Abstract
BACKGROUND: Neutrophil to high-density lipoprotein cholesterol ratio (NHR) is a metabolic inflammatory biomarker reflecting the balance between pro- and anti-inflammatory responses. Extensive research has revealed that NHR is an effective predictor for cardiovascular risks, such as stroke and myocardial infarction. Nevertheless, the association between NHR and incidence risks of aortic dissection (AD) and aortic aneurysm (AA) remains unclear. METHODS: This research, designed as a prospective cohort study, enrolled 409,357 participants based on the UK Biobank project. The cut-off value of NHR i.e., 0.205, was determined using a receiver operating characteristic curve for grouping. Participants were divided into two groups: NHR ≤ 0.205 (n = 293,294) and NHR > 0.205 (n = 116,063). The cumulative incidence of outcome, i.e., AD/AA including AD and AA, was calculated using Kaplan-Meier curves. The dose-response relationship between NHR and AD/AA was evaluated using restricted cubic spline (RCS). Multivariable-adjusted Cox proportional hazards regression models, followed by sensitivity analyses and subgroup analyses, were performed to evaluate the association between NHR and AD/AA onset. RESULTS: A total of 3,408 participants developed AD/AA, including 233 AD cases and 3,259 AA cases, with a median follow-up period of 14.8 years. The incidences of AD/AA, AD and AA were 56.34, 3.85 and 53.87 cases per 100,000 person-years, respectively. A nonlinear relationship between NHR and the incidence risk of AD/AA was documented by RCS (P for nonlinear < 0.001). Participants in the NHR > 0.205 group had a higher risk of developing AD/AA compared to those in the NHR ≤ 0.205 group, with an adjusted HR of 1.47 (95%CI 1.37-1.58). This association was further validated by sensitivity analyses and subgroup analyses. CONCLUSIONS: NHR is an independent risk factor for AD/AA. The disorder of metabolic inflammation may be a potential pathological mechanism for AD/AA. Tailored assessment and management of NHR may serve as effective strategies for the prevention and prediction of AD/AA.