Defensive coping, urbanization, and neuroendocrine function in Black Africans: the THUSA study.

Dissociation between ß-adrenergic behavioral and physiological defensive active coping (AC) responses was associated with cardiometabolic risk in urban but not rural African males. Whether this is partly driven by underlying neuroendocrine dysfunction is not certain. We aimed to assess the association between coping style, urbanization, and neuroendocrine function. Blood pressure (BP) and serum stress hormones were assessed across levels of urbanization (rural vs. urban) and coping style (active vs. passive) in 178 Black African men. Urban men demonstrated increased hypertension prevalence, α-adrenergic hemodynamic pattern, lower testosterone levels, and a larger cortisol:testosterone ratio (Cort:Test) compared to their rural counterparts. This was particularly evident in urban AC men where cortisol and Cort:Test explained 36-40% of the variance in BP. Dissociation between behavioral and physiological ß-adrenergic neuroendocrine responses in urban AC African men was shown. A stressful urban environment might induce an apparent loss of physiological control, thereby facilitating disturbed neuroendocrine AC responses, which could increase cardiovascular disease risk.

Facilitated defensive coping, silent ischaemia and ECG left-ventricular hypertrophy: the SABPA study.

BACKGROUND: Defensive active coping responses (being-in-control, acceptance of the stressor as reality) have been associated with vascular hyper-responsiveness in urban Africans. However, the association between active coping responses, blood pressure (BP), and ECG-derived left-ventricular hypertrophy (LVH) responses is unknown. OBJECTIVES AND METHODS: Associations between BP, silent ischaemia and ECG Cornell product LVH were assessed in 161 African and Caucasian men with active coping responses identified by the Amirkhan Coping Strategy Indicator. BP, ECG and silent ischaemia data were obtained from 24-h ambulatory monitoring. Beat-to-beat BP was continuously recorded during stress testing and fasting resting blood samples obtained for biochemical analyses. RESULTS: Enhanced ß-adrenergic central cardiac responses were evident in active coping Caucasians as opposed to a predomination of α-adrenergic vascular responses in active coping Africans. Active coping African men displayed higher 24-h BP and prevalence of silent ischaemia events compared to the Caucasian men. Regression analyses revealed that α-adrenergic responses were associated with silent ischaemic events, adjusted R 0.21 [ß 1.07, 95% confidence interval (CI) 0.29-1.85] and that ischaemic events predicted LVH in active coping Africans (adjusted R 0.12, ß 0.35, 95% CI 0.11-0.59). Receiver-operated characteristic (ROC) analyses indicated a defensive pathway cut point of 16 in Africans as opposed to 32 in Caucasians predicting silent ischaemia with sensitivity/specificity 100/96%. CONCLUSIONS: A defensive pathway revealed disturbed vascular function showing dissociation between behavioural and physiological ß-adrenergic active coping responses in Africans. Vascular responsiveness facilitated silent ischaemia events and structural LVH changes which potentially explain the increased risk for incident ischaemic stroke in black Africans.