Association of glycemic gap with stroke recurrence in patients with ischemic stroke

Abstract

BackgroundGlycemic gap, as a novel index of acute glycemic excursion, is associated with poor prognosis of different diseases. This study aimed to explore the association of the glycemic gap with long‐term stroke recurrence in patients with ischemic stroke.MethodsThis study included patients with ischemic stroke from the Nanjing Stroke Registry Program. The glycemic gap was calculated by subtracting the estimated average blood glucose from the blood glucose at admission. Multivariable Cox proportional hazards regression analysis was performed to explore the association between the glycemic gap and the risk of stroke recurrence. The Bayesian hierarchical logistic regression model was used to estimate the effects of the glycemic gap on stroke recurrence stratified by diabetes mellitus and atrial fibrillation.ResultsAmong 2734 enrolled patients, 381 (13.9%) patients experienced stroke recurrence during a median follow‐up of 3.02 years. In multivariate analysis, glycemic gap (high group vs. median group) was associated with significantly increased risk for stroke recurrence (adjusted hazard ratio, 1.488; 95% confidence interval, 1.140–1.942; p = .003) and had varying effects on stroke recurrence depending on atrial fibrillation. The restricted cubic spline curve showed a U‐shaped relationship between the glycemic gap and stroke recurrence (p = .046 for nonlinearity).ConclusionOur study found that the glycemic gap was significantly associated with stroke recurrence in patients with ischemic stroke. The glycemic gap was consistently associated with stroke recurrence across subgroups and had varying effects depending on atrial fibrillation.

The Synergistic Relationship Between Atrial Fibrillation and Diabetes Mellitus: Implications for Cardiovascular and Metabolic Health

“…These alterations might induce changes in atrial action potential morphology and duration [ 12 ]. Further comprehensive studies are needed to clarify the molecular processes underpinning T2DM-induced atrial electrical remodeling and identify potential targets for pharmacological intervention [ 13 , 14 ]. The review also establishes that T2DM is associated with a 1.4- to 1.6-fold heightened risk of developing AF, an elevated risk that persists independently of other common risk factors [ 3 ].…”

“…In addition, T2DM might impact the expression and phosphorylation of the L-type calcium channel (LTCC), potentially leading to reduced calcium influx and contractility [12,13]. Furthermore, T2DM could modulate the activity and expression of various potassium channels, including the inward rectifier potassium channel (IK1), transient outward potassium channel (Ito), ultra-rapid delayed rectifier potassium channel (IKur), and acetylcholine-activated potassium channel (IKACh) [11][12][13][14][15]. These alterations might induce changes in atrial action potential morphology and duration [12].…”

“…Nonetheless, the exact reasons for this amplified risk still need to be understood. Plausible explanations encompass subclinical or overt cardiovascular diseases, such as coronary artery disease and the thickening of the left ventricle, diastolic dysfunction, or valvular disease, which may predispose T2DM patients to AF [11][12][13][14][15][16]. Another contributing factor is the increased thromboembolic risk in T2DM patients due to hypercoagulability, endothelial dysfunction, platelet activation, or inflammation [14][15][16][17][18].…”