Reviews in cardiovascular medicine最新文献

{"title":"Enhancer of Zeste Homolog 2 Inhibition Attenuates Atrial Fibrillation Post-Myocardial Infarction Through Reduced Atrial Fibrosis.","authors":"Tian-Peng Wei, Wen-Rui Wang, Xiao-Lu Zhang, Huan-Huan Liu, Ying Liu, Fan Yang, Xiao-Yu Liu, Ru-Xing Wang, Ling-Ling Qian","doi":"10.31083/RCM51343","DOIUrl":"https://doi.org/10.31083/RCM51343","url":null,"abstract":"<p><strong>Background: </strong>Atrial fibrillation (AF) is one of the most prevalent arrhythmias following a myocardial infarction (MI), yet the pathogenesis associated with post-MI AF remains poorly understood. Enhancer of zeste homolog 2 (EZH2), an enzyme that regulates histone modifications, has been implicated in various cardiovascular diseases; however, the role of EZH2 in the development of post-MI AF also remains unclear.</p><p><strong>Methods: </strong>MI was induced in mice by ligation of the left anterior descending coronary artery (LAD), followed by intraperitoneal administration of GSK126 or vehicle control (polyethylene glycol 300 and saline).</p><p><strong>Results: </strong>MI significantly increased the incidence and duration of AF, while electrical mapping revealed decreased conduction velocity. These changes were accompanied by increased atrial fibrosis, which was associated with upregulation of EZH2 and trimethylated histone H3 at lysine 27 (H3K27me3). In GSK126-treated mice, the incidence of AF was reduced, along with a significant decrease in H3K27me3 expression and atrial fibrosis.</p><p><strong>Conclusion: </strong>Upregulation of EZH2 is associated with post-MI AF. Pharmacological inhibition of EZH2 using GSK126 attenuates atrial fibrosis and reduces the incidence of AF. These findings suggest that EZH2 may represent a potential therapeutic candidate for post-MI AF, although further validation is required.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"51343"},"PeriodicalIF":2.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149167806","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":"Lipoprotein(a) Inhibition: Current Evidence, Therapeutic Landscape, and Future Directions.","authors":"Pierre Sabouret, Domenico Mario Giamundo, Joanna Popiolek-Kalisz, Luigi Spadafora, Marco Bernardi, Elad Asher, Mamas A Mamas, Dan Atar, Giuseppe Andò","doi":"10.31083/RCM55004","DOIUrl":"https://doi.org/10.31083/RCM55004","url":null,"abstract":"<p><p>Lipoprotein(a) [Lp(a)] is a genetically determined, apolipoprotein B-containing lipoprotein that contributes to cardiovascular risk through atherogenic, proinflammatory, and potentially antifibrinolytic mechanisms. Genetic, epidemiological, and mechanistic evidence supports a causal role for elevated Lp(a) in atherosclerotic cardiovascular disease and calcific aortic valve disease. In contrast, associations with other cardiovascular phenotypes are less consistent. Since circulating concentrations are largely inherited and only modestly affected by lifestyle measures and conventional lipid-lowering therapies, Lp(a) represents an important component of residual cardiovascular risk. This review summarizes the structural, genetic, and pathogenic characteristics of Lp(a), examines the strength of evidence across coronary artery disease, ischemic stroke, peripheral artery disease, abdominal aortic aneurysm, calcific aortic valve disease, and heart failure, and discusses measurement, clinical interpretation, and potential biomarkers. The therapeutic landscape has expanded rapidly. Antisense oligonucleotides and small interfering RNA agents substantially suppress hepatic apolipoprotein(a) synthesis, oral small-molecule inhibitors prevent Lp(a) particle assembly, and <i>in vivo</i> gene-editing strategies aim to provide highly durable reductions. Early-phase trials have demonstrated marked lowering of circulating Lp(a); however, most were not designed to assess cardiovascular outcomes, so direct comparisons among agents are limited by differences in study populations, assays, dosing schedules, and follow-up. Ongoing cardiovascular outcome trials will determine whether selective Lp(a) lowering reduces clinical events and which patients are most likely to benefit. Until these results are available, Lp(a) measurement can refine risk stratification and support intensive management of modifiable risk factors, whereas biomarker reduction alone should not be equated with proven clinical benefit.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 9","pages":"55004"},"PeriodicalIF":2.2,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166383","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":"A Machine Learning Prediction Model for In-Hospital Mortality in Postoperative Patients With Type A Aortic Dissection.","authors":"Ming-Hao Luo, Xian-Tong Cao, Yin-Rui Huang, Fei-Bai Yao, Guo-Wei Tu, Ying Su, Jun-Yi Hou, Yi-Jie Zhang, Chun-Sheng Wang, Hao Lai, Cong Tian, Yana Yuan, Tao Shi, Zhe Luo","doi":"10.31083/RCM49025","DOIUrl":"10.31083/RCM49025","url":null,"abstract":"<p><strong>Backgrounds: </strong>Scoring systems are increasingly used for risk stratification in the postoperative management of type A aortic dissection (TAAD), but no consensus exists regarding the optimal tool. Thus, this study aimed to develop and validate a machine learning-based model to predict in-hospital mortality among postoperative patients with TAAD.