Short and long term depressive symptoms and arrhythmic pathways to stroke

短期和长期抑郁症状以及心律失常导致中风的途径

• 批准号: 8257465
• 负责人: Paola Gilsanz
• 金额: $ 3.7万
• 依托单位: HARVARD SCHOOL OF PUBLIC HEALTH
• 依托单位国家: 美国
• 财政年份: 2012
• 资助国家: 美国
• 起止时间: 2012-01-01 至 2013-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8257465
• 关键词: Address; Affect; Antidepressive Agents; Arrhythmia; Atherosclerosis; Atrial Fibrillation; Attention; Attenuated; Behavioral Mechanisms; Cardiac; Cardiovascular Diseases; Cardiovascular Physiology; Cardiovascular system; Characteristics; Chronic; Clinical Management; Cohort Studies; Data; Data Sources; Dose; Elderly; Etiology; Fostering; Functional disorder; Future; Health; Health Personnel; Health behavior; Incidence; Individual; Inflammation; Inflammatory Response; Interruption; Intervention; Interview; Investigation; Ischemic Stroke; Learning; Link; Longitudinal Studies; Mediating; Mediator of activation protein; Mental Depression; Moods; Pathway interactions; Patients; Pharmaceutical Preparations; Physical activity; Physiological; Physiological Processes; Public Health; Recording of previous events; Regulation; Research; Research Proposals; Research Training; Resolution; Respondent; Retirement; Risk; Risk Factors; Role; Severities; Smoking; Stroke; Symptoms; Time; Training; United States; cardiovascular disorder epidemiology; cardiovascular risk factor; career; depressive symptoms; design; doctoral student; effective intervention; heart rhythm; innovation; interest; middle age; response; skills; symptom management; treatment planning

DESCRIPTION (provided by applicant): Emerging evidence suggests that elevated depressive symptoms predict stroke onset. However, it remains unclear whether this relationship is causal and, if so, whether the effects are modified by the duration or intensity of depressive symptoms. Furthermore, despite substantial research, we have not been able to establish the mechanisms linking depression and stroke. Addressing these research questions is critical to inform clinical management of depressive symptoms. It also is useful in elucidating the physiological or behavioral mechanisms mediating the link between depression and stroke to identify other opportunities for intervention. Previous research suggests several possible pathways via which depression or depressive symptoms could influence stroke, including health behaviors (e.g. smoking, physical activity) or dysregulation of physiologic processes (e.g. autonomic regulation of cardiac function, inflammatory responses). Many of these mechanisms would operate over a long term time-scale, with pathophysiology (e.g. atherosclerosis) accumulating over years. If only long-term mechanisms link depression and stroke, treatment of depressive symptoms would not be expected to reduce stroke risk immediately; benefits would instead develop over years of successful symptom management. However, if causal mechanisms exert their effects in the short term, interruption of some hypothesized mechanisms might allow nearly immediate benefits by reducing stroke risk after resolution of depressive symptoms. Furthermore, it remains unclear if antidepressant medication affects the risk of stroke. The research on health behaviors and inflammation response has not conclusively established whether these factors fully mediate the relationship between depression and stroke. While no prior research has assessed whether atrial fibrillation (AF) mediates the relationship between depression and stroke, a growing number of studies are examining the impact of mood on AF. As the most common cardiac arrhythmia and a well-known risk factor of stroke, we will examine AF's role as a possible mediator. We propose using data from two complementary longitudinal studies, the Health and Retirement Study (HRS) and the Cardiovascular Health Study (CHS), to examine two aims. The first aim of this proposal is to determine what characteristics (e.g. duration and severity) of depressive symptoms best predict first incidence of all stroke types among middle aged and elderly individuals in the United States. Our second aim is to examine atrial fibrillation as a partial mediator of the association between depressive symptoms and onset of ischemic stroke. The identification of characteristics of depressive symptoms that predict stroke and the underlying etiology can help health practitioners and identify patients at greater risk for stroke. Indentifying whether atrial fibrillation is a mediating factor in the relationship between depression and stroke is clinically important as it may inform treatment plans of at risk patients.

描述（由申请人提供）：新出现的证据表明，抑郁症状加重预示着中风的发生。然而，目前尚不清楚这种关系是否是因果关系，如果是的话，其影响是否会因抑郁症状的持续时间或强度而改变。此外，尽管进行了大量研究，我们仍无法建立抑郁症和中风之间的联系机制。解决这些研究问题对于抑郁症状的临床管理至关重要。它还有助于阐明介导抑郁症和中风之间联系的生理或行为机制，以确定其他干预机会。 先前的研究表明，抑郁或抑郁症状可能通过几种可能的途径影响中风，包括健康行为（例如吸烟、体力活动）或生理过程失调（例如心脏功能的自主调节、炎症反应）。其中许多机制将在长期的时间范围内发挥作用，病理生理学（例如动脉粥样硬化）会多年累积。如果只有长期机制将抑郁症和中风联系起来，那么治疗抑郁症状就不会立即降低中风风险；相反，多年成功的症状管理会带来好处。然而，如果因果机制在短期内发挥作用，那么中断一些假设的机制可能会在抑郁症状缓解后降低中风风险，从而带来近乎立竿见影的好处。此外，尚不清楚抗抑郁药物是否会影响中风风险。关于健康行为和炎症反应的研究尚未最终确定这些因素是否完全介导抑郁和中风之间的关系。虽然之前没有研究评估心房颤动 (AF) 是否介导抑郁和中风之间的关系，但越来越多的研究正在研究情绪对房颤的影响。作为最常见的心律失常和众所周知的中风危险因素，我们将研究房颤作为可能介质的作用。 我们建议使用健康与退休研究（HRS）和心血管健康研究（CHS）这两项补充纵向研究的数据来检验两个目标。该提案的首要目的是确定抑郁症状的哪些特征（例如持续时间和严重程度）最能预测美国中老年人中所有中风类型的首次发病率。我们的第二个目标是检查心房颤动作为抑郁症状与缺血性中风发作之间关联的部分中介因素。识别预测中风的抑郁症状特征及其潜在病因可以帮助健康从业者并识别中风风险较高的患者。确定心房颤动是否是抑郁症和中风之间关系的中介因素具有重要的临床意义，因为它可以为高危患者的治疗计划提供信息。