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; 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）：新兴证据表明，抑郁症状升高预测中风发作。但是，目前尚不清楚这种关系是否是因果关系，如果是的，是否通过抑郁症状的持续时间或强度来改变影响。此外，尽管进行了大量研究，但我们仍无法建立与抑郁和中风联系起来的机制。解决这些研究问题至关重要，对于抑郁症状的临床管理至关重要。它也可用于阐明介导抑郁和中风之间的联系的生理或行为机制，以识别其他干预机会。 先前的研究表明，抑郁症或抑郁症状可能会影响中风的几种可能途径，包括健康行为（例如吸烟，体育活动）或生理过程失调（例如心脏功能的自主性调节，炎症反应）。这些机制中的许多机制将在长期尺度上运作，而病理生理学（例如动脉粥样硬化）多年来积累。如果只有长期机制将抑郁症和中风链接起来，则不会预期对抑郁症状的治疗立即降低中风风险；相反，福利将发展多年来成功的症状管理。但是，如果因果机制在短期内发挥作用，那么某些假设机制的中断可能会通过减少抑郁症状后减少中风风险几乎可以立即获得益处。此外，尚不清楚抗抑郁药是否影响中风的风险。关于健康行为和炎症反应的研究尚未确定这些因素是否完全介导了抑郁症与中风之间的关系。尽管没有先前的研究评估房颤（AF）是否介导抑郁症与中风之间的关系，但越来越多的研究正在研究情绪对AF的影响。作为最常见的心律失常和中风的众所周知的风险因素，我们将研究AF作为可能的介体的作用。 我们建议使用来自两项互补纵向研究的数据，即健康与退休研究（HRS）和心血管健康研究（CHS），以研究两个目标。该提案的第一个目的是确定抑郁症状的哪些特征（例如持续时间和严重性）最好预测美国中年和老年人中所有中风类型的首次发病率。我们的第二个目的是检查房颤，作为抑郁症状与缺血性中风发作之间关联的部分介体。鉴定预测中风和潜在病因的抑郁症状特征可以帮助卫生从业者并确定中风风险更大的患者。坦率的抑制房颤是否是抑郁和中风之间关系的中介因素，在临床上很重要，因为它可以为AT风险患者的治疗计划提供依据。