Posttraumatic stress, heart rate variability, and the mediating role of behavioral health risks.

摘要: Acute stress has long been connected to cardiovascular risk (1). For individuals with posttraumatic disorder (PTSD), a characterized by hyperarousal and frequent physiological symptoms related anxiety stress, dysregulation of the autonomic nervous system identified as an important precursor disease, diabetes, other health risks (2, 3). Indeed, key indicator functioning health, heart-rate variability (HRV), is often depressed amongst PTSD (4). Although link between HRV generally discussed purely psychosomatic phenomenon (5), number behavioral factors—namely smoking, alcohol misuse, obesity, sleep disturbance—may account for this link. In study, was assessed younger adults (18- 39-years-old) without determine whether dysfunction in part attributable higher rates drinking, disturbance that coincide (6-9). Heart-Rate Variability Under normal circumstances, heart rate varies on beat-to-beat basis due dynamic interplay sympathetic (SNS) parasympathetic (PNS). The SNS stimulates excitation (e.g., increased blood pressure) response unexpected changes body and/or environment through release catecholamines (10). PNS restores activity baseline levels via vagal innervation. When these two systems are disequilibrium—either because hyperactive or hypoactive—HRV attenuates (3). Low both disease. It may signal some underlying irregularity, such immune resulting from osteoporosis, arthritis, Alzheimer's cancers (11). Reduced also stimulate deleterious effects health. Lower factor arrhythmia turn predictive disease cardiac arrest (12-14). accelerate atherosclerosis (2) result pressure, which itself independent coronary artery (15). Psychophysiology PTSD Exposure psychological trauma increases developing PTSD, persistent re-experiencing traumatic event, avoidance stimuli associated arousal (16). These have known convey dysregulation, elevated pressure at (17) stressors (18). Even though instrumental etiology disorders, experimental evidence suggests be responsible maintenance physiology psychopathology (15). instance, administration catecholamine antagonists prior induced panic attacks does little reduce rate, suggesting plays minor role (19). However, lactate, suppressor (PNS) activity, accumulates during (20), even administered laboratory studies induce (21) (22). Thus, suppressed consequently reduced implied trauma-related disorders PTSD. exhibit short-term laboratory-based measurements (5, 23-26) 24-hour ambulatory measures (4, 27). turn, more likely than those develop (28) face death (29). Although primarily attributed direct impact factors could partially association. Individuals smoke do so heavily (6), abuse (7), obese (8), suffer stemming flashbacks nightmares (9). Each independently (30-33), relationship frequently accompany PTSD. Current Study In present prediction mediated lifetime dependency, abdominal tested sample (i.e., under 40 years age) Younger were targeted quantify early posed psychopathology. Latent variable modeling used model combination long- minimize measurement error construct. Three sets hypotheses tested: 1) would lower HRV; 2) greater dependence, disturbance; 3) each mediate association HRV. That is, accounting attenuate