Project Heart: Biobehavioral effects on Cardiovascular Risk for Bereaved Spouses

 描述（由申请人提供）：失去配偶是一个高度紧张的事件，使人们在发病率和死亡率的风险增加。心血管疾病（CVD）占配偶丧亲期间死亡人数的20%至53%。压力、抑郁和焦虑会增加促炎细胞因子的产生。事实上，心理应激和抑郁促进转录因子核因子κ B（NF-κ B）活化，这是上调促炎细胞因子产生的主要途径。重要的是，炎症是心血管疾病从初始病变到终末期血栓性并发症的所有阶段的核心。炎症可能是导致心血管疾病的一个关键机制。依恋理论是一个有用的框架，可以用来理解人们在适应失去亲人的能力方面的个体差异。依恋不安全感有两种模式：依恋焦虑和依恋回避。高依恋焦虑的人使用“过度激活”的情绪应对策略。依恋回避程度高的人对依赖他人的支持感到不舒服，他们使用“去激活”的应对策略来抑制或抑制痛苦的经历。依恋方式的个体差异可能是谁最有可能在失去配偶后发生炎症并最终发生CVD的预后因素。心脏迷走神经张力（如呼吸性窦性心律失常或RSA所反映的）与自我调节有关。在紧张的条件下，低RSA的人表现出较差的自我调节控制与高RSA的人相比。低迷走神经张力也是CVD的一个危险因素，部分原因是炎症升高。这个新的/早期阶段的研究人员最近的工作表明，RSA和依恋风格可能共同影响调整的损失。该项目建立在这些初步研究结果的基础上，以研究依恋不安全感，抑郁症，RSA和炎症之间的横向和纵向联系，并在配偶去世后1个月，3个月，6个月和12个月收集这些关键维度的数据。参与者将是最近死于IV期非小细胞肺癌患者的配偶和匹配的对照组。如果炎症是丧亲之痛的一个重要机制，那么旨在减少炎症的心理和药物干预将是开发丧亲之痛治疗方法的重要一步。这些干预措施对具有某些心理特征的人尤其重要。

 DESCRIPTION (provided by applicant): The loss of a spouse is a highly stressful event that puts people at increased risk for morbidity and mortality. Cardiovascular disease (CVD) accounts for 20% to 53% of excess deaths during spousal bereavement. Stress, depression, and anxiety enhance the production of proinflammatory cytokines. Indeed, psychological stress and depression promote transcription factor nuclear factor kappa B (NF-kB) activation, a prime pathway for upregulating proinflammatory cytokine production. Importantly, inflammation is central to all stages of cardiovascular disease from initial lesion to end-stage thrombotic complications. Inflammation may be a key mechanism underlying CVD among the bereaved. Attachment theory is a useful framework for understanding individual differences in people's ability to adjust to the loss of a loved one. There are two patterns of attachment insecurity: attachment anxiety and attachment avoidance. People with high attachment anxiety use "hyperactivating" emotional coping strategies. People with high attachment avoidance are uncomfortable depending on others for support and use "deactivating" coping strategies that inhibit or suppress distressing experiences. Individual differences in attachment style may be prognostic for who is most at risk for enhanced inflammation and ultimately CVD after the loss of a spouse. Cardiac vagal tone (as reflected by respiratory sinus arrhythmia or RSA) is associated with self-regulation. Under stressful conditions individuals with low RSA display poorer self-regulatory control compared to those with high RSA. Low vagal tone is also a risk factor for CVD, partly due to elevations in inflammation. Recent work by this new/early stage investigator suggests that RSA and attachment style may jointly influence adjustment to a loss. This project builds upon these preliminary findings to examine mechanistic connections among attachment insecurity, depression, RSA, and inflammation cross-sectionally and longitudinally, with data on these key dimensions collected 1 month, 3 months, 6 months, and 12 months after the spouse's death. Participants will be spouses of patients who recently passed away to stage IV non-small cell lung cancer and matched controls. If inflammation is an important mechanism underlying bereavement, both psychosocial and pharmaceutical interventions aimed at reducing inflammation would be an important step toward the development of treatments for bereaved individuals. These interventions may be especially important for people with certain psychological characteristics.