pathophysiological mechanisms of cardiac hypertrophy. Future interventions targeting the glutamine metabolic pathway could prevent and treat pathological cardiac hypertrophy.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"51889"},"PeriodicalIF":2.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149167342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Inflammation and Coronary Microvascular Dysfunction.","authors":"Huijing Yao, Jiangwei Cheng, Luqun Yang, Ruiying Wang, Yuanyuan Lin","doi":"10.31083/RCM51873","DOIUrl":"https://doi.org/10.31083/RCM51873","url":null,"abstract":"<p><p>Coronary microvascular dysfunction (CMD) represents a pivotal pathological hallmark across diverse cardiovascular pathologies, the progression of which is tightly coupled to systemic chronic inflammation. Clinically, CMD presents as ischemia with non-obstructive coronary arteries (INOCAs) and myocardial infarction with non-obstructive coronary arteries (MINOCAs), and contributes substantially to heart failure with preserved ejection fraction (HFpEF). Moving beyond conventional risk-factor stratification, this review dissects the mechanistic pathways through which individual comorbidities compromise coronary microcirculatory integrity. In hypertension, increased mechanical wall stress activates proinflammatory Nuclear factor κB (NF-κB)-mitogen-activated protein kinases (MAPK) signaling cascades. In contrast, in diabetes, chronic hyperglycemia drives microvascular injury through the reactive oxygen species (ROS)-advanced glycation end-products (AGEs) axis and Protein Kinase C (PKC)-dependent pathways. In obesity, adipokine dysregulation and gut-derived metabolites, notably trimethylamine N-oxide (TMAO), promote NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, a central mechanism in obesity-related CMD. In the setting of heart failure (HF) and cardiomyopathies, damage-associated molecular pattern (DAMP)-Toll-like receptor (TLR) interactions and TGF-β/Smad signaling promote capillary rarefaction and interstitial fibrosis, thereby linking systemic inflammation to structural microvascular remodeling. Furthermore, both autoimmune-mediated endotheliitis and virus-induced cytokine surges reduce nitric oxide (NO) bioavailability and impair coronary flow reserve (CFR). Thus, by integrating emerging therapeutic strategies, including interleukin-1β (IL-1β) antagonists, SGLT2 inhibitors, and selected traditional medicines, we highlight approaches aimed at restoring microvascular homeostasis. Finally, we propose a personalized framework that leverages multi-omics profiling and artificial intelligence (AI) to modulate the inflammatory milieu, positioning inflammation-targeted interventions as a fundamental strategy for CMD prevention and management.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"51873"},"PeriodicalIF":2.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myocardial Ischemia-Reperfusion Injury: Molecular Mechanisms and Innovative Therapeutic Strategies.","authors":"Dong Zhang, Xiaoting Yang, Shengyu Gong, Gang Zhou, Yunyun Zhao, Xiaolin Zhang, Hui Wu","doi":"10.31083/RCM51415","DOIUrl":"https://doi.org/10.31083/RCM51415","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion injury (MIRI) is a critical pathological paradox following revascularization in acute myocardial infarction, yet effective clinical interventions remain limited. MIRI involves a complex, interlinked hierarchy of programmed cell death modalities, including ferroptosis, pyroptosis, and cuproptosis, which form a network mediated by the stimulator of interferon genes-glutathione peroxidase 4 (STING-GPX4), NOD-like receptor pyrin domain containing 3-gasdermin D (NLRP3-GSDMD), and sirtuin 3-ATPase copper transporting alpha (SIRT3-ATP7A) axes. The dynamic evolution of the immune microenvironment, mitochondrial dysfunction, and non-coding RNA regulatory networks further compound this. Emerging strategies, including bionanotechnology-enabled targeted delivery, intelligent responsive biomaterials, drug repurposing, genome editing, and precise ion channel modulation, demonstrate significant therapeutic potential. Despite bottlenecks in clinical translation related to delivery efficiency, patient heterogeneity, and efficacy evaluation, multidisciplinary integration and technological innovations are propelling a paradigm shift in MIRI treatment from revascularization alone to comprehensive myocardial protection.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"51415"},"PeriodicalIF":2.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of Risk Assessment Strategies Recommended by the 2019 and 2024 European Society of Cardiology Guidelines in Patients With Stable Chest Pain: A Coronary Computed Tomography Angiography Study.","authors":"Hantao Jiang, Chang Liu, Chao Zhang, Chengjian Wang, Minghui Wang, Jia Zhao, Jia Zhou","doi":"10.31083/RCM50177","DOIUrl":"https://doi.org/10.31083/RCM50177","url":null,"abstract":"<p><strong>Background: </strong>The European Society of Cardiology issued guidelines in 2019 and 2024 to help clinicians determine whether patients with stable chest pain (SCP) require advanced cardiovascular imaging testing (CIT). This study aimed to compare the safety and effectiveness of these evaluation strategies.