Coping facilitated troponin T increases and hypo-responsivity in the copeptin-HPA-axis during acute mental stress in a Black cohort : The SABPA study

BACKGROUND: Defensive coping (DefS) was associated with a vulnerable cardiovascular profile in Blacks. The copeptin/vasopressin system is a manifestation of hypothalamic-pituitary-adrenal-axis activity and may act as an acute compensatory mechanism when there is a disruption in volume-loading homeostasis, i.e. when cardiac stress is evident. Whether DefS will influence associations between copeptin and cardiac stress markers, remains unclear. Here we aimed to determine associations between acute mental stress responses of copeptin, vascular responsiveness and biomarkers of cardiomyocyte injury [cardiac troponin T (cTnT)] and cardiac wall-stress [N-terminal pro-brain natriuretic peptide (NT-proBNP)] in DefS race groups.METHODS: South African black and white teachers (n = 378) of both sexes, participated in this target population study. Cases with a history of myocardial infarction, stroke and atrial fibrillation were excluded. We obtained coping scores (Coping Strategy Indicator), beat-to-beat blood pressure and fasting blood samples at rest and after 1-min exposure to the Stroop-Colour-Word-Conflict-test.RESULTS: Interaction effects (p < .05) for copeptin percentage change (%) during the Stroop-Colour-Word-Conflict-test determined stratification of participants into race and DefS (≥26, above-median score) groups. In DefS Blacks, Stroop-Colour-Word-Conflict-test exposure elicited increases in cTnT%, NT-proBNP%, diastolic-blood pressure% and total peripheral resistance%. Again, in these individuals, multiple regression analyses showed positive associations between copeptin% and total peripheral resistance%; with inverse associations between copeptin% and cTnT% (p < .05). None of these associations were found in DefS Whites.CONCLUSIONS: Utilisation of DefS in Blacks provoke vascular hyper-responsiveness and cardiac wall stress (elevated cTnT and NT-proBNP) possibly mediated via the copeptin/vasopressin system. However, a presumably hypo-responsive hypothalamic-pituitary-adrenal-axis during stress exposure could not counteract coronary perfusion deficits via additional copeptin/vasopressin release