Troponin I release after intravenous treatment with high furosemide doses plus hypertonic saline solution in decompensated heart failure trial (Tra-HSS-Fur)

Background High values of cardiac troponin in acute decompensated congestive heart failure (ADHF) identify patientsat higher risk and worsened prognosis. A cardiac troponin increase during therapy indicates the need for more appropriateintervention, aimed at compensating cardiac disease and effectively minimizing myocardial wall stress and subsequentcytolysis. This study evaluated the effects of an intravenous high dose of furosemide with (group A) or without small volumehypertonic saline solution (HSS) (group B) on myocardial cytolysis in patients with ADHF.Methods A total of 248 consecutive patients with ADHF (148 men, mean age 74.9 ± 10.9 years) were randomlyassigned to group A or B. Plasma levels of cardiac troponin-I, brain natriuretic peptide, glomerular filtration rate byModification of Diet in Renal Disease formula, bioelectrical impedance analysis measurements, and delta pressure/delta time(dP/dt) rate were observed on admission and discharge for all patients.Results We observed a significant reduction of cardiac troponin in both groups and a significant improvement in renalfunction, hydration state, pulmonary capillary wedge pressure (P b .0001), end diastolic volume (P b .01), ejection fraction(P b .01), and dP/dt (P b .004) in group A. We also observed a significant reduction in body weight (64.4 vs 75.8 kg)(P b .001), cardiac troponin I (0.02 vs 0.31 ng/mL) (P b .0001) and brain natriuretic peptide (542 vs 1,284 pg/mL) (P b .0001),and hospitalization time (6.25 vs 10.2 days) (P b .0001) in the HSS group.Conclusions These data demonstrate that intravenous high doses of furosemide do not increase myocardial injury and,in addition, when associated to HSS, significantly reduce cardiac troponin I release. This behavior is mirrored by theachievement of improved hemodynamic compensation at echocardiography and body hydration normalization