Abstract P244: Association Between Early Life Trauma and Change in HRV During Mental Stress Among Patients With Recent Myocardial Infarction

Abstract

Background: Early-life traumatic experiences have been associated with increased cardiovascular disease risk. Little is known about how early-life traumatic experiences may affect changes in autonomic function during mental stress among young subjects post-MI. Objective: We hypothesized that those with high exposure to early-life trauma, compared to those with low exposure to early-life trauma, would have increased autonomic dysfunction at baseline, worse stress reactivity, and slower autonomic recovery. Methods: We evaluated 321 subjects with a history of recent myocardial infarction who underwent a laboratory-based mental stress speech task. HRV was measured at rest (T0), during mental stress (T1), and during recovery (T2) with ambulatory electrocardiographic monitoring. We evaluated low frequency (LF) HRV as the primary outcome because of its relationship with baroreflex sensitivity, psychological stress, and cardiovascular disease outcomes. Early life trauma was assessed using the Early Trauma Inventory Self Report - Short Form (ETI-SF) and a binary variable was calculated using one SD above the mean of the ETI-SF score, a previously validated cutpoint, to indicate high early-life trauma exposure and low otherwise. Sociodemographic factors, including race, highest education attained, age, and gender, were considered as potential confounders in multiple linear regression models. Differences amongst stress, rest, and recovery metrics were evaluated as outcomes in separate models. Results: Of 321 subjects with HRV data, 284 were included in the final analytic sample after excluding those with missing covariates. The mean age was 50.7 ± 6.7, 49% were female (139), and 64% were African-American (182); 260 (88.4%) reported experiencing high levels of early-life trauma. There were no associations between early-life trauma during baseline HRV (T0), reactivity to stress (T1 - T0), and prolonged reactivity (T2 - T0). However, those with high early-life trauma had reduced HRV during recovery from stress compared to those with low early-life trauma (T2 - T1; Beta (95% CI) = -0.37 (-0.73, -0.01)). Results were similar after adjustment for sociodemographic factors and did not vary by race/ethnicity or gender. Conclusion: Among subjects with recent MI, high exposure to early-life trauma is associated with prolonged stress-induced autonomic dysfunction during stress and recovery, while the low exposure subjects revert to baseline HRV levels during recovery. This may indicate greater stress-induced cardiotoxicity in those exposed to early life trauma.