Each 10% norepinephrine increase post-stress was linked to ~1 HU lower coronary PCAT attenuation, indicating a lipid-rich perivascular adipose tissue phenotype.
Is acute sympathetic stress reactivity (norepinephrine increase) associated with pericoronary adipose tissue (PCAT) attenuation in male physicians without known cardiovascular disease?
Acute sympathetic stress reactivity is associated with a lipid-rich perivascular adipose tissue phenotype, suggesting excess norepinephrine reactivity may be an early biomarker of coronary vulnerability.
Absolute Event Rate: 0% vs 0%
Pericoronary adipose tissue (PCAT) attenuation from coronary computed tomography angiography (CCTA) is an imaging biomarker of coronary inflammation. Experimental evidence suggests that sympathetic activation and norepinephrine (NE) can alter perivascular adipose tissue (PVAT) composition. Whether NE stress reactivity relates to PVAT phenotype, as reflected by PCAT attenuation, or varies by chronic stress exposure is unclear. We studied 60 male physicians (30 with clinical burnout, 30 controls) without known cardiovascular disease. Participants underwent CCTA for PCAT assessment and Trier Social Stress Test to induce psychosocial stress. Plasma NE was measured at baseline, immediately, +15, +45, and +90 minutes post-stress. Relative NE increase (immediately post-stress minus baseline) was the primary NE index; absolute NE increase, NE area under the curve with respect to increase (AUC-I) and ground (AUC-G; total output) were secondary indices. Multivariable regression adjusted for burnout, age, waist circumference, low-density lipoprotein cholesterol, and segment stenosis score. Greater relative NE stress increase was independently associated with lower total PCAT attenuation (average across three coronary arteries; partial r²=0.12, p=0.010). Each 10% relative NE increase corresponded to ~1 HU lower attenuation. Similarly, an absolute NE increase of 50 pg/mL (partial r²=0.08, p=0.036) and a 5000-unit increase in NE AUC-I (partial r²=0.07, p=0.049) corresponded to ~1 HU lower attenuation, whereas NE AUC-G showed no association (p=0.35). Acute sympathetic stress reactivity, reflected by NE increase, is associated with a lipid-rich PVAT phenotype, as indicated by lower PCAT attenuation, supporting PVAT responsiveness to adrenergic stimulation. Excess NE reactivity may represent a biomarker of early coronary vulnerability.
Borovicka et al. (Mon,) reported a other. Each 10% norepinephrine increase post-stress was linked to ~1 HU lower coronary PCAT attenuation, indicating a lipid-rich perivascular adipose tissue phenotype.