Key result
Higher admission serum sodium shows no independent association with mortality after adjusting for shock severity.
Why the study?
Does admission serum sodium level predict all-cause mortality in patients with cardiogenic shock complicated by acute myocardial infarction?
Cohort (n=312)
No
Does admission serum sodium level predict all-cause mortality in patients with cardiogenic shock complicated by acute myocardial infarction?
Hazard Ratio: 1.02 (95% CI 0.98–1.06)
p-value: p=0.46
Admission serum sodium is an early integrative marker of shock severity in AMI-CS, but its association with mortality is largely explained by concurrent hyperlactatemia rather than being an independent predictor.
Admission sodium should not guide prognosis in AMI-CS; leaves open whether it adds value beyond lactate in prospective models.
Background: Serum sodium is an important laboratory value in hospitalized patients, but its relationship with mortality in patients with cardiogenic shock complicated by acute myocardial infarction (AMI-CS) has not been evaluated. We assessed the association between admission serum sodium and mortality in AMI-CS. Methods: A total of 312 patients with AMI-CS treated at a single center were retrospectively enrolled in this study. The primary endpoint was all-cause mortality. Patients were divided into three groups by tertiles based on admission serum sodium levels. The prognostic value of admission serum sodium levels was evaluated using Kaplan–Meier survival curves and Cox regression. Restricted cubic splines, subgroup analyses, and sensitivity analyses were also performed. Results: Over a follow-up of 4.5 years, 51.9% of enrolled patients died. In unadjusted analyses, higher admission serum sodium was associated with mortality, as well as rates of sepsis, dialysis, and brain injury during hospitalization, and patients with sodium > 141.2 mmol/L had higher short-term mortality; a J-shaped relationship was observed on unadjusted spline analysis. However, this association did not persist after adjustment for shock severity: the fully adjusted hazard ratio per 1 mmol/L was 1.02 (95% CI 0.98–1.06, p = 0.46) for long-term and 1.03 (95% CI 0.98–1.07, p = 0.28) for 30-day mortality, and the spline association was no longer significant (p for overall association = 0.40; p for nonlinearity = 0.33). Adding severity variables one at a time showed that the association was abolished specifically by arterial lactate. Conclusions: Higher admission serum sodium is associated with mortality in AMI-CS, but this association is largely explained by concurrent shock severity, particularly hyperlactatemia. Admission sodium may serve as an early, readily available integrative marker of shock severity for risk stratification, but whether sodium-directed treatment strategies affect outcomes requires prospective study.
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Wang et al. (2026) conducted a cohort in Cardiogenic shock complicated by acute myocardial infarction (AMI-CS) (n=312). Admission serum sodium vs. Lower admission serum sodium was evaluated on All-cause mortality (HR 1.02, 95% CI 0.98-1.06, p=0.46). Higher admission serum sodium was associated with mortality in unadjusted analyses, but this association was abolished after adjusting for shock severity, particularly arterial lactate (fully adjusted HR 1.02).
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