Higher aggregate index of systemic inflammation was independently associated with in-hospital new-onset atrial fibrillation in patients with MINOCA (OR 2.335; 95% CI 1.532-3.560; P<0.001).
Cohort (n=409)
No
Is the aggregate index of systemic inflammation (AISI) associated with in-hospital new-onset atrial fibrillation in patients with MINOCA?
Higher aggregate index of systemic inflammation (AISI) is independently associated with in-hospital new-onset atrial fibrillation in patients with MINOCA, serving as a potential adjunctive risk marker.
Odds Ratio: 2.335 (95% CI 1.532–3.56)
p-value: p=< .001
In recent years, with a growing understanding of coronary microvascular dysfunction, myocardial infarction with nonobstructive coronary arteries (MINOCA) has been proposed as a distinct type of myocardial infarction. The management of atrial fibrillation (AF) coexisting with myocardial infarction remains a major challenge in clinical practice. This study aims to explore the association between the inflammatory marker aggregate index of systemic inflammation (AISI) and new-onset AF (NOAF) in patients with MINOCA. In this single-center, retrospective study, we consecutively enrolled patients with MINOCA from January 2019 to June 2025. AISI was calculated as (Neutrophil count × Platelet count × Monocyte count)/Lymphocyte count from procedural complete blood count. NOAF was defined as new-onset AF after admission in patients with no previous history of AF. Multivariable logistic regression was employed to screen for factors associated with NOAF. Restricted cubic spline was used to characterize the dose-response relationships between AISI and NOAF. Receiver operating characteristic curves were constructed to evaluate the discriminative performance of AISI. Among 409 patients with MINOCA, 38 (9.3%) developed NOAF. In multivariable analysis, AISI (odds ratio 2.335, 95% confidence interval CI 1.532–3.560, P < .001) and C-reactive protein (odds ratio 1.009, 95% CI 1.002–1.017, P = .015) remained independently associated with NOAF, which suggests that AISI provides additional information independent of the traditional inflammatory marker C-reactive protein in relation to NOAF. Restricted cubic spline analysis suggested an initial nonlinear dose-response relationship between AISI and NOAF in the unadjusted model; however, this association was no longer statistically significant after adjustment for relevant clinical covariates. In receiver operating characteristic analysis, AISI yielded an area under the curve of 0.712 with an optimal cutoff of 750 (sensitivity 0.737, specificity 0.650, 95% CI 0.617–0.808, P < .001). Higher AISI is independently associated with in-hospital NOAF in patients with MINOCA, although its discriminative performance is moderate, suggesting that AISI may serve as an adjunctive rather than a standalone risk marker.
Shen et al. (Fri,) conducted a cohort in Myocardial infarction with nonobstructive coronary arteries (MINOCA) (n=409). Aggregate index of systemic inflammation (AISI) was evaluated on In-hospital new-onset atrial fibrillation (NOAF) (OR 2.335, 95% CI 1.532-3.560, p=< .001). Higher aggregate index of systemic inflammation was independently associated with in-hospital new-onset atrial fibrillation in patients with MINOCA (OR 2.335; 95% CI 1.532-3.560; P<0.001).