PubMed · 13775055
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P J TALSO. 1961. Recent developments in diuretics.. https://pubmed.ncbi.nlm.nih.gov/13775055/
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Hyponatremia has been identified as a risk factor for increased morbidity and mortality in patients with congestive heart failure (CHF) and other edematous disorders and can lead to severe neurologic derangements. Low cardiac output and blood pressure associated with CHF triggers a compensatory response by the body that activates several neurohormonal systems designed to preserve arterial blood volume and pressure. Hyponatremia in patients with CHF is primarily caused by increased activity of arginine vasopressin (AVP). AVP increases free-water reabsorption in the renal collecting ducts, increasing blood volume and diluting plasma sodium concentrations. Hyponatremia may also be triggered by diuretic therapy used in the management of symptoms of CHF. Hyponatremic disorders occur when the normal ratio of solutes to body water content is altered by parallel changes in serum sodium and osmolality. Hyponatremia is generally defined as a serum sodium ion concentration <135 to 136 mmol/L and can be broadly categorized into 2 types, dilutional or depletional. Dilutional hyponatremia is the most common form of hyponatremia and is caused by excess water retention. Depletional hyponatremia is usually hypovolemic, with an absolute deficiency of water but a relative excess of body water compared with sodium concentration.
CONTEXT: Nesiritide improves symptoms in patients with acutely decompensated heart failure compared with placebo and appears to be safer than dobutamine. Its short-term safety relative to standard diuretic and vasodilator therapies is less clear. OBJECTIVE: To investigate the safety of nesiritide relative to noninotrope-based control therapies, primarily consisting of diuretics or vasodilators. DATA SOURCES: Primary reports of completed clinical trials as of December 2004 were obtained from the US Food and Drug Administration (FDA), the study sponsor (Scios Inc), a PubMed literature search using the terms nesiritide, clinical trials, and humans, and a manual search of annual meetings of 3 heart associations. STUDY SELECTION: Of 12 randomized controlled trials evaluating nesiritide, 3 met all inclusion criteria: randomized double-blind study of patients with acutely decompensated heart failure, therapy administered as single infusion (> or =6 hours), inotrope not mandated as control, and reported 30-day mortality. DATA EXTRACTION: Data were extracted from FDA and sponsor documents and corroborated with published articles when available. Thirty-day survival was assessed by meta-analysis using a fixed-effects model and time-dependent risk by Kaplan-Meier analysis with Cox proportional hazards regression modeling. Where deaths were described within a range of days after treatment, an extreme assumption was made favoring nesiritide over control therapy, an approach relevant to the time-dependent analyses. DATA SYNTHESIS: In the 3 trials, 485 patients were randomized to nesiritide and 377 to control therapy. Death within 30 days tended to occur more often among patients randomized to nesiritide therapy (35 [7.2%] of 485 vs 15 [4.0%] of 377 patients; risk ratio from meta-analysis, 1.74; 95% confidence interval [CI], 0.97-3.12; P = .059; and hazard ratio after adjusting for study, 1.80; 95% CI, 0.98-3.31; P = .057). CONCLUSIONS: Compared with noninotrope-based control therapy, nesiritide may be associated with an increased risk of death after treatment for acutely decompensated heart failure. The possibility of an increased risk of death should be investigated in a large-scale, adequately powered, controlled trial before routine use of nesiritide for acutely decompensated heart failure.
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