Key result
Hyponatremia in ACS is linked to ~11-fold higher 30-day mortality compared to normonatremia.
Why the study?
Simple laboratory markers may support early risk stratification in ACS, and although hyponatremia is linked to adverse cardiovascular outcomes, its prognostic relevance in patients with ACS required clinical evaluation.
Does hyponatremia (serum sodium <135 mmol/L) predict adverse in-hospital outcomes and 30-day mortality compared to normonatremia in patients admitted with acute coronary syndrome?
Cohort (n=75)
No
Does hyponatremia (serum sodium <135 mmol/L) predict adverse in-hospital outcomes and 30-day mortality compared to normonatremia in patients admitted with acute coronary syndrome?
In patients presenting with acute coronary syndrome, hyponatremia (<135 mmol/L) is strongly associated with lower left ventricular ejection fraction, higher clinical severity, increased adverse in-hospital outcomes, and substantially higher 30-day mortality.
High mortality in this small observational cohort merits caution; leaves open hyponatremia's independent prognostic value pending larger prospective studies.
Acute coronary syndrome (ACS) remains an important cause of morbidity and mortality, and simple laboratory markers that identify patients at increased risk may support early clinical risk stratification. Hyponatremia has been associated with neurohormonal activation and adverse outcomes in cardiovascular disease, but its prognostic relevance in patients with ACS requires evaluation in the clinical setting. This prospective single-centre study included 75 patients admitted with ACS to the intensive care unit of Government Royapettah Hospital, Chennai, between April and September 2016. Patients presenting within 12 hours of symptom onset with electrocardiographic evidence of ST-elevation myocardial infarction, non-ST-elevation myocardial infarction, or unstable angina were enrolled. Patients with previous coronary artery disease, arrhythmias, cardiomyopathy or heart failure, previous diuretic use, cirrhosis, hypothyroidism, renal disease, marked renal dysfunction, or refusal to participate were excluded. Serum sodium was measured at admission, 48 hours, and discharge, with sodium <135 mmol/L defining hyponatremia. Patients were followed weekly for 30 days for morbidity and mortality. Nine patients (12.0%) were hyponatremic and 66 (88.0%) were normonatremic. Mean ejection fraction was lower in the hyponatremic group (46.67±7.70%) than in the normonatremic group (53.77±9.96%; p=0.0436), while serum sodium remained significantly lower at all three assessment points (p<0.0001 for each comparison). Killip class also differed significantly between groups (p=0.0461). Adverse in-hospital outcome occurred in 44.44% of hyponatremic patients compared with 10.61% of normonatremic patients (p=0.0071). Thirty-day mortality was 66.67% and 6.06%, respectively (p<0.0001). The reported logistic regression model identified admission, 48-hour, and discharge hyponatremia as significant predictors of mortality. In this cohort, hyponatremia was associated with lower ventricular systolic function, higher clinical severity, adverse in-hospital outcome, and substantially higher 30-day mortality. Serum sodium may therefore provide an accessible prognostic marker in ACS, although confirmation in larger multicentre cohorts is required.
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Mishra et al. (2026) conducted a cohort in Acute coronary syndrome (n=75). Hyponatremia (serum sodium <135 mmol/L) vs. Normonatremia (serum sodium >=135 mmol/L) was evaluated on 30-day mortality (p=<0.0001). Hyponatremia in acute coronary syndrome was associated with higher 30-day mortality (66.67% vs 6.06%; p<0.0001) and adverse in-hospital outcomes (44.44% vs 10.61%; p=0.0071) compared to normonatremia.
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