Coping and autonomic dysfunction act in tandem with alcohol-related subclinical atherosclerosis: the SAPBA study

Abstract

"Introduction: Alcohol abuse is among the Westernized world‘s most common lifestyle factors contributing to sensitization of vascular structure and pathology. Gamma glutamyl transferase (γ-GT), as a marker of alcohol abuse, may indicate increased sensitization and vascular disease risk when using chronic defense coping (DefS). DefS was contradicted as a promoter of health, as it was related with dissociation between self-reported behavioral (―in-control‖) albeit physiological (―loss-of–control‖) responses. Therefore, we aimed to assess if DefS may mask autonomic dysfunction and induce alcohol-related subclinical atherosclerosis. Methods: A black African male teacher cohort with similar socioeconomic standing and without atrial fibrillation (N=101) from the North-West Province of South Africa, was recruited and investigated. Fasting blood values, 24h ambulatory blood pressure (ABPM) and -ECG, Coping Strategy Indicator (CSI) scores and ultrasound left carotid intima media far wall scanning values, were obtained. The standard deviation between successful R-R intervals (SDNN) was utilized as a marker of time-domain 24h heart rate variability (HRV). Multivariate regression analyses were computed. Results: A hypertensive state in the men was evident at a much lower ROC γ-GT cut point than the suggested MERCK cut-point of 78 U/L [55.7 U/L, sensitivity/specificity 60%/86% (AUC 0.78; 95% CI: 0.67; 0.88]. Hereafter, males were stratified into low (<55.7 U/l) and high (≥55.7 U/l) γ-GT groups. Overall, the high γ-GT group, revealed a poorer lifestyle profile, mean higher 24h ABPM, depressed 24h HRV and more 24h silent ischemic events (14 vs. 2) compared to their low γ-GT counterparts (P ≤ 0.01). HRV responses were inversely associated with γ-GT when utilizing DefS (r = -0.28; P = 0.015). Additionally, ABPM predicted 24h silent ischemia (OR 1.11; P ≤ 0.01) whereas 24h silent ischemia predicted a trend for structural vascular disease in the DefS African men (OR 1.06; p ≤ 0.06). Conclusion: DefS revealed behavioral ―in-control‖ responses directly opposing or masking physiological ―loss-of-control‖ responses, underpinning a dissociative response. Alcohol, which is a central nervous system depressant, enhanced vasoconstriction in the vasculature. Indeed, alcohol abuse was related to depressed heart rate variability, when utilizing DefS, sensitizing the vasculature, induced silent ischemia and ultimately structural vascular remodeling. The detrimental effects of DefS acting in tandem with autonomic dysfunction augment alcohol-related ischemia and may increase the risk for early sub-clinical atherosclerosis. "