November 23, 2020Journal of Clinical MedicineOpen Access

Social Stress-Induced Oxidative DNA Damage Is Related to Prospective Cardiovascular Risk

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Why the study?

Psychosocial stress increases cardiovascular risk and oxidative DNA damage, but whether acute stress-induced DNA damage relates to cardiovascular risk profiles and sympathetic response remained to be tested.

Does acute psychosocial stress induce oxidative DNA damage in healthy volunteers, and is it related to their prospective cardiovascular risk profile?

Structured PICO

Does acute psychosocial stress induce oxidative DNA damage in healthy volunteers, and is it related to their prospective cardiovascular risk profile?

Population

95 healthy volunteers (83 male, 12 female), stratified by prospective cardiovascular Münster score (PROCAM) into 33 subjects with prospective risk of myocardial infarction (risk+) and 59 subjects without risk (risk-).

Intervention

Trier social stress test for groups (TSST-G) to induce acute psychosocial stress

Comparator

Comparison between subjects with (risk+) and without (risk-) prospective risk of myocardial infarction

Outcome

Oxidative DNA damage determined using whole-blood single-cell gel electrophoresis ('tail moment' in the 'comet assay')surrogate

Acute psychosocial stress induces oxidative DNA damage specifically in individuals with an elevated prospective risk of myocardial infarction, linking sympathetic stress responses to potential cardiotoxicity.

Implication

Stress-induced DNA damage tracks higher CV risk; leaves open mechanistic mediation of events in prospective cohorts.

Abstract

Psychosocial stress increases cardiovascular risk, which coincides with enhanced oxidative DNA damage. Increased sympathetic tone-related catecholamine release causes oxidative stress, which contributes to catecholamine-related cardiotoxicity. Therefore, we tested the hypothesis whether acute psychosocial stress induces oxidative DNA damage, its degree being related to the cardiovascular risk profile and depending on the sympathetic stress response. After assessment of the prospective cardiovascular Münster score (PROCAM) to determine the risk of acute myocardial infarction, 83 male and 12 female healthy volunteers underwent the Trier social stress test for groups (TSST-G). Heart rate variability was quantified by measuring the standard deviation (SDNN) and root mean square of successive differences (RMSSD) between normal-to-normal inter-beat intervals. Salivary α-amylase (sAA) activity was assessed as a surrogate for noradrenaline plasma concentrations. Oxidative DNA damage was determined using whole-blood single-cell gel electrophoresis ("tail moment" in the "comet assay"). A total of 33 subjects presented with a prospective risk of myocardial infarction (risk+) vs. 59 subjects without risk (risk-). The TSST-G stress significantly increased blood pressure, heart rate, and sAA in both groups, while oxidative DNA damage was only increased in the risk+ group. Immediately after the TSST-G, the "tail moment" showed significant inverse linear relations with both SDNN and RMSSD. Acute psychosocial stress may cause oxidative DNA damage, the degree of which is directly related to the individual cardiovascular risk profile and depends on the stress-induced increase in the sympathetic tone.