</p><p><strong>Methods: </strong>Data from postoperative TAAD patients treated at two centers were analyzed retrospectively. The primary outcome was in-hospital all-cause mortality. Clustering methods were implemented for feature selection. A random forest algorithm was selected from a range of machine learning methods to develop a postoperative mortality risk prediction tool. Receiver operating characteristic (ROC) curves were employed to assess predictive accuracy and reliability. Model calibration was evaluated by plotting calibration curves. SHapley Additive exPlanations (SHAP) values were calculated to quantify the contribution of each feature. Model performance was compared with the European System for Cardiac Operative Risk Evaluation II (EuroSCORE II).</p><p><strong>Results: </strong>A total of 983 patients who underwent surgical repair for TAAD were included in the study. Eight features were identified as significant predictors of in-hospital mortality. On postoperative day (POD) 1, the final random forest model achieved an area under the receiver operating characteristic curve (AUROC) of 0.8899 (95% confidence interval (CI): 0.7988-0.9469). External validation on POD 1 yielded an AUROC of 0.8331 (95% CI: 0.7722-0.8871). The model demonstrated significantly higher discriminative performance than EuroSCORE II.</p><p><strong>Conclusions: </strong>This study developed and primarily validated an accurate machine learning model to predict the all-cause in-hospital mortality of patients with TAAD undergoing surgical repair.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 8","pages":"49025"},"PeriodicalIF":2.2,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13539989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888079","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":"Clinical Prognostic Impact of CALLY in Heart Failure Patients With Different Ejection Fractions: A Retrospective Study.","authors":"Xinuo Ma, Jianping Yang, Zijie Liu, Ying Li, Sirui Yang, Tao Shi, Fazhi Yang, Yujuan Peng, Lixing Chen","doi":"10.31083/RCM49108","DOIUrl":"10.31083/RCM49108","url":null,"abstract":"<p><strong>Background: </strong>Chronic heart failure (CHF) is closely linked to high morbidity and mortality rates, with inflammation and changes in nutritional status being key contributors to disease progression. Thus, this study aimed to evaluate the prognostic utility of the novel composite index CALLY, which incorporates albumin (ALB) level, lymphocyte count (LYM), and C-reactive protein (CRP) level, for predicting all-cause mortality in patients with CHF and varying ejection fractions.</p><p><strong>Methods: </strong>This retrospective cohort study included 1193 patients with CHF who were admitted to the First Affiliated Hospital of Kunming Medical University between January 2017 and October 2021. Restricted cubic spline analysis was used to determine the CALLY index cutoff value and classify patients into two groups. Kaplan-Meier and multivariable Cox regression analyses were performed to assess the prognostic value of CALLY in the overall cohort and in subgroups with HFrEF, HFmrEF, and HFpEF. Model performance was evaluated using receiver operating characteristic curves with DeLong's test, calibration curves with bootstrap resampling, and decision curve analysis.</p><p><strong>Results: </strong>Kaplan‒Meier analysis revealed that lower CALLY levels were associated with higher all-cause mortality in all patients with CHF and in the twoCHF subgroups. Multivariable Cox proportional hazards analysis demonstrated that CALLY independently predicted all-cause mortality across all heart failure subtypes. Receiver operating characteristic curve analysis indicated that models incorporating CALLY exhibited improved predictive performance. Calibration and decision curve analyses further supported the clinical utility of the CALLY index.</p><p><strong>Conclusions: </strong>Amongpatients with CHF in this cohort, a lower CALLY index was independently associated with higher all-cause mortality across different ejection fraction categories. These findings suggest that CALLY may serve as a potential risk marker.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 8","pages":"49108"},"PeriodicalIF":2.2,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888476","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":"Cardiac Sympathetic Nerve Terminals in the Pathogenesis of Takotsubo Syndrome: A Brief Review and Novel Analytical Approach.","authors":"Shams Y-Hassan","doi":"10.31083/RCM49787","DOIUrl":"10.31083/RCM49787","url":null,"abstract":"<p><p>Takotsubo syndrome (TS) is an acute cardiac condition that clinically resembles acute coronary syndrome; however, TS is not caused by acute coronary obstruction. Moreover, TS is characterized by a distinctive regional, often circumferential, and typically reversible left ventricular wall motion abnormality, which can also involve the right ventricle. In addition to the takotsubo sign, the disease has several other characteristic features, including a history of an emotional or physical trigger, repolarization changes on electrocardiography, moderate elevations of biomarkers of myocardial cell necrosis, and histopathological myocardial changes in the form of contraction band necrosis (coagulative myocytolysis) with characteristic