In adults with acute STEMI treated with primary PCI, serum sodium concentration did not independently predict in-hospital arrhythmias (OR 1.02; 95% CI 0.94-1.11; p=0.62).
Cohort (n=398)
Does serum sodium concentration predict in-hospital arrhythmias in STEMI patients treated with primary PCI?
Serum sodium concentration does not independently predict in-hospital arrhythmias in acute STEMI patients undergoing primary PCI.
Odds Ratio: 1.02 (95% CI 0.94–1.11)
p-value: p=0.62
Abstract Background Rhythm and conduction disturbances are critical determinants of ST-elevation myocardial infarction (STEMI) outcomes. While potassium and calcium imbalances are well-established contributors to arrhythmogenesis, the role of serum sodium, a key electrolyte modulating myocardial excitability, remains underexplored in acute STEMI. Purpose To evaluate whether serum sodium concentration independently predicts in-hospital arrhythmias (ventricular tachycardia (VT), ventricular fibrillation (VF), and atrial fibrillation (AF)) in STEMI patients treated with primary percutaneous coronary intervention (pPCI), after adjusting for key covariates. Methods This retrospective cohort study investigated the impact of serum sodium concentration on arrhythmias in 398 adults with acute STEMI who underwent pPCI. We excluded hypo-/hyperkalemia and abnormal glomerular filtration rate (GFR). Patients were stratified into two groups: Group 1 with plasma sodium level ≤140 mmol/L (n = 279), and Group 2 with plasma sodium level 140 mmol/L (n = 119). Baseline characteristics, including GFR, diabetes mellitus (DM), plasma potassium level, and left ventricular ejection fraction (LVEF), were comparable between the groups. Backward stepwise logistic regression (Wald method) assessed predictors of arrhythmia, adjusting for LVEF, potassium, DM, and sodium groups. Results The analysis showed no statistically significant differences in baseline characteristics between Group 1 and Group 2. Specifically, GFR was 106.1 ± 18.1 vs. 109.8 ± 24.2 mL/min/1.73m² (p = 0.84), potassium 4.16 ± 0.40 vs. 4.15 ± 0.40 mmol/L (p = 0.74), DM prevalence 23.3% vs. 19.3% (p = 0.75), and LVEF was 37.99% ± 7.31 vs. 39.64% ± 7.36 (p = 0.067). The mean serum sodium level was 136.7 ± 3.3 mmol/L in Group 1 and 141± 2.3 mmol/L in Group 2 (p = 0.83). Among the study cohort, 25 cases of arrhythmia (including VT, VF, AF) were identified, representing 6.3% of the total population. However, serum sodium levels were not found to be predictive of in-hospital arrhythmias (OR:1.02, 95% CI: 0.94–1.11, p = 0.62). In contrast, reduced LVEF (OR: 0.95, 95% CI: 0.92–0.98, p = 0.001) and potassium levels (OR: 1.89, 95% CI: 1.12–3.20, p = 0.017) emerged as significant predictors of arrhythmic events. Conclusion In this cohort of STEMI patients treated with primary PCI, serum sodium concentration did not independently influence the incidence of in-hospital arrhythmias. These findings suggest that serum sodium concentration (≤140 vs. 140 mmol/L) may not have a clinically significant impact on arrhythmogenesis in acute STEMI.
Hayrapetyan et al. (Mon,) conducted a cohort in Acute STEMI (n=398). Serum sodium concentration ≤140 mmol/L vs. Serum sodium concentration >140 mmol/L was evaluated on In-hospital arrhythmias (ventricular tachycardia, ventricular fibrillation, and atrial fibrillation) (OR 1.02, 95% CI 0.94-1.11, p=0.62). In adults with acute STEMI treated with primary PCI, serum sodium concentration did not independently predict in-hospital arrhythmias (OR 1.02; 95% CI 0.94-1.11; p=0.62).