(PS6-C70) Heart Rate Variability Moderates Change in Depressive Symptoms in Individuals in Early Alcohol Use Disorder Recovery

Impairment in central autonomic network (CAN) regulatory functioning reflected by reduced parasympathetically mediated heart rate variability (HRV) and increased sympathetic activation is thought to impede alcohol use disorder (AUD) recovery. We previously showed that parasympathetically mediated HRV is negatively associated with alcohol use over 90-day follow-up among treatment receiving individuals in early recovery from AUD. Here we sought to explore how parasympathetically mediated HRV and sympathetic activation may moderate change in depressive symptoms over 90-day follow-up in this sample. In this study, 42 participants in the first year of a current AUD recovery attempt were monitored for four days using ambulatory electrocardiogram (ECG) device, with indices of parasympathetically mediated HRV (SDNN and RMSSD) and sympathetic activation (heart rate and the Kubios sympathetic index) calculated from these ECG recordings. Depressive symptoms were assessed with the Beck Depression Inventory II (BDI-II) at baseline and at 90-day follow-up. Four generalized linear models were fitted with follow-up BDI-II score as the dependent variable, and baseline BDI-II score, HRV/sympathetic activation, and the baseline BDI-II score × HRV/sympathetic activation interaction term as independent variables, controlling for alcohol use over follow-up (percent days abstinent), age, and accelerometry measured movement. Based on previous laboratory-based research measuring resting, parasympathetically mediated HRV, we hypothesized that higher parasympathetically mediated HRV would be associated with reductions in depressive symptoms from baseline to follow-up, whereas lower HRV would predict an increase or no change in depressive symptoms. Additionally, we precited that greater sympathetic activation would be associated with increases or no change in depressive symptoms from baseline to follow-up, whereas lesser sympathetic activation would predict a decrease in depressive symptoms. Contrary to our predictions, inspection of the interaction terms indicated that for those with higher SDNN (χ²= 5.26, p= .02) and RMSSD (χ²= 11.40, p= .0007) reflecting parasympathetically mediated HRV, depression scores remained fairly constant from baseline to 90-day follow-up. Conversely, those with lower SDNN and RMSSD tended to experience reductions in depressive symptoms from baseline to 90-day follow-up. Further, the interaction terms for the heart rate (χ²= 8.30, p= .004) and the Kubios sympathetic index (χ²= 17.37, p< .0001) reflecting sympathetic activation, indicated that for those with lesser sympathetic activation, depression scores remained fairly constant from baseline to 90-day follow-up. Conversely, those with greater heart rate and Kubios sympathetic index scores tended to experience decreases in depressive symptoms from baseline to 90-day follow-up. Additional work is needed to explain these findings that were counter to our predictions. One possibility is that HRV under laboratory-based, resting conditions, and real-time, ambulatory conditions interact differently with depression. More work is needed to better describe HRV/negative affect associations under ambulatory conditions.