Objective: The impedance cardiogram (ICG) is a non-invasive sensing modality for assessing the mechanical aspects of cardiac function, but is sensitive to artifacts from respiration, speaking, motion, and electrode displacement. Electrocardiogram (ECG)-synchronized ensemble averaging of ICG (conventional ensemble averaging method) partially mitigates these disturbances, as artifacts from intra-subject variability (ISVar) of ICG morphology and event latency remain. This paper describes an automated algorithm for removing noisy beats for improved artifact suppression in ensemble-averaged (EA) ICG beats. Approach: Synchronized ECG and ICG signals from 144 male subjects at rest in different psychological conditions were recorded. A 'three-stage EA ICG beat' was formed by passing 60-seconds non-overlapping ECG-synchronized ICG signals through three filtering stages. The amplitude filtering stage removed spikes/noisy beats with amplitudes outside of normal physiological ranges. Cross-correlation was applied to remove noisy beats in coarse and fine filtering stages. The accuracy of the algorithm-detected artifacts was measured with expert-identified artifacts. Agreement between the expert and the algorithm was assessed using intraclass correlation coefficients (ICC) and Bland-Altman plots. The ISVar of the cardiac parameters was evaluated to quantify improvement in these estimates provided by the proposed method. Main results: The proposed algorithm yielded an accuracy of 96.3% and high inter-rater reliability (ICC > 0.997). Bland-Altman plots showed consistently accurate results across values. The ISVar of the cardiac parameters derived using the proposed method was significantly lower than those derived via conventional ensemble averaging method (p < 0.0001). Enhancement in resolution of fiducial points and smoothing of higher-order time derivatives of the EA ICG beats were observed. Significance: The proposed algorithm provides a robust framework for removal of noisy beats and accurate estimation of ICG-based parameters. Importantly, the methodology reduced the ISVar of cardiac parameters. An open-source toolbox has been provided to enable other researchers to readily reproduce and improve upon this work.

Posttraumatic stress disorder (PTSD) is a highly disabling condition associated with alterations in multiple neurobiological systems, including increases in inflammatory function. Vagus nerve stimulation (VNS) decreases inflammation, however few studies have examined the effects of non-invasive VNS on physiology in human subjects, and no studies in patients with PTSD. The purpose of this study was to assess the effects of transcutaneous cervical VNS (tcVNS) on inflammatory responses to stress. Thirty subjects with a history of exposure to traumatic stress with (N ​= ​10) and without (N ​= ​20) PTSD underwent exposure to stressful tasks immediately followed by active or sham tcVNS and measurement of multiple biomarkers of inflammation (interleukin-(IL)-6, IL-2, IL-1β, Tumor Necrosis Factor alpha (TNFα) and Interferon gamma (IFNγ) over multiple time points. Stressful tasks included exposure to personalized scripts of traumatic events on day 1, and public speech and mental arithmetic (Mental Stress) tasks on days 2 and 3. Traumatic scripts were associated with a pattern of subjective anger measured with Visual Analogue Scales and increased IL-6 and IFNγ in PTSD patients that was blocked by tcVNS (p ​< ​.05). Traumatic stress had minimal effects on these biomarkers in non-PTSD subjects and there was no difference between tcVNS or sham. No significant differences were seen between groups in IL-2, IL-1β, or TNFα. These results demonstrate that tcVNS blocks behavioral and inflammatory responses to stress reminders in PTSD.

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Post-traumatic stress disorder (PTSD) is an independent risk factor for incident heart failure, but the underlying cardiac mechanisms remained elusive.Impedance cardiography (ICG), especially when measured during stress, can help understand the underlying psychophysiological pathways linking PTSD with heart failure. We investigated the association between PTSD and ICG-based contractility metrics (pre-ejection period (PEP) and Heather index (HI)) using a controlled twin study design with a laboratory-based traumatic reminder stressor.PTSD status was assessed using structured clinical interviews. We acquired synchronized electrocardiograms and ICG data while playing personalized-trauma scripts. Using linear mixed-effects models, we examined twins as individuals and within PTSD-discordant pairs. We studied 137 male veterans (48 pairs, 41 unpaired singles) from Vietnam War Era with a mean (standard deviation) age of 68.5(2.5) years. HI during trauma stress was lower in the PTSD vs. non-PTSD individuals (7.2 vs. 9.3 [ohm/s 2 ], p = .003). PEP reactivity (trauma minus neutral) was also more negative in PTSD vs. non-PTSD individuals (−7.4 vs. −2.0 [ms], p = .009). The HI and PEP associations with PTSD persisted for adjusted models during trauma and reactivity, respectively. For within-pair analysis of eight PTSD-discordant twin pairs (out of 48 pairs), PTSD was associated with lower HI in neutral, trauma, and reactivity, whereas no association was found between PTSD and PEP. PTSD was associated with reduced HI and PEP, especially with