Inflammatory and Cardiovascular Responses to Active and Passive Acute Psychological Stress.

Abstract

Objective: Acute psychological stress is a risk factor for cardiovascular disease (CVD), possibly through promoting a heightened inflammatory profile. Active stressors are commonly used to investigate cardiovascular and immune reactivity; however, this response may not translate to other stress modalities. We aimed to decipher potential differences in immune responses to passive and active stressors.

Methods: Eighty-eight participants completed this study. After a baseline period, a passive (International Affective Picture System [IAPS]) and active stress task (Paced Auditory Serial Addition Test [PASAT]) were completed in a randomized order, with 45-minute rest post-tasks. Cardiovascular measures (including SBP, DBP, HR) were collected continuously. Blood samples were collected after each time point determining inflammatory responses, including circulating and stimulated interleukin-6 (IL-6), systemic inflammation response index (SIRI), neutrophil/lymphocyte ratio (NLR), TNF-α, and P- and E-selectin.

Results: Cardiovascular measures were higher during the PASAT than IAPS (p < .001). Circulating IL-6 levels increased from baseline to 45-minutes after both tasks (p ≤ .001), with no difference between 45-minute post-PASAT and 45-minute post-IAPS (p > .05). SIRI increased from baseline to post-IAPS (p = .013), 45-minute post-IAPS (p = .004), and 45-minute post-PASAT (p < .001). No difference in SIRI between 45-minute post-PASAT and 45-minute post-IAPS existed. NLR increased from baseline to 45-minute post-PASAT (p = .008). There were no significant time effects for TNF-α, P-selectin, or E-selectin (all p > .05).

Conclusion: Both stressors increased circulating IL-6 levels and SIRI. Cardiovascular measures were higher during the active task, but the magnitude of inflammatory responses did not significantly differ between tasks. Regardless of stress modality, an immune response ensues, potentially increasing the risk of CVD over time.