time-related evolutionary changes. Several pathophysiologic mechanisms underlying the disease process remain under debate. However, there is evidence of sympathetic nervous system involvement, including local cardiac sympathetic hyperactivation and disruption at cardiac sympathetic nerve terminals, with excessive norepinephrine release and spillover. Hence, the pathogenetic term autonomic neurocardiogenic syndrome (ANCA), with or without a takotsubo phenotype, has been introduced. For decades, the histopathological cardiac lesions of focal or multifocal coagulative myocytolysis and focal or multifocal \"myocarditis\" in TS/ANCA syndrome have been described as diagnostic terms in the medical literature. However, the circumferential and multifocal nature of this disease, along with the characteristic time-related histopathological changes and its presence within normal myocardium, provide further evidence that TS/ANCA syndrome is a disorder of the cardiac sympathetic nerve terminals. Therefore, this review presents evidence supporting the previously unquestioned pathogenetic mechanism, with a focus on the specific role of cardiac sympathetic nerve terminals in this syndrome.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 8","pages":"49787"},"PeriodicalIF":2.2,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888408","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":"A New Option for the Management of Dyslipidemias: Advances in Research on the Small Interfering RNA Drug Inclisiran.","authors":"Xuebing Wu, Jing Zhang","doi":"10.31083/RCM48237","DOIUrl":"10.31083/RCM48237","url":null,"abstract":"<p><p>Atherosclerotic cardiovascular disease (ASCVD) is associated with increased morbidity and mortality rates. Numerous studies have shown that lowering low-density lipoprotein cholesterol (LDL-C) levels can reduce the occurrence of cardiovascular disease (CVD). Current data indicate that 80% of patients with ASCVD do not achieve the LDL-C targets recommended by clinical guidelines. Nearly 15% of patients with hypercholesterolemia exhibit statin intolerance, with some experiencing severe adverse reactions such as liver function abnormalities and rhabdomyolysis. Statins require daily administration, and proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies should be injected 12 to 26 times annually. Frequent dosing reduces patient adherence. This review comprehensively discusses inclisiran, the first lipid-lowering small interfering RNA (siRNA) drug, focusing on the associated mechanism of action, pharmacology, clinical trial data, efficacy, safety, use in special populations, and adverse effects. The objective is to provide evidence to guide the appropriate clinical use of inclisiran, a novel option for lipid-lowering therapy. Inclisiran may represent another milestone in the treatment of dyslipidemia.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 8","pages":"48237"},"PeriodicalIF":2.2,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888028","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":"Erratum: Yan et al. Association Between Serum Lipid-Bilirubin Ratio and Clinical Prognosis Among Patients Undergoing Percutaneous Coronary Intervention After Coronary Artery Bypass Grafting. Reviews in Cardiovascular Medicine. 2025; 26(11): 39827.","authors":"Xu Yan, Muhib Ur Rehman, Qiuxuan Li, Zhiqiang Yang, Lixia Yang, Zhijian Wang, Yujie Zhou","doi":"10.31083/RCM57380","DOIUrl":"10.31083/RCM57380","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.31083/RCM39827.].</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 8","pages":"57380"},"PeriodicalIF":2.2,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13539986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888423","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":"Integrated Assessment of Stress Hyperglycemia and Glycemic Variability for Mortality Prediction in Non-St-Segment Elevation Myocardial Infarction and St-Segment Elevation Myocardial Infarction: A Glycometabolic Phenotype-Stratified Analysis.","authors":"Jinlin Hu, Jingyu Bo, Kunyang He, Liangbing Yang, Miao Zhang, Teng Ge, Bo Ning, Guanmou Li, Rongjun Zou, Xiaoping Fan","doi":"10.31083/RCM50449","DOIUrl":"10.31083/RCM50449","url":null,"abstract":"<p><strong>Background: </strong>Precise risk stratification in myocardial infarction (MI) remains challenging, particularly when integrating acute dysglycemia with chronic metabolic status. Prior evaluations of stress hyperglycemia ratio (SHR) and glycemic variability (GluCV) have seldom accounted for underlying glucose metabolic phenotypes, potentially obscuring their prognostic utility in distinct MI subtypes.</p><p><strong>Methods: </strong>In this retrospective cohort study, we identified 3628 non-ST-segment elevation myocardial infarction (NSTEMI) and 825 ST-segment elevation myocardial infarction (STEMI) patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Participants were stratified by glycemic status: normal glucose regulation (NGR), pre-diabetes (Pre-DM), and diabetes mellitus (DM). We assessed the individual and combined prognostic value of SHR and GluCV for one-year all-cause mortality. Machine learning (ML) models were subsequently developed to optimize risk prediction.