Background: Dysregulated psychobiological reactivity to acute psychological stress is associated with subclinical cardiovascular disease (CVD) risk, but its association with clinical CVD and mortality remains unclear-especially when considering both exaggerated and blunted responses, non-cardiovascular biomarkers, and potential racial/ethnic differences. This study aimed to test (1) relationships between multi-system stress reactivity and CVD/mortality, and (2) effect modification by race/ethnicity.
Methods: Participants were CVD-free adults (N = 957, age=69 ± 9 years, 56 % female, 27 % non-Hispanic White, 32 % non-Hispanic Black, 41 % Hispanic) enrolled in the Multi-Ethnic Study of Atherosclerosis. The following responses to a standardized psychological stress protocol were recorded: blood pressure (BP), heart rate, heart rate variability (HRV), salivary alpha-amylase (sAA), and cortisol. Participants were followed for a median of 8 years. Covariate-adjusted Cox proportional hazard models investigated associations of stress reactivity (baseline-to-stress changes: low/blunted: ≤25th percentile; intermediate/moderate [reference]: 26-74th; high/exaggerated: ≥75th) with incident CVD (N = 111) and all-cause mortality (N = 114). Race/ethnicity was tested as an effect modifier.
Results: Stress reactivity was not linked with CVD incidence. Blunted diastolic BP reactivity was associated with premature all-cause mortality (HR=1.92, 95 % CI: 1.03-3.56). Exaggerated (HR=0.58, 95 % CI: 0.35-0.98) and blunted (HR=0.52, 95 % CI: 0.30-0.89) sAA reactivity were associated with reduced mortality risk. Race/ethnicity was not an effect modifier (all p for interaction > 0.05).
Conclusions: Blunted DBP reactivity may serve as an early marker of increased mortality risk; randomized trials should test whether interventions that normalize DBP reactivity improve long-term survival. Further research should explore why dysregulated sAA reactivity was associated with lower mortality risk.
Keywords: Acute stress; Chronic disease prevention; Physiological responses; Reactivity hypothesis; Stress reactivity.
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