</p><p><strong>Methods: </strong>A total of 17,612 symptomatic patients referred for coronary computed tomography angiography (CCTA) were included and followed over time. Each patient was classified into a deferral or referral group according to the 2019 and 2024 strategies, respectively. Obstructive coronary artery disease (CAD) was primarily defined as a lesion with ≥50% diameter stenosis on CCTA. Associations between major adverse cardiovascular events (MACEs) and the deferral and referral groups were evaluated using hazard ratios (HRs). Net reclassification improvement (NRI) and the number needed to test (NNT) to prevent unnecessary CIT were used to compare the two strategies.</p><p><strong>Results: </strong>Under the 2019 and 2024 strategies, 40% and 46% of patients, respectively, were categorized into deferral groups. These groups demonstrated a low prevalence of obstructive CAD (9.8% and 9.4%) and MACE (3.9% and 3.9%), suggesting that only limited intensive clinical follow-up was needed. Compared with the 2019 strategy, the 2024 strategy revealed a stronger association with MACEs (HR: 3.64 vs. 3.28) and a positive NRI (6.11%; <i>p</i> < 0.001), resulting in an NNT of 17.</p><p><strong>Conclusions: </strong>The 2024 strategy maintained a safety profile comparable to that of the 2019 strategy while potentially reducing unnecessary CIT in patients presenting with SCP suggestive of chronic coronary syndrome (CCS).</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"50177"},"PeriodicalIF":2.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Inflammation in the Development of Heart Failure After Myocardial Infarction.","authors":"Yachao Li, Mengjie Lei, Zengming Xue","doi":"10.31083/RCM49888","DOIUrl":"https://doi.org/10.31083/RCM49888","url":null,"abstract":"<p><p>Inflammation plays a key role in the onset and progression of heart failure (HF) after myocardial infarction (MI), which represents one of the leading causes of mortality in patients with cardiovascular disease. This review summarizes the inflammatory mechanisms involved at different stages of HF after MI, including the infiltration and activation of inflammatory cells, the release of inflammatory mediators, and the effects of these mediators on cardiomyocytes, the extracellular matrix, and cardiac function. In addition, this review discusses therapeutic strategies that target inflammatory pathways, providing a theoretical basis for the prevention and treatment of HF after MI.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"49888"},"PeriodicalIF":2.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation After Transcatheter Aortic Valve Implantation: Mechanisms, Risk Stratification, and Therapeutic Implications.","authors":"Mihail Celeski, Michele Marchetta, Emanuele Sammartini, Antonio Sorropago, Mattia Basile, Matteo Morello, Carmine Salzillo, Marco Bernardi, Pasquale Mollo, Francisco José Romeo, Arturo Cesaro, Michele Golino","doi":"10.31083/RCM52850","DOIUrl":"https://doi.org/10.31083/RCM52850","url":null,"abstract":"<p><p>Transcatheter aortic valve implantation (TAVI) elicits a sterile inflammatory response that is almost universal, yet highly heterogeneous in both magnitude and clinical impact. Initiated by endothelial injury, ischemia-reperfusion, and residual bioprosthetic immunogenicity, peri-procedural inflammation converges on activation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and downstream interleukin-1β (IL-1β) and IL-6 signaling, leading to increased C-reactive protein levels. This response is further modulated by patient susceptibility, procedural complexity, and device-specific characteristics. While a controlled response promotes tissue repair and healing, exaggerated activation, which manifests as systemic inflammatory response syndrome in up to two-thirds of patients, has been consistently associated with higher mortality, conduction disturbances, new-onset atrial fibrillation, acute kidney injury (AKI), and subclinical leaflet thrombosis. Emerging evidence also implicates gut microbiome-derived metabolites and xenoantigen-driven adaptive immunity as additional contributors to the overall inflammatory burden. Serial biomarker assessment, including C-reactive protein trajectories, neutrophil-to-lymphocyte ratio, cancer antigen 125 (CA-125), and novel composite indices such as the neutrophil percentage-to-albumin ratio, combined with multimodality imaging, allows increasingly refined risk stratification. However, no anti-inflammatory therapy is currently established for routine use after TAVI. Colchicine has shown proof-of-concept signals, sodium-glucose cotransporter 2 inhibitors have demonstrated clinical benefit with pleiotropic anti-inflammatory properties, and lessons from IL-1 and IL-6 inhibition trials in ischemic heart disease provide a translational roadmap. This narrative review synthesizes the epidemiology, mechanisms, clinical consequences, and assessment of peri-TAVI inflammation. Moreover, this review proposes a pragmatic inflammatory subphenotyping framework that integrates baseline risk, procedural exposure, and biomarker kinetics. Such a framework may help bridge the gap between observational associations and precision-based therapeutic strategies, shifting peri-TAVI inflammation from a prognostic marker to a modifiable determinant of outcome.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"52850"},"PeriodicalIF":2.2,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}