| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3002018 | Nutrition, Metabolism and Cardiovascular Diseases | 2011 | 8 Pages |
Background and AimsNeurohormonal activation and inflammation characterizes heart failure, relates to outcome, and is a therapeutic target.The aim of this study was to evaluate the effects of high-dose furosemide plus small-volume hypertonic saline solutions (HSS) on natriuretic peptides and immuno-inflammatory marker levels and to analyze, after treatment, the response to acute saline loading.Methods and Results120 patients with heart failure treated with high-dose furosemide + HSS (Furosemide/HSS group) were matched with: 30 subjects with heart failure treated with high-dose furosemide (furosemide group), 30 controls with asymptomatic left-ventricular dysfunction (ALVD) (asymptomatic group) and 30 controls without heart failure or ALVD (Healthy group). We evaluated plasma levels of natriuretic peptides and cytokine levels in baseline, after treatment and after acute saline load.After treatment with high-dose furosemide + HSS compared to treatment with furosemide alone we observed a significant lowering of ANP [96 (46.5–159.5) pg/ml vs 64 (21–150) pg/ml], BNP [215.5 (80.5–487) pg/ml vs 87 (66–141.5) pg/ml], TNF-α [389.5 (265–615.5) pg/ml vs 231.5 (156–373.5) pg/ml], IL-1β [8 (7–9) pg/ml vs 4 (3–7) pg/ml], IL-6 [5 (3–7.5) pg/ml vs 3 (2–4) pg/ml], plasma values and after an acute saline load, a lower percentage change of ANP (+18.6% vs +28.03% vs +25% vs +29%), BNP (+14.5% vs +29.2% vs +30% vs +29.6%) TNF-α (+10.8% vs +15.8% vs +17.8% vs +11.3%), IL-1β (+20% vs 34.4% vs 40% vs 34.4%) compared to control groups.ConclusionsTreatment with HSS could be responsible for a stretching relief that could influence natriuretic and immuno-inflammatory markers.
