Abstract

Furosemide is a drug that has not only a renal effect, but also a vascular one, resulting in decreased left atrial and ventricularfilling pressure accompanied by an increase in venous compliance, all of this with significant effects on central cardiac hemodynamics.In dialysis patients, it is still unclear the efficiency of furosemide, a diuretic drug that inhibits the Na+, K+, 2CL� cotransporter in the renal tubular system. Also, furosemide need to be used at much higher doses because of its pharmacokinetic changes in the context of impaired renal clearance.The aim of our study was to investigate whether furosemide induces changes in cardiovascular hemodynamics in end-stage renal disease (ESRD) patients, using standard echocardiography and Tissue Doppler Imaging (TDI).We foundcorrelations between furosemide useand improved cardiac parameters, assessed by multiple echocardiographic variables, and we consider that furosemide has complementary effects in dialysis patients with residual diuresis.

Highlights

  • Diuretics are often stopped when patients start dialysis

  • Furosemide need to be used at much higher doses because of its pharmacokinetic changes in the context of impaired renal clearance.The aim of our study was to investigate whether furosemide induces changes in cardiovascular hemodynamics in end-stage renal disease (ESRD) patients, using standard echocardiography and Tissue Doppler Imaging (TDI).We foundcorrelations between furosemide useand improved cardiac parameters, assessed by multiple echocardiographic variables, and we consider that furosemide has complementary effects in dialysis patients with residual diuresis

  • Novel Doppler techniques should be able to detect even more subtle changes in cardiac function induced by furosemide [2, 8-11], E-wave velocity reflects the left atrium(LA)-left ventricle(LV) pressure gradient during early diastole filling and is affected by impaired LV relaxation andleft atrial pressure(LAP)[8,9].A-wave velocity reflects the LA-LV pressure gradient during late diastole, and it depends by LV compliance and LA contractile function.Mitral E-velocity deceleration time(DT) is influenced by LV relaxation, LV diastolic pressures after mitral valve opening, and left ventricular stiffness.Isovolumetric relaxation time(IVRT) is prolonged in patients with impaired LV relaxation but normal LV filling pressures

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Summary

Introduction

Diuretics are often stopped when patients start dialysis. Some studies have shown that preserved residual renal function in dialysis patients is associated with bettercardiovascular status and the association between diuretic and preserved residual renal function is still in debating, the clinical and paraclinical benefits offered by furosemide make it valuable in dialysis patients with urine output [1-3].In dialysis patients,even with someresidual diuresis, furosemide has been shown to induce a rapid vascular effect, besides the diuretic effect. A decrease in cardiac preload and filling pressures[1,2,4] Several parameters, such as left ventricular hypertrophy (LVH) and left ventricular (LV) systolic dysfunction, have been identified as independent outcome predictorsin dialysis patients [5-7]. Diastolic heart failure and increased filling pressures in dialysis patients often exists without the presence of significant systolic heart failure, and that may be assessed by Doppler techniques, especially Tissue Doppler Imaging (TDI), that has demonstrated its significant prognostic value for all-cause mortality and cardiovascular death [8-10]. E/E2 ratio was calculated, and significant LV diastolic dysfunction was defined as E/ E’ ≥ 14, septal E’ velocity 34mL/m2 [8,9].E/E’ ratio < 8 isassociated with normal LV filling pressures (PCWP < 15 mmHg), while a ratio > 15 is associated with increased filling pressures (PCWP > 15mmHg) [ 10,12,]. Comparisons between baseline and month measurements were performed using ANOVA with the Turkey post hoc test.Statistical significance was considered if p

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