OBJECTIVE:To identify predictors of low cardiac output and mortality in decompensated heart failure.INTRODUCTION:Introduction: Patients with decompensated heart failure have a high mortality rate, especially those patients with low cardiac output. However, this clinical presentation is uncommon, and its management is controversial.METHODS:We studied a cohort of 452 patients hospitalized with decompensated heart failure with an ejection fraction of <0.45. Patients underwent clinical‐hemodynamic assessment and Chagas disease immunoenzymatic assay. Low cardiac output was defined according to L and C clinical‐hemodynamic profiles. Multivariate analyses assessed clinical outcomes. P<0.05 was considered significant.RESULTS:The mean age was 60.1 years; 245 (54.2%) patients were >60 years, and 64.6% were men. Low cardiac output was present in 281 (63%) patients on admission. Chagas disease was the cause of heart failure in 92 (20.4%) patients who had higher B type natriuretic peptide levels (1,978.38 vs. 1,697.64 pg/mL; P = 0.015). Predictors of low cardiac output were Chagas disease (RR: 3.655, P<0.001), lower ejection fraction (RR: 2.414, P<0.001), hyponatremia (RR: 1.618, P = 0.036), and renal dysfunction (RR: 1.916, P = 0.007). Elderly patients were inversely associated with low cardiac output (RR: 0.436, P = 0.001). Predictors of mortality were Chagas disease (RR: 2.286, P<0.001), ischemic etiology (RR: 1.449, P = 0.035), and low cardiac output (RR: 1.419, P = 0.047).CONCLUSIONS:In severe decompensated heart failure, predictors of low cardiac output are Chagas disease, lower ejection fraction, hyponatremia, and renal dysfunction. Additionally, Chagas disease patients have higher B type natriuretic peptide levels and a worse prognosis independent of lower ejection fraction.

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OBJECTIVE:We aimed to evaluate angiotensin receptor blocker add-on therapy in patients with low cardiac output during decompensated heart failure.METHODS:We selected patients with decompensated heart failure, low cardiac output, dobutamine dependence, and an ejection fraction <0.45 who were receiving an angiotensin-converting enzyme inhibitor. The patients were randomized to losartan or placebo and underwent invasive hemodynamic and B-type natriuretic peptide measurements at baseline and on the seventh day after intervention. ClinicalTrials.gov: NCT01857999.RESULTS:We studied 10 patients in the losartan group and 11 patients in the placebo group. The patient characteristics were as follows: age 52.7 years, ejection fraction 21.3%, dobutamine infusion 8.5 mcg/kg.min, indexed systemic vascular resistance 1918.0 dynes.sec/cm5.m2, cardiac index 2.8 L/min.m2, and B-type natriuretic peptide 1,403 pg/mL. After 7 days of intervention, there was a 37.4% reduction in the B-type natriuretic peptide levels in the losartan group compared with an 11.9% increase in the placebo group (mean difference, -49.1%; 95% confidence interval: -88.1 to -9.8%, p = 0.018). No significant difference was observed in the hemodynamic measurements.CONCLUSION:Short-term add-on therapy with losartan reduced B-type natriuretic peptide levels in patients hospitalized for decompensated severe heart failure and low cardiac output with inotrope dependence.