Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to dissemintate knowledge & skills of Acute Cardiovascular Care
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
ESC Councils goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Mariell Jessup,
Presenter | see Discussant report
Marco , FESC (Italy)
List of Authors: Metra M, O’Connor C, Massie B, Cotter G, Weatherley B, Dittrich H, Teerlink J, Bloomfield D. Ponikowski P. The PROTECT Executive Committee. Abstract: Background: Patients hospitalized with acute decompensated heart failure (ADHF) often develop worsening renal function (WRF) and reduced diuretic response during their treatment. This clinical problem is associated with longer hospital stays and worse inpatient and post-discharge clinical outcomes. Recent studies have demonstrated that treatment with selective adenosine A1 antagonists (A1RA) can both enhance diuresis and prevent WRF. We hypothesized that early treatment with the A1RA, rolofylline, would facilitate early clinical improvement and reduce the risk of WRF and also reduce the rate of post-discharge death and readmissions for cardiovascular and renal causes. Methods: PROTECT was a multicenter, randomized (rolofylline vs placebo in a 2:1 ratio), double-blind, placebo-controlled trial in patients hospitalized for ADHF manifest by dyspnea at rest and signs of volume overload requiring iv loop diuretic therapy, Patients were anticipated to require ongoing IV furosemide ≥40 mg/day for at least 24 hours after enrollment and had to have impaired renal function (estimated creatinine clearance 20-80 mls/min). Additionally, patients were required to have a BNP level ≥500 pg/ml or NT-proBNP ≥2000 pg/ml. Key exclusions were ongoing or planned IV vasoactive therapy (except for nitrates), mechanical/circulatory support, ultrafiltration, dialysis, acute coronary syndromes within 2 weeks, severe cardiac valve stenosis or high risk for seizures (a known adverse effect of A1RA). Randomization was to occur within 24 hours and rolofylline 30 mg/day IV or matching placebo was infused shortly thereafter for 4 hours/day for up to 3 days. The primary endpoint was a 3 category ordered outcome of treatment success, lack of change, or treatment failure, assessed through Day 7 or discharge. Treatment success was defined as moderate to marked improvement in dyspnea at both 24 and 48 hours after randomisation in the absence of treatment failure. Treatment failure included any of the following: death or readmission for HF through Day 7, worsening symptoms and/or signs of HF after Day 2 through 7 or discharge with the need for rescue therapy, persistent renal impairment (SCr increase ≥0.3 mg/dL through Day 7 confirmed at Day 14, or initiation of hemofiltration or dialysis through Day 7). Secondary endpoints included time to death or rehospitalization for cardiovascular or renal causes through Day 60 and the proportion of patients with persistent renal impairment (SCr increase ≥0.3 mg/dL from randomization to Day 7, confirmed at Day 14, initiation of hemofiltration or dialysis, or death up to day 7). Results: Patients (n=2033) were randomized between May 2, 2007 and January 23, 2009 at 173 sites in North America, Argentina, Israel, Europe, and Russia to rolofylline (n=1356) and placebo (n=677). For the primary endpoint (Table 1), rolofylline was associated with more successes than placebo, but also more failure (odds ratio versus placebo 0.92, 95%CI 0.78, 1.09, p=0.348). The secondary composite endpoint of death or cardiovascular or renal hospitalization occurred in 30.7% of rolofylline patients ( 25.7% were hospitalized and 8.9% died) and 31.9% of placebo patients (25.6% were hospitalized and 9.5% died), yielding a time to first event hazard ratio of 0.98, 95% CI 0.83-1.17, p=0.86). Rolofylline did not reduce the incidence of renal impairment compared to placebo (15.0% vs 13.7%, respectively, odds ratio versus placebo 1.11, 95% CI 0.85, 1.46; p = 0.44). The number of patients experiencing one or more AE was similar between rolofylline (62.9%) and placebo (61.4%). However, more patients on rolofylline experienced nervous system disorders, with 11 patients (0.8%) experiencing seizure and 16 patients (1.2%) experiencing stroke on rolofylline, with no patients experiencing seizure and 3 patients (0.5%) experiencing stroke on placebo.
Conclusions: The primary efficacy endpoint of the study, that rolofylline 30 mg would provide a favorable shift in the distribution of the primary endpoint of success, unchanged, and failure compared to placebo was not met. Nor were either of the two key secondary efficacy endpoints met. The overall safety profiles of the placebo and rolofylline groups were similar. No increase in cardiac AEs were seen. However, treatment with rolofylline 30 mg was associated with a higher incidence of seizures and a trend towards more strokes.
Discussant | see Presenter abstract
Mariell Jessup, FESC (United States of America)
Effects of Rolofylline in Patients with Acute Heart Failure Syndrome and Renal Impairment: Findings from the PROTECT- Study
This congress report accompanies a presentation given at the ESC Congress 2009. Written by the author himself/herself, this report does not necessarily reflect the opinion of the European Society of Cardiology.
© 2016 European Society of Cardiology. All rights reserved