Mechanisms of Sympathetic Overactivity in Post-traumatic Stress Disorder
创伤后应激障碍中交感神经过度活跃的机制
基本信息
- 批准号:8921491
- 负责人:
- 金额:--
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2015
- 资助国家:美国
- 起止时间:2015-07-01 至 2019-06-30
- 项目状态:已结题
- 来源:
- 关键词:AddressAfghanistanAnxiety DisordersArithmeticBaroreflexBiofeedbackBiological MarkersBlood PressureBlood VesselsBreathingCardiovascular DiseasesCardiovascular systemChronicClinicalDataDevicesDiseaseElectrocardiogramExhibitsFunctional disorderFutureGeneral PopulationGoalsHeart RateHumanHyperactive behaviorHypertensionInflammationInflammatoryInterventionInvestigationIraqLiteratureLong-Term EffectsMajor Depressive DisorderMeasurableMeasuresMediatingMeditationMuscleNerveNerve EndingsPatientsPhysiologyPopulationPost-Traumatic Stress DisordersPressoreceptorsPsyche structureReactionRegulationRelaxationResearchRestRiskRoleStagingStimulusStressSympathetic Nervous SystemSystemTechniquesTestingTherapeuticTranslatingTraumaVeteransbaseblood pressure reductioncardiovascular disorder riskcardiovascular risk factorcombatdisorder controlheart disease riskheart rate variabilityhemodynamicshigh riskimprovedinsightnovelpilot trialpreventprogramspublic health relevancerelating to nervous systemresearch studyrespiratoryresponsevirtual realityyoung manyoung woman
项目摘要
DESCRIPTION (provided by applicant):
Post-traumatic stress disorder (PTSD) is a highly prevalent anxiety disorder that is associated with an increased risk of cardiovascular (CV) disease and hypertension. Given the large numbers of Veterans returning from Iraq and Afghanistan afflicted with PTSD, addressing this under-recognized but highly significant consequence of PTSD is of paramount importance. The mechanisms underlying increased CV risk in PTSD remains unknown. One potential mechanism is overactivation of the sympathetic nervous system (SNS), both at rest and during stress. Previous studies have shown that PTSD patients have higher resting heart rates and blood pressure (BP), greater cardiovascular reactivity during stress, and reduced heart rate variability, suggesting a state of heightened sympathetic activity. Although SNS hyperactivity is implicated in PTSD based on these observed indirect derangements, SNS regulation has never before been rigorously investigated in this population, and the underlying mechanisms and potential interventions targeting SNS activity and CV risk remain unexplored. The goals of this study are to determine if: 1) PTSD patients have higher resting SNS activity, and greater SNS reactivity during mental stress; 2) PTSD patients have abnormal arterial baroreflex sensitivity (BRS) that underlies SNS overactivity at baseline and during mental stress; 3) device-guided slow breathing (DGB) acutely improves SNS activity and BRS in PTSD patients; and 4) 8 weeks of daily DGB therapy improves SNS activity and hemodynamic profiles at rest and during mental stress. Furthermore, given that around half of PTSD patients have comorbid major depression (MD), and MD is independently associated with CV risk and SNS dysregulation, we hypothesize that comorbid MD augments SNS reactivity at rest and during mental stress in PTSD patients. To achieve these goals, we will measure sympathetic nerve activity directly using microneurography in young, prehypertensive veterans with PTSD (with and without MD) compared to non-PTSD controls (with and without MD) at rest and during mental stress, perform arterial baroreflex testing using the modified Oxford technique, and perform an 8-week pilot trial on the benefits of DGB on SNS reactivity and regulation. We hypothesize that PTSD patients have greater SNS activity at baseline and greater SNS reactivity during sympathoexcitation with mental stress, both related to combat recall and other forms of mental stress. We expect that these derangements are independent of MD, but that comorbid MD augments SNS reactivity in PTSD. We further propose that SNS overactivity is mediated by arterial baroreflex dysfunction at rest and during mental stress. Finally, previous studies have shown that device guided slow breathing (DGB), in which breathing is slowed to subphysiologic rates (of 5-6 breaths/minute) via an interactive biofeedback device, reduces BP, SNS activity, and improves BRS in patients with hypertension. DGB has never previously been tested in PTSD and may be a novel nonpharmacologic approach to reducing SNS activity and restoring BRS in these patients. We hypothesize that DGB acutely improves SNS overactivity, BP, and BRS, and chronically leads to sustained reductions in SNS and BRS at rest and during stress, in prehypertensive patients with PTSD. Improving SNS overactivity and BRS may have long term benefits on reducing CV risk in PTSD patients.
