Growing evidence links posttraumatic stress disorder (PTSD) to cardiovascular morbidity and mortality, but the mechanisms are incompletely understood. Abnormal sleep is a modifiable behavior that is a known contributor to cardiovascular risk and a hallmark symptom of PTSD. Our preliminary data and data from other labs show that PTSD is associated with profound sleep disturbance and with abnormal autonomic function (dysautonomia) especially at night. We propose a rigorous twin study to test the new paradigm that abnormal sleep is linked in a bidirectional way with nighttime dysautonomia to increase cardiovascular risk in PTSD. We will add comprehensive autonomic and sleep assessments to an ongoing NHLBI-funded twin study of PTSD and ischemic heart disease (IHD), the Emory Twin Study Follow-up (ETSF). The ETSF will re-examine 180 monozygotic and dizygotic twin pairs (360 individuals) from the Vietnam Era Twin Registry to reassess PTSD status and cardiac status using positron emission tomography (PET) myocardial perfusion imaging. In a previous examination of this sample, we found that twins with PTSD had worse myocardial perfusion and coronary microvascular function compared with twins without PTSD. As part of the proposed ancillary study, we will add both at home and in-lab objective sleep and autonomic monitoring, which will allow for both ?real- world? and controlled psychophysiological assessments. Twins will undergo in-lab polysomnography when on site and will be equipped patches for electrocardiogram monitoring and actigraphy wristbands for sleep monitoring to use at home for 14 days. During their visit, they will be examined in a controlled environment which matches their brothers' and allows for the most controlled analyses of within-pair difference. We will address the following hypotheses: (1) Twins with PTSD will exhibit more disturbed sleep (shorter sleep duration, more sleep fragmentation, and more sleep-disordered breathing) compared with twins without PTSD. (2) Twins with PTSD will exhibit more nocturnal dysautonomia (lower nighttime HRV) compared with twins without PTSD. (3) Disturbed sleep and nighttime dysautonomia will be positively related to quantitative indicators of IHD using PET imaging, including perfusion deficits and lower coronary flow reserve. We will also explore dynamic associations among PTSD, sleep disturbance and dysautonomia in the lab and at home. Our proposed twin study should fill a significant gap in evidence regarding the mechanisms of cardiovascular risk in PTSD. If our hypotheses are met, this study will place abnormal sleep and nighttime altered autonomic function at the forefront as interrelated biobehavioral pathways linking PTSD to IHD. The long-term goal is to provide targets for novel interventions that collectively help reduce IHD risk, sleep disturbance, and PTSD symptom burden.
Ischemic heart disease (IHD) continues to be the leading cause of disability, hospitalizations, health care expenditures, and death in the United States. Identification of pathways of risk through which PTSD affects IHD risk is important in order to understand of IHD pathophysiology and develop effective interventions. Our rigorous twin study will elucidate whether abnormal sleep and nighttime autonomic nervous system imbalance represent interrelated biobehavioral pathways linking PTSD to IHD.
