6533b7d7fe1ef96bd126863e

RESEARCH PRODUCT

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

Rossella IatrinoPietro Di PasqualeMauro CardilloGaspare ParrinelloUmberto LupoDaniele TorresSalvatore GiambancoCaterina SchimmentiSalvatore PaternaCarla MontainaRossella Petrantoni

subject

Malemedicine.medical_specialtySettore MED/09 - Medicina InternaHemodynamicsRenal functionDouble-Blind MethodFurosemideInternal medicineTroponin INatriuretic Peptide BrainmedicineElectric ImpedanceHumansPulmonary wedge pressureDiureticsAgedAged 80 and overHeart FailureSaline Solution Hypertonicbusiness.industryTroponin IFurosemideTRoponin I Heart Failure Hypertonic saline furosemideMiddle AgedBrain natriuretic peptidemedicine.diseaseSurgeryEchocardiography Doppler ColorHeart failureCardiologyPotassiumAdministration IntravenousDrug Therapy CombinationFemaleCardiology and Cardiovascular MedicinebusinessBioelectrical impedance analysismedicine.drug

description

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 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 the achievement of improved hemodynamic compensation at echocardiography and body hydration normalization

yearjournalcountryeditionlanguage
2012-09-01
10.1016/j.ahj.2012.05.025http://hdl.handle.net/10447/66423