Wleklik Marta, Lee Christopher S, Lewandowski Łukasz, Czapla Michał, Jędrzejczyk Maria, Aldossary Heba, Uchmanowicz Izabella
Division of Research Methodology, Department of Nursing, Faculty of Nursing and Midwifery, Wroclaw Medical University, Wrocław, Poland.
Boston College William F. Connell School of Nursing, Chestnut Hill, Massachusetts, USA.
ESC Heart Fail. 2025 Jun;12(3):2010-2022. doi: 10.1002/ehf2.15208. Epub 2025 Jan 23.
This study aimed to identify factors associated with frailty in heart failure (HF) patients, focusing on demographic, biochemical and health-related variables. It also explored the correlation between frailty and comorbidities such as malnutrition, cognitive impairment and depression, assessing how these factors interact to influence frailty risk.
A total of 250 HF patients (mean age 73.5 ± 7.2 years; 45.6% female) hospitalized for acute decompensated HF were included. Frailty was assessed using Fried phenotype criteria. Cognitive function, depression and nutritional status were evaluated using validated instruments [Mini-Mental State Examination (MMSE), Patient Health Questionnaire-9 (PHQ-9) and Mini Nutritional Assessment (MNA)]. Biochemical markers included C-reactive protein (CRP), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), haemoglobin, estimated glomerular filtration rate (eGFR) and systolic blood pressure (SBP). Statistical analyses, including logistic regression, were performed to assess associations and odds ratios (ORs) for frailty, adjusted for inflammation and HF type.
Frailty was present in 60.4% of patients. Frail individuals exhibited significantly higher CRP (median 4.60 vs. 2.54 mg/L, P < 0.001) and NT-proBNP (median 2558.8 vs. 1102.6 pg/mL, P = 0.001) and lower haemoglobin (13.7 vs. 14.3 g/dL, P = 0.012), eGFR (62 vs. 71 mL/min/1.73 m, P = 0.025) and SBP (130 vs. 134 mmHg, P = 0.026). Each 10% increase in CRP was associated with a 5.5% increase in frailty odds (P < 0.001). Frailty was linked to cognitive impairment (OR 2.1, P = 0.018), malnutrition (OR 3.0, P < 0.001) and depression (OR 3.1, P < 0.001), while high adherence to treatment reduced frailty risk by 78.9% (P = 0.027). Interactions were observed between cognitive impairment and body mass index (BMI) (P = 0.020), where higher BMI mitigated the frailty odds difference between cognitively impaired and unimpaired patients. Depression's association with frailty odds varied by adherence levels (P = 0.034) and central obesity (P = 0.047), with the absence of depression offering protection against frailty in patients with central obesity. These interactions remained significant after adjustment for HF type and left ventricular ejection fraction (LVEF) and were consistent across stratifications by these factors.
Frailty in HF is influenced by inflammatory markers, cognitive impairment and psychosocial factors. Elevated CRP and NT-proBNP were strong predictors of frailty. Cognitive impairment and depression were key modifiable factors, interacting with BMI, adherence and obesity. Targeting these factors with early interventions could mitigate frailty risk, improving outcomes and quality of life in HF patients.
本研究旨在确定与心力衰竭（HF）患者虚弱相关的因素，重点关注人口统计学、生化和健康相关变量。它还探讨了虚弱与营养不良、认知障碍和抑郁等合并症之间的相关性，评估这些因素如何相互作用以影响虚弱风险。
共纳入250例因急性失代偿性HF住院的患者（平均年龄73.5±7.2岁；45.6%为女性）。使用Fried表型标准评估虚弱。使用经过验证的工具[简易精神状态检查表（MMSE）、患者健康问卷9项（PHQ-9）和微型营养评定量表（MNA）]评估认知功能、抑郁和营养状况。生化标志物包括C反应蛋白（CRP）、脑钠肽前体N末端（NT-proBNP）、血红蛋白、估计肾小球滤过率（eGFR）和收缩压（SBP）。进行了包括逻辑回归在内的统计分析，以评估虚弱的相关性和比值比（OR），并根据炎症和HF类型进行调整。
60.4%的患者存在虚弱。虚弱个体的CRP（中位数4.60对2.54mg/L，P<0.001）和NT-proBNP（中位数2558.8对1102.6pg/mL，P=0.001）显著更高，而血红蛋白（13.7对14.3g/dL，P=0.012）、eGFR（62对71mL/min/1.73m²，P=0.025）和SBP（130对134mmHg，P=0.026）更低。CRP每增加10%，虚弱几率增加5.5%（P<0.001）。虚弱与认知障碍（OR 2.1，P=0.018）、营养不良（OR 3.0，P<0.001）和抑郁（OR 3.1，P<0.001）相关，而高治疗依从性使虚弱风险降低78.9%（P=0.027）。观察到认知障碍与体重指数（BMI）之间存在相互作用（P=0.020），较高的BMI减轻了认知障碍患者与未受损患者之间的虚弱几率差异。抑郁与虚弱几率的关联因依从性水平（P=0.034）和中心性肥胖（P=0.047）而异，在中心性肥胖患者中，无抑郁可预防虚弱。在调整HF类型和左心室射血分数（LVEF）后，这些相互作用仍然显著，并且在按这些因素分层时是一致的。
HF患者的虚弱受炎症标志物、认知障碍和社会心理因素影响。CRP和NT-proBNP升高是虚弱的强预测因素。认知障碍和抑郁是关键的可改变因素，与BMI、依从性和肥胖相互作用。通过早期干预针对这些因素可以降低虚弱风险，并改善HF患者的结局和生活质量。
