Project Heart: Biobehavioral effects on Cardiovascular Risk for Bereaved Spouses

 描述(由申请人提供)：失去配偶是一种高度紧张的事件，使人们面临更高的发病率和死亡率风险。在配偶丧亲期间额外死亡的20%到53%是心血管疾病(CVD)。压力、抑郁和焦虑会增加促炎细胞因子的产生。事实上，心理压力和抑郁促进了转录因子核因子kappaB(NF-kB)的激活，这是上调促炎细胞因子产生的主要途径。重要的是，炎症是心血管疾病所有阶段的中心，从最初的病变到终末期血栓并发症。炎症可能是导致丧亲者心血管疾病的关键机制。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类型：依恋焦虑和依恋回避。高度依恋焦虑的人会使用“过度激活”的情绪应对策略。高度依恋回避的人会感到不舒服，会依赖他人的支持，并使用抑制或抑制痛苦经历的“去激活”应对策略。依恋方式的个体差异可能预示着谁最有可能在失去配偶后患上炎症加剧，并最终患上心血管疾病。心脏迷走神经张力(反映为呼吸性窦性心律失常或RSA)与自我调节有关。在压力条件下，与高RSA个体相比，低RSA个体表现出更差的自我调节控制。迷走神经张力低也是心血管疾病的危险因素，部分原因是炎症升高。这位新的/早期研究人员最近的研究表明，RSA和依恋风格可能共同影响对损失的适应。这个项目建立在这些初步发现的基础上，从横向和纵向上考察依恋不安全感、抑郁、RSA和炎症之间的机制联系，收集配偶死亡后1个月、3个月、6个月和12个月这些关键维度的数据。参与者将是最近去世的第四期非小细胞肺癌患者的配偶和匹配的对照组。如果炎症是导致丧亲的一个重要机制，那么旨在减少炎症的心理社会和药物干预将是开发针对丧失亲人的治疗方法的重要一步。这些干预措施可能对具有某些心理特征的人特别重要。

 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.