Biological and Physiological Mechanisms of Symptom Clusters in Heart Failure (BIOMES-HF)

心力衰竭症状群的生物学和生理机制 (BIOMES-HF)

基本信息

批准号：
10208572
负责人：
Quin Eleanor Denfeld
金额：
$ 50.15万
依托单位：
OREGON HEALTH & SCIENCE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2021
资助国家：
美国
起止时间：
2021-04-23 至 2025-01-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10208572
关键词：
Acute Address Adult Affective Symptoms Age Anxiety Biological Biological Markers Body Weight decreased Cardiovascular system Chronic Clinical Coupled Dyspnea EFRAC Elderly Event Failure Fibrosis Functional disorder Gender Growth Heart failure Heterogeneity Hospitalization Hospitals Impairment Inflammation Insulin Resistance Intervention Knowledge Light Longitudinal Studies Malignant Neoplasms Measures Mediating Mediation Mental Depression Methods Modeling Myocardial Nature Outcome Pain Patient Outcomes Assessments Patients Phase Phenotype Physical activity Physiological Process Pump Quality of life Research Risk Role Skeletal Muscle Sleep Stress Symptoms Time United States associated symptom base biomarker panel cognitive function endothelial dysfunction exhaustion frailty hemodynamics hospital readmission improved individualized medicine infancy innovation physical symptom programs symptom cluster symptom management symptom science symptomatic improvement therapy development time use

项目摘要

PROJECT SUMMARY Symptom burden continues to be a significant problem for millions of adults living with heart failure (HF), the fastest growing cardiovascular condition in the U.S. Symptoms, which often co-occur or cluster together, are of utmost importance in HF because they predict quality of life and clinical events. There is considerable heterogeneity in symptoms in HF, however, that is particularly evident in the vulnerable transition period after a hospitalization for acute decompensated HF. While symptoms improve for some patients and they have longer periods of relative stability, others are plagued by enduring symptoms leading to poor outcomes, including rehospitalization. Given little-to-no association between hemodynamic markers (e.g. ejection fraction) and symptoms in HF, our clinical efforts to optimize hemodynamic stability during a hospitalization may not translate to improvement in symptoms post-hospitalization. Many studies have shown that HF is not just a hemodynamic, “pump failure” problem, but that it is a multifactorial, systemic condition involving processes such as inflammation, sympathetic dysregulation, and endothelial dysfunction. Based on research by our group and others, we propose that a multi-biomarker panel and the physical frailty phenotype that capture the multifaceted nature of HF might tell us more about symptoms in HF than our current objective markers. Therefore, the purpose of the proposed research is to 1) identify clusters of change in symptoms after a HF hospitalization and 2) quantify longitudinal associations between symptoms, biomarkers, and physical frailty. We will address the following aims through a gender- and age-balanced longitudinal study of 240 adults during the 6 month transition period after a hospitalization for acute decompensated HF: 1) identify clusters of change in physical symptoms among adults with heart failure, 2) quantify longitudinal associations between biomarkers and physical symptoms among adults with heart failure, and 3) quantify longitudinal associations between physical frailty and physical symptoms among adults with heart failure. We will use advanced quantitative modeling, including growth mixture modeling and longitudinal mediation modeling, to examine changes in symptoms, biomarkers, and physical frailty post-HF hospitalization and associations therein. This innovative study will advance HF symptom science by utilizing a multi-biomarker panel and the physical frailty phenotype that capture the multifaceted nature of HF, coupled with advanced quantitative modeling, to characterize heterogeneity and identify potential mechanisms of symptoms in HF. As a result, this research will inform the next phase of this program of research by pinpointing amenable targets for intervention to provide better, individualized treatment to improve symptom burden in HF.

项目概要对于数百万患有心力衰竭 (HF) 的成年人来说，症状负担仍然是一个重大问题。在美国，心血管疾病发展最快。这些症状经常同时出现或聚集在一起，包括在心力衰竭中至关重要，因为它们可以预测生活质量和临床事件。然而，心力衰竭症状的异质性在心力衰竭后的脆弱过渡期尤为明显。因急性失代偿性心力衰竭而住院，虽然一些患者的症状有所改善，但他们的住院时间更长。在相对稳定的时期，其他人则受到导致不良结果的持久症状的困扰，包括考虑到血流动力学指标（例如射血分数）与再住院之间几乎没有关联。心力衰竭的症状，我们在住院期间优化血流动力学稳定性的临床努力可能不会许多研究表明，心衰不仅仅是一种住院后症状的改善。血流动力学，“泵衰竭”问题，但它是一个涉及过程的多因素、系统性状况根据我们小组的研究，例如炎症、交感神经失调和内皮功能障碍。和其他人，我们建议使用多生物标志物组和捕捉身体虚弱表型心力衰竭的多方面性质可能比我们目前的客观标志物更能告诉我们心力衰竭的症状。因此，本研究的目的是 1) 识别心力衰竭后症状的集群变化住院治疗；2) 症状、生物标志物和身体虚弱之间的定量纵向关联。我们将通过对 240 名成年人进行性别和年龄平衡的纵向研究来实现以下目标：因急性失代偿性心力衰竭住院后 6 个月的过渡期：1) 识别变化集群在患有心力衰竭的成人的身体症状中，2) 量化生物标志物之间的纵向关联心力衰竭成人患者的身体症状和身体症状，以及 3) 之间的纵向定量关联我们将使用先进的定量方法来评估患有心力衰竭的成人的身体虚弱和身体症状。建模，包括增长混合模型和纵向中介模型，以检查心衰住院后的症状、生物标志物和身体虚弱及其关联。研究将利用多生物标志物组和身体虚弱表型推进心力衰竭症状科学捕捉 HF 的多方面性质，结合先进的定量模型，来表征因此，这项研究将为心力衰竭症状的潜在机制提供信息。该研究计划的下一阶段将确定可行的干预目标，以提供更好的、个体化治疗以改善心力衰竭的症状负担。