Abstract 1178: Endothelial Cell Activation, Impaired Nitric Oxide Bioavailability and Reduced Endothelial Repair Capacity After Anger Provocation
Background: Studies have demonstrated that anger increases the risk of incident cardiovascular disease (CVD). Endothelial cell health is an important determinant of atherosclerosis development and CVD onset. We investigated whether anger provocation induces acute dysfunction in the vascular endothelium in apparently healthy individuals.
Methods: Twenty-four subjects (58.3% female, mean age 38.1±12.4 years) underwent a standardized and validated 12-minute anger induction. Blood was drawn at baseline (pre-induction), 30, and 90 minutes post-anger induction. Nitric oxide-dependent vasodilation was determined by assessing reactive hyperemia index (RHI) using peripheral arterial tonometry. CD62E+ and CD51+ endothelial microparticles (EMPs), and KDR+, CD34+, and CD133+ endothelial progenitor cells (EPCs), were used to assess endothelial activation and repair, respectively. EMPs and EPCs were quantified by flow cytometry from blood samples.
Results: RHI decreased from baseline to 30-minutes (2.33±0.46 vs. 1.98±0.45, p=0.01) and 90 minutes (2.33±0.46 vs. 2.01±0.53, p=0.04) post-anger induction. There was no difference between 30 and 90 minutes (p=0.80). In addition, levels of CD62E+ EMPs increased from baseline to 90 minutes post-induction (614±502 EMP/uL vs. 999±898 EMP/uL, p=0.007). There were nonsignificant differences between baseline and 30 minutes (614±502 vs. 862±880 EMP/uL, p=0.10) and 30 and 90 minutes (862±880 vs. 999±898 EMP/uL, p=0.18). CD51+ EMP levels consistently showed an increase post-induction, however, only the increase from baseline to 90 minutes approached significance (p=0.06). Finally, EPCs significantly decreased from baseline to 30-minutes (0.034±0.026% vs. 0.018±0.019%, p=0.02) with a return toward baseline values at 90 minutes (0.027%±0.039%). There were no significant differences between 30 and 90 minutes (p=0.58) or baseline and 90 minutes (p=0.37).
Conclusion: Anger directly affects the endothelium by inducing endothelial cell activation while impairing nitric oxide bioavailability and endothelial regenerative capacity in healthy participants. Endothelial cell dysfunction and injury may explain the link between anger and incident CVD events.