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 η2=0.074) or age and metabolic syndrome factors (P=0.030, partial η2=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.