{"title":"移植物抗宿主病是异基因造血干细胞移植后心力衰竭的危险因素:一项回顾性队列研究","authors":"Tong Wang, Qian Zhu, Hongfei Zhao, Huan Liu","doi":"10.1016/j.transproceed.2025.05.030","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a critical therapeutic option for hematologic malignancies. However, it is associated with severe complications, including graft-versus-host disease (GVHD). While GVHD is widely recognized for its impact on various organs, its role in the development of heart failure (HF) remains insufficiently understood. This study investigates the association between GVHD and HF following allo-HSCT, focusing on identifying key risk factors contributing to HF development.</p><p><strong>Methods: </strong>A retrospective cohort study was conducted on 220 patients who underwent allo-HSCT between 2005 and 2024. HF was defined by clinical criteria and left ventricular ejection fraction. The association of GVHD severity (acute and chronic), inflammatory markers (tumor necrosis factor-alpha, interleukin-6), and cardiac biomarkers (B-type natriuretic peptide) with HF was analyzed. Multivariate logistic regression was performed to identify independent predictors of HF.</p><p><strong>Results: </strong>Patients with HF demonstrated significantly lower left ventricular ejection fraction (33.92% ± 6.73% vs 61.51% ± 6.18%, P = .021) and higher levels of B-type natriuretic peptide (393.29 ± 71.29 ng/L vs 307.92 ± 76.28 ng/L, P = .042), tumor necrosis factor-alpha (80.3 ± 20.4 pg/mL vs 40.2 ± 10.1 pg/mL, P < .001), and interleukin-6 (65.1 ± 15.7 pg/mL vs 25.4 ± 8.6 pg/mL, P < .001) compared to controls. Severe acute GVHD (Grade ≥III) significantly increased the risk of HF (odds ratio = 3.5, P < .001). Patients with multiple GVHD-related complications had a 3.6-fold higher likelihood of HF development (P < .01). Echocardiographic findings revealed significant cardiac remodeling in HF patients, with increased left ventricular end-diastolic diameter (68.76 ± 7.23 mm vs 44.18 ± 7.16 mm, P = .004) and left ventricular posterior wall thickness (12.18 ± 4.32 mm vs 4.46 ± 2.19 mm, P = .002). Additionally, HF patients experienced more severe transplant-related complications, including infections (29.0% vs 10.6%, P = .041) and hemorrhagic cystitis (23.4% vs 7.1%, P = .027). Mortality was significantly higher in the HF group (86.0% vs 41.6%, P < .001), with infection (71.0%) and HF (21.5%) being the leading causes of death. GVHD significantly heightens the risk of HF after allo-HSCT.</p><p><strong>Conclusions: </strong>These findings underscore the necessity for proactive cardiovascular monitoring and targeted therapeutic interventions in GVHD patients to prevent the development of HF.</p>","PeriodicalId":94258,"journal":{"name":"Transplantation proceedings","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Graft-Versus-Host Disease as a Risk Factor for Heart Failure After Allogeneic Hematopoietic Stem Cell Transplantation: A Retrospective Cohort Study.\",\"authors\":\"Tong Wang, Qian Zhu, Hongfei Zhao, Huan Liu\",\"doi\":\"10.1016/j.transproceed.2025.05.030\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a critical therapeutic option for hematologic malignancies. However, it is associated with severe complications, including graft-versus-host disease (GVHD). While GVHD is widely recognized for its impact on various organs, its role in the development of heart failure (HF) remains insufficiently understood. This study investigates the association between GVHD and HF following allo-HSCT, focusing on identifying key risk factors contributing to HF development.</p><p><strong>Methods: </strong>A retrospective cohort study was conducted on 220 patients who underwent allo-HSCT between 2005 and 2024. HF was defined by clinical criteria and left ventricular ejection fraction. The association of GVHD severity (acute and chronic), inflammatory markers (tumor necrosis factor-alpha, interleukin-6), and cardiac biomarkers (B-type natriuretic peptide) with HF was analyzed. Multivariate logistic regression was performed to identify independent predictors of HF.</p><p><strong>Results: </strong>Patients with HF demonstrated significantly lower left ventricular ejection fraction (33.92% ± 6.73% vs 61.51% ± 6.18%, P = .021) and higher levels of B-type natriuretic peptide (393.29 ± 71.29 ng/L vs 307.92 ± 76.28 ng/L, P = .042), tumor necrosis factor-alpha (80.3 ± 20.4 pg/mL vs 40.2 ± 10.1 pg/mL, P < .001), and interleukin-6 (65.1 ± 15.7 pg/mL vs 25.4 ± 8.6 pg/mL, P < .001) compared to controls. Severe acute GVHD (Grade ≥III) significantly increased the risk of HF (odds ratio = 3.5, P < .001). Patients with multiple GVHD-related complications had a 3.6-fold higher likelihood of HF development (P < .01). Echocardiographic findings revealed significant cardiac remodeling in HF patients, with increased left ventricular end-diastolic diameter (68.76 ± 7.23 mm vs 44.18 ± 7.16 mm, P = .004) and left ventricular posterior wall thickness (12.18 ± 4.32 mm vs 4.46 ± 2.19 mm, P = .002). Additionally, HF patients experienced more severe transplant-related complications, including infections (29.0% vs 10.6%, P = .041) and hemorrhagic cystitis (23.4% vs 7.1%, P = .027). Mortality was significantly higher in the HF group (86.0% vs 41.6%, P < .001), with infection (71.0%) and HF (21.5%) being the leading causes of death. GVHD significantly heightens the risk of HF after allo-HSCT.