描述(由申请人提供):
创伤后应激障碍 (PTSD) 是一种非常普遍的焦虑症,与心血管 (CV) 疾病和高血压的风险增加有关,鉴于大量从伊拉克和阿富汗返回的退伍军人患有 PTSD,解决这一问题尚未得到充分认识。但 PTSD 的一个非常重要的后果是,PTSD 患者心血管风险增加的机制仍然未知,其中一个潜在机制是交感神经系统 (SNS) 的过度激活,无论是在休息时还是在压力期间。有更高的休息时间心率和血压 (BP)、应激期间心血管反应性增强以及心率变异性降低,表明呼吸交感神经活动处于一种状态。对该人群进行了调查,但针对 SNS 活动和 CV 风险的潜在机制和潜在干预措施尚未探索。本研究的目标是确定是否:1) PTSD 患者在静息时具有较高的 SNS 活动性,在精神状态下具有较高的 SNS 反应性。 2) PTSD 患者的动脉压力反射敏感性 (BRS) 异常,这是基线时和精神压力期间 SNS 过度活跃的原因;3) 设备引导的缓慢呼吸 (DGB) 可显着改善 PTSD 患者的 SNS 活动和 BRS;4) 8 周;每日 DGB 治疗可改善休息时和精神压力期间的 SNS 活动和血流动力学特征。此外,鉴于约一半的 PTSD 患者患有重度抑郁症 (MD),且 MD 是独立相关的。由于心血管风险和 SNS 失调,我们认为共病 MD 会增强 PTSD 患者在休息和精神压力期间的 SNS 反应性。为了实现这些目标,我们将使用显微神经造影直接测量患有 PTSD 的年轻高血压前期退伍军人的交感神经活动。 MD)与非 PTSD 对照(有和没有 MD)在休息和精神压力期间进行比较,使用改良的牛津技术进行动脉压力反射测试,并进行为期 8 周的试点试验,了解 DGB 对SNS 反应性和调节。我们发现 PTSD 患者在基线时具有较高的 SNS 活动性,并且在精神压力引起的交感神经兴奋期间具有较高的 SNS 反应性,这两者都与战斗回忆和其他形式的精神压力有关。我们预计这些紊乱与 MD 无关。共病 MD 会增强 PTSD 患者的 SNS 反应性,我们进一步提出,SNS 过度活动是由休息时和精神压力期间的动脉压力反射功能障碍介导的。 (DGB) 通过交互式生物反馈装置将呼吸减慢至亚生理频率(5-6 次呼吸/分钟),从而降低血压、SNS 活动,并改善高血压患者的 BRS。DGB 以前从未在 PTSD 和 PTSD 中进行过测试。可能是减少这些患者的 SNS 活性和恢复 BRS 的一种新颖的非药物方法,我们发现 DGB 可以显着改善 SNS 过度活动、血压和 BRS,并长期导致持续降低。在患有 PTSD 的高血压前期患者中,改善 SNS 过度活动和 BRS 可能对降低 PTSD 患者的心血管风险具有长期益处。
项目成果
期刊论文数量(0)
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Jeanie Park其他文献
Jeanie Park的其他文献
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Mechanisms of Sympathetic Overactivity in Post-traumatic Stress Disorder
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