Test of a new theory to explain excess risk in cardiac PTSD

测试解释心脏创伤后应激障碍（PTSD）过度风险的新理论

• 批准号: 8938870
• 负责人: William Whang
• 金额: $ 70.73万
• 依托单位: COLUMBIA UNIVERSITY HEALTH SCIENCES
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-07-15 至 2019-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8938870
• 关键词: Accident and Emergency department; Acute; Adherence; Adrenergic beta-Antagonists; American; Awareness; Behavior; Behavioral; Cardiac; Cardiovascular Diseases; Cardiovascular system; Caring; Characteristics; Clinic; Cohort Studies; Complex; Distress; Dose; Elderly; Electrocardiogram; Electronics; Enrollment; Event; Frequencies; Goals; Heart Rate; Hospitalization; Hospitals; Hour; Intervention; Investigation; Laboratories; Lead; Life; Modeling; Monitor; Morbidity - disease rate; Movement; Myocardial Infarction; Outcome; Parasympathetic Nervous System; Participant; Patients; Persons; Pharmaceutical Preparations; Population; Post-Traumatic Stress Disorders; Posture; Process; Public Health; Reaction; Recurrence; Relative (related person); Reporting; Research; Risk; Risk Marker; Secondary Prevention; Secondary to; Survivors; Sympathetic Nervous System; Symptoms; Testing; Thinking; Time; Unstable angina; Veterans; Withdrawal; acute coronary syndrome; adverse outcome; avoidance behavior; base; cardiovascular risk factor; cohort; experience; heart rate variability; heart rhythm; high risk; indexing; insight; mortality; novel; outcome forecast; public health relevance; response; theories

 DESCRIPTION (provided by applicant): The goal of the proposed research is to identify targets for new interventions to reduce the doubled cardiac event recurrence and mortality risk faced by the 1 in 8 survivors of non-ST elevation myocardial infarction (NSTEMI) and unstable angina (UA) who develop PTSD secondary to their life-threatening cardiac event. Research on the mechanisms likely to carry that risk is converging on autonomic dysregulation as the culprit. PTSD is associated with high heart rate (HR) and low heart rate variability (HRV), both established secondary risk markers in NSTEMI/UA patients. In our recently offered Enduring Somatic Threat (EST) model, we propose a vicious cycle in which PTSD intrusion symptoms cause acute autonomic imbalance, leading to heart rhythm alterations that are perceived as threatening by the patient, causing further autonomic imbalance. Further, the model proposes that this vicious cycle is exacerbated by non-adherence to beta-blockers (medications that blunt sympathetic influences on HR), a common avoidance behavior in patients with PTSD. Surprisingly, although autonomic imbalance is the leading candidate for PTSD's influence on cardiovascular morbidity and mortality in populations from young veterans to older adults with cardiovascular disease, its candidacy is based almost solely on research conducted in the clinic or the laboratory. No study has ever tested the association of PTSD symptoms and cardiovascular parameters in the real world. We propose to test the EST model in our Reactions to Acute Care and Hospitalization observational cohort study of 1,741 NSTEMI/UA patients. We will enroll 100 participants with NSTEMI/UA-induced PTSD, and 100 without, at 1-month after hospital discharge. For 1 week, participants will (1) report on PTSD intrusion symptoms in the 30 minutes prior to each of 10 daily electronic momentary assessments (EMA); (2) wear an ambulatory smart shirt embedded with ECG and an accelerometer, from which we will derive heart rate and heart rate variability (HRV); and (3) have their adherence to beta blockers electronically monitored. We will test whether NSTEMI/UA patients with PTSD have higher 24-hr HR and lower 24-hr HRV than those without PTSD and, if so, whether the frequency and intensity of intrusive thought(s) explains the difference. Further, we will test whether HR is higher, and HRV lower, for epochs in which patients report intrusions relative to those in which they do not and whether the difference is more pronounced in patients with PTSD. Finally, we will test whether patients with PTSD are less adherent to beta-blockers, and explore whether associations of intrusions with HR/HRV are more pronounced on days that patients miss their dose. More than 150,000 Americans develop PTSD secondary to NSTEMI/UA each year, and they are at high risk for adverse outcomes. This research will determine whether autonomic dysregulation in the real world is truly a candidate mechanism, describe the dynamics by which PTSD causes it, identify the factors most important to target and the point in the vicious cycle to intervene, and suggest new interventions to offset risk.

 描述（由申请人提供）：拟议研究的目标是确定新干预措施的目标，以减少非ST段抬高心肌梗死（NSTEMI）和不稳定型心绞痛（UA）幸存者中1/8的患者所面临的心脏事件复发和死亡风险增加一倍，这些患者继发于危及生命的心脏事件而发生PTSD。对可能带来这种风险的机制的研究正集中在自主神经失调作为罪魁祸首。创伤后应激障碍与高心率（HR）和低心率变异性（HRV）相关，这两者都是NSTEMI/UA患者的次要风险标志物。在我们最近提供的持久躯体威胁（EST）模型中，我们提出了一个恶性循环，其中PTSD侵入症状导致急性自主神经失衡，导致患者认为具有威胁性的心律改变，导致进一步的自主神经失衡。此外，该模型提出，这种恶性循环因不坚持使用β受体阻滞剂（减弱交感神经对HR影响的药物）而加剧，这是PTSD患者常见的回避行为。令人惊讶的是，尽管自主神经失调是PTSD对从年轻退伍军人到患有心血管疾病的老年人的心血管发病率和死亡率的影响的主要候选者，但其候选资格几乎完全基于在临床或实验室进行的研究。还没有研究测试过创伤后应激障碍症状和心血管参数在真实的世界中的关联。我们建议在我们对1，741名NSTEMI/UA患者的急性护理和住院反应观察性队列研究中测试EST模型。我们将在出院后1个月招募100名患有NSTEMI/UA诱导的PTSD的参与者，100名没有。在1周内，参与者将（1）在每天10次电子瞬时评估（EMA）之前的30分钟内报告PTSD侵入症状;（2）穿着嵌入ECG和加速度计的动态智能衬衫，我们将从中获得心率和心率变异性（HRV）;（3）电子监测他们对β受体阻滞剂的依从性。我们将测试患有PTSD的NSTEMI/UA患者是否比没有PTSD的患者有更高的24小时HR和更低的24小时HRV，如果是这样，侵入性思维的频率和强度是否可以解释这种差异。此外，我们将测试HR是否更高，HRV是否更低，对于患者报告入侵相对于他们没有报告入侵的时期，以及PTSD患者的差异是否更明显。最后，我们将测试PTSD患者是否对β受体阻滞剂的依从性较低，并探索在患者错过剂量的日子里，侵入与HR/HRV的关联是否更明显。每年有超过150，000名美国人继发于NSTEMI/UA的PTSD，他们面临着不良后果的高风险。这项研究将确定自主神经失调在真实的世界中是否是一个真正的候选机制，描述PTSD导致它的动力学，确定最重要的目标因素和恶性循环的点， 干预，并提出新的干预措施，以抵消风险。