CARDIAC RISK MARKERS AND UNREMITTING DEPRESSION IN ACUTE CORONARY SYNDROME

急性冠脉综合征中的心脏风险标志物和持续抑郁

• 批准号: 8054977
• 负责人: ROBERT M CARNEY
• 金额: $ 74.47万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-03-01 至 2013-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8054977
• 关键词: Aftercare; Area; Cardiac; Cardiovascular system; Cessation of life; Clinical Trials; Cognitive Therapy; DSM-IV; Depressed mood; Enrollment; Equation; Frequencies; Hamilton Rating Scale for Depression; Health; Hospitalization; Hospitals; Individual; Lead; Link; Literature; Measures; Mediator of activation protein; Medical; Mental Depression; Modeling; Myocardial Infarction; Participant; Patients; Process; Questionnaires; Recruitment Activity; Research; Research Personnel; Resistance; Risk; Risk Factors; Risk Marker; Sampling; Sertraline; Severities; Survival Rate; Testing; Universities; Washington; acute coronary syndrome; cardiovascular risk factor; dosage; effective intervention; high risk; improved; medical schools; meetings; mortality; patient population; response; single episode major depressive disorder; standard care

DESCRIPTION (provided by investigator): Depression is a risk factor for mortality after hospitalization for acute coronary syndrome (ACS). However, converging evidence from several recent clinical trials suggests that the mortality risk is higher among patients with treatment-resistant depression than those who respond to standard treatments for depression. Interestingly, some of the strongest predictors of treatment resistance in depressed psychiatric patients also happen to be cardiac risk markers, including indicators of cardiovascular autonomic dysregulation, HPA axis dysregulation, and proinflammatory and procoagulant processes. Furthermore, these markers have also been identified as potential mediators of the effect of depression on post-ACS mortality. The purpose of this study is to test the hypotheses that 1) depressed post-ACS patients who fail to respond to aggressive treatment for depression have higher levels of specific cardiac risk markers at the end of treatment than do otherwise comparable patients who do respond; 2) high levels of these cardiac risk markers prior to treatment predict poor response to depression treatment; and 3) these risk markers improve as depression improves in treatment responders. Participants will be recruited from three St. Louis area hospitals affiliated with Washington University School of Medicine. One hundred seventy patients, who meet the DSM-IV criteria for a current major depressive episode and who score 17 or higher on the HAM-D-17 approximately 3 months after hospitalization for ACS, will be enrolled in the study. All participants will be treated with individual cognitive behavior therapy (CBT) for up to 6 months. The frequency of CBT sessions will decrease when specific improvement criteria are met. Patients who have not improved >50 percent on the BDI-II depression questionnaire by 3 months will continue in CBT but will also be given sertraline at an initial dosage of 50 mg/day. If necessary and if tolerated, the dosage will be gradually increased to a maximum of 200 mg/day. Depression will be assessed, and cardiac risk markers will be measured, at baseline, 3 months, and 6 months. Structural equation models will be used to test the primary hypotheses. Relevance: Depression doubles the risk of death after a heart attack, for reasons that are not well understood. Initial efforts to reduce this risk by treating depression have not been successful. This study will help to clarify how depression increases the risk of dying, and it may suggest ways to develop more effective interventions. PUBLIC HEALTH RELEVANCE: Depression doubles the risk of death after a heart attack, for reasons that are not well understood. Initial efforts to reduce this risk by treating depression have not been successful. This study will help to clarify how depression increases the risk of dying, and it may suggest ways to develop more effective interventions.

描述（由研究者提供）：抑郁是急性冠脉综合征 (ACS) 住院后死亡的危险因素。然而，最近几项临床试验的综合证据表明，难治性抑郁症患者的死亡风险高于对标准抑郁症治疗有反应的患者。有趣的是，抑郁症精神病患者治疗抵抗的一些最强预测因素也恰好是心脏风险标志物，包括心血管自主神经失调、HPA 轴失调以及促炎和促凝血过程的指标。此外，这些标志物也被确定为抑郁症对 ACS 后死亡率影响的潜在中介因素。本研究的目的是检验以下假设：1) 对抑郁症积极治疗无反应的 ACS 后抑郁患者在治疗结束时比有反应的其他类似患者具有更高水平的特定心脏风险标记物； 2) 治疗前这些心脏病风险标志物水平高预示着抑郁症治疗反应不佳； 3）随着治疗反应者抑郁症的改善，这些风险标记也随之改善。参与者将从华盛顿大学医学院附属的三家圣路易斯地区医院招募。 170 名符合当前重度抑郁发作 DSM-IV 标准且因 ACS 住院约 3 个月后 HAM-D-17 得分为 17 或更高的患者将参加该研究。所有参与者都将接受长达 6 个月的个体认知行为疗法 (CBT)。当满足特定的改进标准时，CBT 课程的频率将会减少。 3 个月内 BDI-II 抑郁症问卷改善未超过 50% 的患者将继续接受 CBT，但也将给予舍曲林，初始剂量为 50 毫克/天。如有必要且可耐受，剂量将逐渐增加至最大 200 mg/天。将在基线、3 个月和 6 个月时评估抑郁症并测量心脏风险标志物。结构方程模型将用于检验主要假设。相关性：抑郁症会使心脏病发作后的死亡风险增加一倍，其原因尚不清楚。通过治疗抑郁症来降低这种风险的初步努力并未成功。这项研究将有助于阐明抑郁症如何增加死亡风险，并可能提出制定更有效干预措施的方法。公共卫生相关性：抑郁症会使心脏病发作后的死亡风险增加一倍，其原因尚不清楚。通过治疗抑郁症来降低这种风险的初步努力并未成功。这项研究将有助于阐明抑郁症如何增加死亡风险，并可能提出制定更有效干预措施的方法。