Abstract
Defensive coping (DefS) was associated with cardiovascular disease (CVD) susceptibility in Blacks. Whether coping strategies will associate with sub-clinical left ventricular hypertrophy (electrocardiographic-left ventricular hypertrophy [ECG-LVH] or Cornell product), cardiomyocyte injury and blood pressure (BP), is unclear. Therefore, we assessed relationships between ECG-LVH, cardiac troponin T (cTnT) and 24-hour BP in bi-ethnic groups when habitually utilising a certain coping style, and these groups when having a stress-related cTnT cut-point of 4.2ng/L. A target population study included a Black (n=190) and White (n=204) teachers' gender cohort (20-65years) from South Africa. The Coping Strategy Indicator determined DefS, social support and avoidance coping scores. Fasting blood samples, 10-lead ECG, 24-hour BP and ECG data were obtained. Interaction effects showed no gender, social support and avoidance coping differences. Stratification of groups was done for ethnicity and DefS. Blacks sought more social support, used less avoidance coping and presented with higher CVD susceptibility. Hypertension prevalence and ECG-LVH levels in DefS Blacks (63%) were higher compared to DefS Whites (40%). Multivariate regression analyses showed positive associations between Cornell product, cTnT and BP [p≤0.05] in DefS Blacks only. Their 24-hour systolic blood pressure (SBP) was associated with time-domain depressed heart-rate-variability and prolonged ST-segment-depression especially when applying an established stress-related cTnT ≥ 4.2ng/L cut-point. Defensive coping facilitated autonomic hyperactivity, myocardial injury and subsequent compensatory BP elevations as possible homeostatic reflexes to alleviate myocardial perfusion deficits. The resulting pressure overload increased sub-clinical wall remodelling and ischaemic heart disease risk in Blacks utilising habitual defensiveness. We therefore recommend regular ECG and high sensitivity cTnT screening in asymptomatic patients with emotional stress susceptibility. Longitudinal evidence is needed to confirm causality and progression of cardiomyopathy risk.
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