Abstract 2980: Elevated Interleukin-6 Levels are Independently Associated with Neurocardiogenic Injury
Introduction: Inflammation and inflammatory cytokines (IC) have been associated with the development of several cardiovascular diseases such as atherosclerosis, acute coronary syndromes, and heart failure. IC levels are also increased in patients with subarachnoid hemorrhage (SAH). The role of inflammation in neurocardiogenic injury after SAH is not known. We aimed to explore the association between IC levels and adverse cardiac outcomes in this setting.
Methods: This was a prospective cohort study of consecutive patients with aneurysmal SAH admitted to UCSF. Plasma was collected for measurements of levels of tumor necrosis factor alpha (TNFa) and the following interleukins (IL): IL-1a, IL-1b, IL-6, and IL-10, soon after enrollment. These levels served as predictor values. Cardiac troponin I (cTi) was measured, clinical data were collected, and two-dimensional echocardiography was performed 1, 3, and 6 days after enrollment. The following outcome data were collected and treated dichotomously: left ventricular ejection fraction (LVEF), regional wall motion abnormalities (RWMA), cTi, and B-type natriuretic peptide (BNP) levels. The association between each predictor and outcome variable was quantified by univariate and multivariate logistic regression (adjusted for SAH severity grade, age, sex, race, history of hypertension of smoking) and reporting odds ratios (OR) and 95% confidence intervals (95% CI).
Results: The study included 142 patients. By multivariate analysis, elevated levels of IL-6 were independently predictive of cTi release, decreased LVEF, and elevated BNP (Table⇓). Elevated levels of other ICs were not associated with adverse cardiac outcomes. However, increased levels of IL-10 were independently predictive of death (OR 10.4, 95% CI 2.1–51.2, p = 0.004).
Conclusions: Elevated levels of IL-6 are associated with adverse cardiac outcomes after SAH. Inflammation may play a role in the development of neurocardiogenic injury after SAH.