</p><p><strong>Results: </strong>The combination of SHR and GluCV effectively stratified mortality risk across all glycemic phenotypes in both NSTEMI and STEMI patients. Notably, within NSTEMI cohorts, the subgroup characterized by both high GluCV and low SHR exhibited the poorest survival. In comparative analyses, GluCV demonstrated superior prognostic performance over SHR for NSTEMI outcomes. Among five ML algorithms tested, the Random Forest model achieved the highest predictive accuracy [NGR (area under the curve (AUC): 0.885, 95% confidence interval (CI): 0.882-0.888), Pre-DM (AUC: 0.854, 95% CI: 0.85-0.857), DM (AUC: 0.87, 95% CI: 0.868-0.871)], with GluCV consistently identified as a top-ranking feature.</p><p><strong>Conclusions: </strong>By concurrently evaluating SHR and GluCV within a glycemic stratification framework, this study refines mortality prediction in MI patients. Our findings advocate for a shift from uniform glycemic targets to phenotype-specific management strategies. The developed ML tool offers a practical approach for individualized risk assessment in clinical practice.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 8","pages":"50449"},"PeriodicalIF":2.2,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888561","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":"Pathological Mechanisms and Therapeutic Potential of Mitochondrial Dysfunction in Heart Failure.","authors":"Shige San, Xi Yang, Liang Shen, Kun Meng","doi":"10.31083/RCM51920","DOIUrl":"10.31083/RCM51920","url":null,"abstract":"<p><p>Heart failure (HF) is a clinical syndrome resulting from structural or functional cardiac abnormalities and represents a growing global public health challenge. Common etiologies include myocardial infarction, cardiomyopathy, and myocarditis. Mitochondrial dysfunction is now recognized as a central event in the initiation and progression of HF, making this pathogenesis a key focus of recent research. Recent studies have confirmed that HF with reduced ejection fraction (HFrEF) is driven by defects in excitation-contraction coupling, leading to mechano-energetic uncoupling. In contrast, HF with preserved ejection fraction (HFpEF) is characterized by an imbalance between cardiac workload and mitochondrial energy supply. Mitochondrial dysfunction is evident in both forms of HF, with metabolic disturbances serving as both biomarkers and drivers of disease progression. However, key knowledge gaps remain, including uncertainty regarding the regulation of mitochondrial networks and the limited clinical translation of targeted therapies. Thus, the precise modulation of mitochondrial quality control and the correction of metabolic and oxidative imbalances may offer a promising approach for overcoming current therapeutic limitations. This review analyzes the current literature to summarize the pathological mechanisms and therapeutic strategies targeting mitochondrial dysfunction in HF, as a deeper understanding of these mechanisms may support the development of individualized treatment strategies for HF.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 8","pages":"51920"},"PeriodicalIF":2.2,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887534","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":"Progress in Understanding Brain Injury After Cardiopulmonary Bypass in Cardiac Surgery: A Narrative Review.","authors":"Si Zhang, Jianing Hao, Weijie Fan, Bo Liu, Wei Li, Li Wen, Dong Zhang","doi":"10.31083/RCM50277","DOIUrl":"10.31083/RCM50277","url":null,"abstract":"<p><p>The application of cardiopulmonary bypass (CPB) has significantly advanced cardiovascular surgery. However, CPB-associated brain injury remains a critical complication that affects patient prognosis and quality of life. Overt stroke occurs in approximately 1-5% of cases, while postoperative delirium affects 20-50% of patients, and perioperative neurocognitive disorders are reported in 10-40%, depending on the diagnostic criteria used. This narrative review provides a comprehensive summary of recent research progress on CPB-associated brain injury in cardiac surgery, along with a critical appraisal of the supporting evidence. While the main focus is on adult patients, various pediatric conditions are also discussed. We review the evolution of CPB technology; the classification and clinical burden of brain injury; detailed pathophysiological mechanisms, including hemodynamic injury, microembolism, systemic inflammatory response, and blood-brain barrier disruption; current cerebral protection strategies advances in personalized cerebral perfusion. Furthermore, special consideration is given to genetic susceptibility (such as apolipoprotein E (<i>APOE</i>) polymorphisms), and pediatric cardiac surgery. A systematic screening of high-quality literature from the past five years highlights the challenges that continue to impede clinical translation, despite progress in neuromonitoring and minimally invasive CPB technologies. Future research directions include the application of artificial intelligence and real-time cerebral autoregulation monitoring to support the transition from empirical medicine to precision, individualized cerebral protection.</p>","PeriodicalId":20989,"journal":{"name":"Reviews in cardiovascular medicine","volume":"27 8","pages":"50277"},"PeriodicalIF":2.2,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888084","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}