Biblioteca
Results of a non-specific immunomodulation therapy in chronic heart failure (ACCLAIM trial): a placebo-controlled randomised trial
Resultados de uma terapia imunomodulatória não específica em falência artertial crônica: um estudo controlado randomisado
OBS da ABOZ: este estudo utiliza auto-hemoterapia menor com ozônio, ver pagina 3 : "The blood sample was exposed to oxygen/ozone gas mixture (ozone concentration of 15·35 g/m³)".
Background: Evidence suggests that inflammatory mediators contribute to development and progression of chronic heart failure. We therefore tested the hypothesis that immunomodulation might counteract this pathophysiological mechanism in patients.
Methods: We did a double-blind, placebo-controlled study of a device-based non-specifi c immunomodulation therapy (IMT) in patients with New York Heart Association (NYHA) functional class II–IV chronic heart failure, left ventricular (LV) systolic dysfunction, and hospitalisation for heart failure or intravenous drug therapy in an outpatient setting within the past 12 months. Patients were randomly assigned to receive IMT (n=1213) or placebo (n=1213) by intragluteal injection on days 1, 2, 14, and every 28 days thereafter. Primary endpoint was the composite of time to death from any cause or fi rst hospitalisation for cardiovascular reasons. The study continued until 828 primary endpoint events had accrued and all study patients had been treated for at least 22 weeks. Analysis was by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00111969.
Findings: During a mean follow-up of 10·2 months, there were 399 primary events in the IMT group and 429 in the placebo group (hazard ratio 0·92; 95% CI 0·80–1·05; p=0·22). In two prespecifi ed subgroups of patients—those with no history of previous myocardial infarction (n=919) and those with NYHA II heart failure (n=689)—IMT was associated with a 26% (0·74; 0·57–0·95; p=0·02) and a 39% (0·61; 95% CI 0·46–0·80; p=0·0003) reduction in the risk of primary endpoint events, respectively.
Interpretation: Non-specifi c immunomodulation may have a role as a potential treatment for a large segment of the heart failure population, which includes patients without a history of myocardial infarction (irrespective of their functional NYHA class) and patients within NYHA class II.
Background: Evidence suggests that inflammatory mediators contribute to development and progression of chronic heart failure. We therefore tested the hypothesis that immunomodulation might counteract this pathophysiological mechanism in patients.
Methods: We did a double-blind, placebo-controlled study of a device-based non-specifi c immunomodulation therapy (IMT) in patients with New York Heart Association (NYHA) functional class II–IV chronic heart failure, left ventricular (LV) systolic dysfunction, and hospitalisation for heart failure or intravenous drug therapy in an outpatient setting within the past 12 months. Patients were randomly assigned to receive IMT (n=1213) or placebo (n=1213) by intragluteal injection on days 1, 2, 14, and every 28 days thereafter. Primary endpoint was the composite of time to death from any cause or fi rst hospitalisation for cardiovascular reasons. The study continued until 828 primary endpoint events had accrued and all study patients had been treated for at least 22 weeks. Analysis was by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00111969.
Findings: During a mean follow-up of 10·2 months, there were 399 primary events in the IMT group and 429 in the placebo group (hazard ratio 0·92; 95% CI 0·80–1·05; p=0·22). In two prespecifi ed subgroups of patients—those with no history of previous myocardial infarction (n=919) and those with NYHA II heart failure (n=689)—IMT was associated with a 26% (0·74; 0·57–0·95; p=0·02) and a 39% (0·61; 95% CI 0·46–0·80; p=0·0003) reduction in the risk of primary endpoint events, respectively.
Interpretation: Non-specifi c immunomodulation may have a role as a potential treatment for a large segment of the heart failure population, which includes patients without a history of myocardial infarction (irrespective of their functional NYHA class) and patients within NYHA class II.
Download
Autor: Guillermo Torre-Amione, Stefan D Anker, Robert C Bourge, Wilson S Colucci, Barry H Greenberg, Per Hildebrandt, Andre Keren, Michael Motro, Lemuel A Moyé, Jan Erik Otterstad, Craig M Pratt, Piotr Ponikowski, Jean Lucien Rouleau, Francois Sestier, Bern
Revista: Lancet