Troponin I release after intravenous treatment with high furosemide doses plus
hypertonic saline solution in decompensated heart failure trial (Tra-HSS-Fur).
Author(s): Parrinello G(1), Di Pasquale P, Torres D, Cardillo M, Schimmenti C, Lupo U,
Iatrino R, Petrantoni R, Montaina C, Giambanco S, Paterna S.
Affiliation(s): Author information:
(1)Department of Internal and Specialty Medicine, Chair of Clinical
Pathophysiology, University of Palermo, Italy. gaspare.parrinello@unipa.it
Publication date & source: 2012, Am Heart J. , 164(3):351-7
BACKGROUND: High values of cardiac troponin in acute decompensated congestive
heart failure (ADHF) identify patients at higher risk and worsened prognosis. A
cardiac troponin increase during therapy indicates the need for more appropriate
intervention, aimed at compensating cardiac disease and effectively minimizing
myocardial wall stress and subsequent cytolysis. This study evaluated the effects
of an intravenous high dose of furosemide with (group A) or without small volume
hypertonic 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 randomly assigned to group A or B. Plasma levels of cardiac
troponin-I, brain natriuretic peptide, glomerular filtration rate by Modification
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 renal function, hydration state, pulmonary
capillary wedge pressure (P < .0001), end diastolic volume (P < .01), ejection
fraction (P < .01), and dP/dt (P < .004) in group A. We also observed a
significant reduction in body weight (64.4 vs 75.8 kg) (P < .001), cardiac
troponin I (0.02 vs 0.31 ng/mL) (P < .0001) and brain natriuretic peptide (542 vs
1,284 pg/mL) (P < .0001), and hospitalization time (6.25 vs 10.2 days) (P <
.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 the
achievement of improved hemodynamic compensation at echocardiography and body
hydration normalization.
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