</p><p><strong>Conclusions: </strong>These findings underscore the necessity for proactive cardiovascular monitoring and targeted therapeutic interventions in GVHD patients to prevent the development of HF.</p>\",\"PeriodicalId\":94258,\"journal\":{\"name\":\"Transplantation proceedings\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-06-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Transplantation proceedings\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1016/j.transproceed.2025.05.030\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Transplantation proceedings","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.transproceed.2025.05.030","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
背景:同种异体造血干细胞移植是恶性血液病的重要治疗选择。然而,它与严重的并发症相关,包括移植物抗宿主病(GVHD)。虽然GVHD因其对各种器官的影响而被广泛认识,但其在心力衰竭(HF)发展中的作用仍未得到充分了解。本研究调查了同种异体造血干细胞移植后GVHD与HF之间的关系,重点是确定导致HF发展的关键危险因素。方法:对2005年至2024年间接受同种异体造血干细胞移植的220例患者进行回顾性队列研究。根据临床标准和左心室射血分数来定义HF。分析GVHD严重程度(急性和慢性)、炎症标志物(肿瘤坏死因子- α、白细胞介素-6)和心脏生物标志物(b型利钠肽)与HF的关系。采用多变量logistic回归来确定心衰的独立预测因素。结果:HF患者左心室射血分数明显低于对照组(33.92%±6.73% vs 61.51%±6.18%,P = 0.021), b型利钠肽(393.29±71.29 ng/L vs 307.92±76.28 ng/L, P = 0.042)、肿瘤坏死因子- α(80.3±20.4 pg/mL vs 40.2±10.1 pg/mL, P < 0.001)、白细胞介素-6(65.1±15.7 pg/mL vs 25.4±8.6 pg/mL, P < 0.001)水平明显高于对照组。严重急性GVHD(≥III级)显著增加HF的风险(优势比= 3.5,P < 0.001)。合并多种gvhd相关并发症的患者发生HF的可能性高出3.6倍(P < 0.01)。超声心动图结果显示HF患者心脏重构明显,左室舒张末期内径(68.76±7.23 mm vs 44.18±7.16 mm, P = 0.004)和左室后壁厚度(12.18±4.32 mm vs 4.46±2.19 mm, P = 0.002)增加。此外,HF患者经历了更严重的移植相关并发症,包括感染(29.0% vs 10.6%, P = 0.041)和出血性膀胱炎(23.4% vs 7.1%, P = 0.027)。心衰组死亡率明显高于对照组(86.0% vs 41.6%, P < 0.001),其中感染(71.0%)和心衰(21.5%)是主要死亡原因。GVHD显著增加了同种异体造血干细胞移植后发生HF的风险。结论:这些发现强调了对GVHD患者进行主动心血管监测和有针对性的治疗干预以预防HF发展的必要性。
Graft-Versus-Host Disease as a Risk Factor for Heart Failure After Allogeneic Hematopoietic Stem Cell Transplantation: A Retrospective Cohort Study.
Background: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a critical therapeutic option for hematologic malignancies. However, it is associated with severe complications, including graft-versus-host disease (GVHD). While GVHD is widely recognized for its impact on various organs, its role in the development of heart failure (HF) remains insufficiently understood. This study investigates the association between GVHD and HF following allo-HSCT, focusing on identifying key risk factors contributing to HF development.
Methods: A retrospective cohort study was conducted on 220 patients who underwent allo-HSCT between 2005 and 2024. HF was defined by clinical criteria and left ventricular ejection fraction. The association of GVHD severity (acute and chronic), inflammatory markers (tumor necrosis factor-alpha, interleukin-6), and cardiac biomarkers (B-type natriuretic peptide) with HF was analyzed. Multivariate logistic regression was performed to identify independent predictors of HF.
Results: Patients with HF demonstrated significantly lower left ventricular ejection fraction (33.92% ± 6.73% vs 61.51% ± 6.18%, P = .021) and higher levels of B-type natriuretic peptide (393.29 ± 71.29 ng/L vs 307.92 ± 76.28 ng/L, P = .042), tumor necrosis factor-alpha (80.3 ± 20.4 pg/mL vs 40.2 ± 10.1 pg/mL, P < .001), and interleukin-6 (65.1 ± 15.7 pg/mL vs 25.4 ± 8.6 pg/mL, P < .001) compared to controls. Severe acute GVHD (Grade ≥III) significantly increased the risk of HF (odds ratio = 3.5, P < .001). Patients with multiple GVHD-related complications had a 3.6-fold higher likelihood of HF development (P < .01). Echocardiographic findings revealed significant cardiac remodeling in HF patients, with increased left ventricular end-diastolic diameter (68.76 ± 7.23 mm vs 44.18 ± 7.16 mm, P = .004) and left ventricular posterior wall thickness (12.18 ± 4.32 mm vs 4.46 ± 2.19 mm, P = .002). Additionally, HF patients experienced more severe transplant-related complications, including infections (29.0% vs 10.6%, P = .041) and hemorrhagic cystitis (23.4% vs 7.1%, P = .027). Mortality was significantly higher in the HF group (86.0% vs 41.6%, P < .001), with infection (71.0%) and HF (21.5%) being the leading causes of death. GVHD significantly heightens the risk of HF after allo-HSCT.
Conclusions: These findings underscore the necessity for proactive cardiovascular monitoring and targeted therapeutic interventions in GVHD patients to prevent the development of HF.