Artur Kovenskiy, Zhussipbek Mukhatayev, Aliya Sailybayeva, Makhabbat Bekbossynova, Almagul Kushugulova
{"title":"循环生物标志物在心力衰竭中的诊断和预后价值。","authors":"Artur Kovenskiy, Zhussipbek Mukhatayev, Aliya Sailybayeva, Makhabbat Bekbossynova, Almagul Kushugulova","doi":"10.3389/fcvm.2025.1633164","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Heart failure (HF) represents a global health burden with distinct phenotypes characterized by varying left ventricular ejection fraction (LVEF). Despite shared endothelial dysfunction, heart failure with reduced (HFrEF) and preserved ejection fraction (HFpEF) exhibit fundamentally different pathophysiological mechanisms, comorbidity profiles, and treatment responses.</p><p><strong>Methods: </strong>This systematic review and meta-analysis examine inflammatory, cardiac remodelling and congestion, and myocardial injury biomarkers across HF phenotypes, integrating data from 78 studies encompassing 58,076 subjects.</p><p><strong>Results: </strong>Our analysis reveals a significant elevation of IL-6, TNF-alpha, and hs-CRP in HF compared to controls, with distinct biomarker profiles emerging between phenotypes. While inflammatory markers universally increase with disease severity, their utility in phenotypic differentiation remains limited due to substantial overlap. Comorbidity burden significantly influences inflammatory profiles, creating diagnostic challenges that multi-biomarker approaches may address. NT-proBNP, sST2, GDF-15, and cardiac troponins demonstrate complementary value when combined with inflammatory markers, potentially enabling more precise phenotypic classification.</p><p><strong>Conclusion: </strong>Our findings highlight the central role of inflammation in HF pathophysiology while identifying critical knowledge gaps, particularly regarding HFpEF-specific inflammatory signatures. This comprehensive analysis provides a foundation for developing targeted immunomodulatory therapies and personalized diagnostic approaches in heart failure management.</p><p><strong>Systematic review registration: </strong>https://www.crd.york.ac.uk/PROSPERO/view/CRD42025639405, PROSPERO CRD42025639405.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1633164"},"PeriodicalIF":2.8000,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504382/pdf/","citationCount":"0","resultStr":"{\"title\":\"Diagnostic and prognostic value of circulating biomarkers in heart failure.\",\"authors\":\"Artur Kovenskiy, Zhussipbek Mukhatayev, Aliya Sailybayeva, Makhabbat Bekbossynova, Almagul Kushugulova\",\"doi\":\"10.3389/fcvm.2025.1633164\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Heart failure (HF) represents a global health burden with distinct phenotypes characterized by varying left ventricular ejection fraction (LVEF). Despite shared endothelial dysfunction, heart failure with reduced (HFrEF) and preserved ejection fraction (HFpEF) exhibit fundamentally different pathophysiological mechanisms, comorbidity profiles, and treatment responses.</p><p><strong>Methods: </strong>This systematic review and meta-analysis examine inflammatory, cardiac remodelling and congestion, and myocardial injury biomarkers across HF phenotypes, integrating data from 78 studies encompassing 58,076 subjects.</p><p><strong>Results: </strong>Our analysis reveals a significant elevation of IL-6, TNF-alpha, and hs-CRP in HF compared to controls, with distinct biomarker profiles emerging between phenotypes. While inflammatory markers universally increase with disease severity, their utility in phenotypic differentiation remains limited due to substantial overlap. Comorbidity burden significantly influences inflammatory profiles, creating diagnostic challenges that multi-biomarker approaches may address. NT-proBNP, sST2, GDF-15, and cardiac troponins demonstrate complementary value when combined with inflammatory markers, potentially enabling more precise phenotypic classification.</p><p><strong>Conclusion: </strong>Our findings highlight the central role of inflammation in HF pathophysiology while identifying critical knowledge gaps, particularly regarding HFpEF-specific inflammatory signatures. This comprehensive analysis provides a foundation for developing targeted immunomodulatory therapies and personalized diagnostic approaches in heart failure management.</p><p><strong>Systematic review registration: </strong>https://www.crd.york.ac.uk/PROSPERO/view/CRD42025639405, PROSPERO CRD42025639405.</p>\",\"PeriodicalId\":12414,\"journal\":{\"name\":\"Frontiers in Cardiovascular Medicine\",\"volume\":\"12 \",\"pages\":\"1633164\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-09-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504382/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Frontiers in Cardiovascular Medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3389/fcvm.2025.1633164\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Cardiovascular Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fcvm.2025.1633164","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Diagnostic and prognostic value of circulating biomarkers in heart failure.
Background: Heart failure (HF) represents a global health burden with distinct phenotypes characterized by varying left ventricular ejection fraction (LVEF). Despite shared endothelial dysfunction, heart failure with reduced (HFrEF) and preserved ejection fraction (HFpEF) exhibit fundamentally different pathophysiological mechanisms, comorbidity profiles, and treatment responses.
Methods: This systematic review and meta-analysis examine inflammatory, cardiac remodelling and congestion, and myocardial injury biomarkers across HF phenotypes, integrating data from 78 studies encompassing 58,076 subjects.
Results: Our analysis reveals a significant elevation of IL-6, TNF-alpha, and hs-CRP in HF compared to controls, with distinct biomarker profiles emerging between phenotypes. While inflammatory markers universally increase with disease severity, their utility in phenotypic differentiation remains limited due to substantial overlap. Comorbidity burden significantly influences inflammatory profiles, creating diagnostic challenges that multi-biomarker approaches may address. NT-proBNP, sST2, GDF-15, and cardiac troponins demonstrate complementary value when combined with inflammatory markers, potentially enabling more precise phenotypic classification.
Conclusion: Our findings highlight the central role of inflammation in HF pathophysiology while identifying critical knowledge gaps, particularly regarding HFpEF-specific inflammatory signatures. This comprehensive analysis provides a foundation for developing targeted immunomodulatory therapies and personalized diagnostic approaches in heart failure management.
期刊介绍:
Frontiers? Which frontiers? Where exactly are the frontiers of cardiovascular medicine? And who should be defining these frontiers?
At Frontiers in Cardiovascular Medicine we believe it is worth being curious to foresee and explore beyond the current frontiers. In other words, we would like, through the articles published by our community journal Frontiers in Cardiovascular Medicine, to anticipate the future of cardiovascular medicine, and thus better prevent cardiovascular disorders and improve therapeutic options and outcomes of our patients.