PURPOSE: Numerous multicenter inpatient and outpatient registries have shown low serum sodium to be a poor prognostic indicator with respect to all cause mortality in congestive heart failure (CHF) patients. The purpose of this study is to replicate this finding in an outpatient population consisting largely of indigent African-American CHF patients on maximal combined ACE-I and beta-blocker therapy.
METHODS: 1037 consecutive outpatients with CHF were enrolled in the study. Of these patients, 364 had baseline serum sodium measured. All 364 patients presented with EF<40%. The mean NYHA functional class was 2.12 (+/− 0.845), and the mean percent ejection fraction was 29.5 (+/− 9.1). The patient population had an average mean serum sodium of 138.2 with a range of 120 to 156. In a prospective analysis, we evaluated the relationship between hyponatremia (defined as <135 mEq/L) and all cause mortality after enrollment. Of the 364 enrollees with baseline serum sodium, 48 (13%) had hyponatremia.
RESULTS: At 40 months follow-up, 8 patients in the hyponatremia group compared to 31 in the normonatremic group died (Odds ratio = 1.84 with 95% CI 0.790–4.279, p = .15). However, results of Kaplan Meier analyses indicated there were no significant differences in mortality between the hyponatremia and normonatremic groups (log rank test = 0.39).
CONCLUSION: The relationship between baseline serum sodium and all cause mortality did not reach significance. Low baseline serum sodium did not predict mortality in an indigent largely African-American population on maximal ACE-I and beta-blocker therapy.
CLINICAL IMPLICATIONS: This was the first study that looked at the predictive value of sodium in an extremely well-managed ambulatory CHF population with a significant number of African-American patients. While our results need to be duplicated, the study suggests that low serum sodium as a marker of mortality in CHF patients may not generalize to predominately African-American populations on high dose medical therapy. This finding, if validated by subsequent studies, could be of prognostic value and therapeutic importance.
DISCLOSURE: Andrew DeWolfe, No Financial Disclosure Information; No Product/Research Disclosure Information