Physician burnout and type D personality relate to pericoronary fat phenotype and role of sympathetic activation: a cross-sectional study

Biological pathways linking psychosocial stress to coronary pathology remain elusive. Burnout and type D personality (TDP), defined by negative affectivity and social inhibition, are prevalent among physicians and associated with cardiovascular risk. We investigated whether burnout and TDP relate to pericoronary adipose tissue (PCAT) attenuation, a noninvasive imaging marker of fat composition and coronary inflammatory signaling. We further investigated whether sympathetic activation is implicated as an indirect pathway in this association. Systemic inflammation was examined as a downstream correlate. Sixty male physicians (30 with burnout, 30 controls) underwent coronary computed tomography angiography and cold pressor testing to assess PCAT attenuation and peak rate pressure product (RPP) as a measure of sympathetic activation. Burnout and TDP traits were measured using validated questionnaires. Regression models tested associations among burnout, negative affectivity-by-social inhibition interaction, peak RPP, PCAT attenuation, and high-sensitivity C-reactive protein. Burnout was associated with lower PCAT attenuation after adjustment for TDP and cardiovascular risk factors (− 3.79 Hounsfield units, 95% CI: − 7.55, − 0.029; p = 0.048; ΔR 2 = 0.060). The negative affectivity-by-social inhibition interaction was significantly associated with lower PCAT attenuation ( p = 0.011; ΔR 2 = 0.102) and higher peak RPP ( p = 0.013; ΔR 2 = 0.093). Peak RPP showed an indirect effect consistent with partial statistical mediation of the association between TDP and PCAT attenuation. PCAT attenuation moderated the relationship between peak RPP and C-reactive protein (interaction p = 0.023), with stronger inflammatory responses observed at lower attenuation. Burnout and synergistic TDP traits were associated with altered PCAT attenuation, with findings consistent with an indirect effect via heightened sympathetic activity. Lower PCAT attenuation amplified sympathetic associations with systemic inflammation, consistent with an outside-in pathway. Lipid-rich perivascular fat may mark an early stage of coronary vulnerability, raising the possibility that psychosocial stress relates to coronary biology before overt vascular inflammation.