Synergistic Effects of Type D (“Distressed”) Personality Traits on Coronary Microvascular Function in Male Physicians With Occupational Burnout: A Cross‐Sectional Study

Background Psychosocial factors like type D personality (TDP) and occupational burnout are associated with increased coronary artery disease risk. This cross‐sectional study investigated a potential mechanism linking TDP, characterized by negative affectivity (NA) and social inhibition (SI), to coronary microvascular function in male physicians and examined burnout's potential moderating role through a balanced, stratified design. Methods Sixty male physicians, evenly divided into burnout and nonburnout groups, underwent positron emission tomography to measure endothelium‐dependent coronary flow reserve (CFR) during the cold pressor test and endothelium‐independent CFR during adenosine‐induced hyperemia. TDP effects were primarily analyzed using a dimensional approach based on continuous NA and SI scores and their interaction, adjusting for physical activity and Systematic Coronary Risk Evaluation 2 or age and metabolic syndrome factors. Results Fourteen participants (23.3%) exhibited TDP (NA and SI scores ≥10), with 92.9% also experiencing burnout. Moderator analysis was limited by the high co‐occurrence of burnout and TDP. A significant positive NA×SI interaction was associated with increased endothelium‐dependent CFR, independent of burnout, physical activity, and either Systematic Coronary Risk Evaluation 2 ( P =0.044, partial η 2 =0.074) or age and metabolic syndrome factors ( P =0.030, partial η 2 =0.087). CFR increased with higher SI scores when NA was high, and with higher NA scores when SI was high. This effect was mediated by peak rate–pressure product, an indicator of sympathetic stimulation. Conclusions TDP components may synergistically affect coronary microvascular function via heightened sympathetic activity. Exaggerated CFR during sympathetic stimulation may reflect a compensatory or early‐stage response, potentially indicative of maladaptive hyperemia and future microvascular impairment.