Depression and Biobehavioral Processes in Heart Failure

心力衰竭的抑郁和生物行为过程

• 批准号: 7099994
• 负责人: Willem Johan Kop
• 金额: $ 37.06万
• 依托单位: HENRY M. JACKSON FDN FOR THE ADV MIL/MED
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-08-15 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7099994
• 关键词: behavioral /social science research tag; behavioral medicine; biomarker; catecholamines; clinical research; cortisol; depression; disease /disorder etiology; echocardiography; heart failure; heart function; human subject; inflammation; outcomes research; pathologic process; patient oriented research; prognosis; psychophysiology

DESCRIPTION (provided by applicant): Heart failure (HF) is a major health problem with a high annual mortality rate in the US. The incidence of HF continues to rise despite medical progress in heart failure interventions. Depression is an important psychosocial predictor of HF, with a 2 to 3-fold risk of increased mortality. To understand the role of depression in HF morbidity and mortality, there is a need to determine pathophysiological mechanisms linking depression to HF outcomes. Inflammatory processes play a primary pathophysiologic role in HF, and there is substantial overlap between inflammatory markers related to adverse HF outcomes and those known to be increased in depression. Using a prospective design, the proposed research will determine the role of pro-inflammatory markers (IL6, TNFa, CRP) as measures linking depression to heart failure progression. Two hundred heart failure patients will be monitored repeatedly for depression and inflammatory markers for 2 years. This study will: (1) determine the association between depression and inflammation and the role of neurohormones (catecholamines and cortisol) in this relationship; and (2) determine whether inflammatory processes play a role in the pathophysiological pathways linking depression to adverse heart failure outcome (mortality and HF-related hospitalization). Unique to this study is the use of repeated measures to document the temporal associations between depression and inflammatory markers. Such assessments are important to disentangle whether depression precedes, coincides with, or follows inflammation in heart failure patients. Information from this research will provide important knowledge for patient risk stratification, will elucidate pathophysiological mechanisms by which depression increases risk of adverse heart failure outcomes, and may lead to novel treatment targets in patients at high-risk of life- threatening heart failure complications. Lay language: Heart failure is a serious health problem, with a high mortality rate. Many patients with heart failure also suffer from depression, and these patients are at a substantially greater risk of being hospitalized or dying. This study examines the role of inflammation and immune pathways by which depression results in poor heart failure outcomes. This knowledge will help identify high risk patients and may lead to potential new treatments for depressed heart failure patients.

描述（由申请人提供）：心力衰竭（HF）是美国年度死亡率高的主要健康问题。尽管心力衰竭干预了医学进展，HF的发病率仍在继续上升。抑郁症是HF的重要社会心理预测指标，死亡率增加了2至3倍。为了了解抑郁症在HF发病率和死亡率中的作用，有必要确定将抑郁症与HF结局联系起来的病理生理机制。炎症过程在HF中起主要的病理生理作用，并且与不良HF结局有关的炎症标志物与已知在抑郁症中增加的炎症标志物之间存在很大的重叠。使用前瞻性设计，拟议的研究将确定促炎性标记（IL6，TNFA，CRP）的作用，将抑郁症与心力衰竭进展联系起来。将对抑郁症和炎症标志物反复监测两百例心力衰竭患者2年。这项研究将：（1）确定抑郁症与炎症之间的关联以及神经激素（儿茶酚胺和皮质醇）在这种关系中的作用； （2）确定炎症过程是否在将抑郁症与不良心力衰竭预后的病理生理途径（死亡率和与HF相关的住院）联系起来。这项研究独有的是使用重复措施来记录抑郁症和炎症标记之间的时间关联。这样的评估对于解开抑郁症之前的抑郁症是否与心力衰竭患者的炎症相吻合或跟随抑郁症很重要。这项研究的信息将为患者风险分层提供重要的知识，将阐明抑郁症增加心力衰竭结果的风险，并可能导致患者的新治疗靶标的病理生理机制，并可能导致患者高风险的心脏衰竭并发症。外行语言：心力衰竭是一个严重的健康问题，死亡率很高。许多心力衰竭的患者也患有抑郁症，这些患者患住院或死亡的风险要大得多。这项研究研究了抑郁症会导致心力衰竭结局不佳的炎症和免疫途径的作用。这些知识将有助于识别高风险患者，并可能导致心力衰竭患者的潜在新疗法。