Ben Halima1, Yaakoubi1, Boudiche1, Rekik1, Mghaieth1, Larbi1, Ouali1, Mourali1

1Rabta Hospital, Tunis, Tunisia

Atrial fibrillation (AF) is mediated by oxidative stress, neurohormonal activation, and inflammatory activation. Serum uric acid (SUA) is a surrogate marker of oxidative stress. hyperuricemia has been widely accepted to be associated with the incidence of AF. But the role of SUA in left atrial (LA) remodeling and new-onset atrial fibrillation (NOAF) during acute coronary syndrome (ACS) has not been fully explored. The aim  of the study was to evaluate the association between SUA, LA remodeling and NOAF in patients with ischemic heart disease.

It was a study which included patients hospitalized for ACS between 1st January 2019 to 31 December 2019. Non inclusion criteria were: gout and/or treatment with allopurinol, chronic lung disease with hypoxemia and severe chronic kidney disease. Fasting blood samples were obtained to dose SUA.

Totally, 402 patients with ACS were included in the study. Of all, 39 patients (9.7%) had developed NOAF during hospitalization. Hyperuricemia was found in 39 patients (9,7%).  SUA was significantly increased in patients with NOAF compared with non-NOAF patients            (78±26 vs 56±21, p=0.001). According to the ROC curve for predicting NOAF, the cut-off value of SUA was about 62 mg/l with a sensitivity of 68% and specificity of 70%.

In multivariate analysis, age>62 years (adjusted OR=4.83 ; p=0.02), chronic renal failure (adjusted OR=6.16 ; p=0.04), history of stroke (adjusted OR=44 ; p=0.002) and  SUA >62mg/l (adjusted OR=4.4 ; p= 0.04) remained independent predictors of  NOAF.

In our study conducted in a Tunisian population with ACS, we have demonstrated a significant association between the increased levels of SUA and NOAF. So it seems to be interesting to propose a closer monitoring and event the use of more efficient tools, in patients having ACS and hyperuricemia, whose main goal is to better detect NOAF in order to offer adequate and early treatment .