Lipopolysaccharide responsiveness is an independent predictor of death in patients with chronic heart failure |
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| Affiliation: | 1. Innovative Clinical Trials, University of Medicine Goettingen, Department of Cardiology and Pneumology, Goettingen, Germany;2. National Heart and Lung Institute, Imperial College London, UK;3. Institute for Experimental Endocrinology, Charité Medical School, Campus Virchow-Klinikum, Berlin, Germany;4. Laboratory for Applied Research on Cardiovascular System, Department of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland;5. Katholisches Klinikum Mainz, Innere Medizin 1, Mainz, Germany;6. Centre for Stroke Research Berlin, Charité — University Medical School, Berlin, Germany;1. Department of Cellular and Molecular Medicine, University of Arizona, 1656 East Mabel Street, Tucson, AZ 85724, USA;2. Department of Anaesthesiology and Operative Intensive Care, University Hospital Mannheim, Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany;1. Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, OH, USA;2. The Institute of Organ Transplantation, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China;1. Center of Translational Medicine, Temple University School of Medicine, Philadelphia, PA, USA;2. Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA, USA;3. Department of Cellular and Molecular Physiology, The Pennsylvania State University College of Medicine, Hershey, PA, USA;4. Cardiovascular Division, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, VA, USA;1. Vanderbilt Center for Arrhythmia Research and Therapeutics, Vanderbilt University School of Medicine, Nashville, TN, USA;2. Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA;3. Department of Cell and Regenerative Biology, School of Medicine and Public Health, University of Wisconsin, Madison, WI, USA |
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| Abstract: | BackgroundThe origin of pro-inflammatory activation in chronic heart failure (HF) remains a matter of debate. Lipopolysaccharide (LPS) may enter the blood stream through the morphologically altered and leaky gut barrier. We hypothesized that lower LPS reactivity would be associated with worse survival as compared to normal or higher LPS reactivity.MethodsLPS responsiveness was studied in 122 patients with chronic HF (mean ± SD: age 67.3 ± 10.3 years, 24 female, New York Heart Association class [NYHA] class: 2.5 ± 0.8, left ventricular ejection fraction [LVEF]: 33.5 ± 12.5%) and 27 control subjects of similar age (63.7 ± 7.7 years, p > 0.05). Reference LPS was added at increasing doses to ex vivo whole blood samples and necrosis factor-α (TNFα) was measured. Patients were subgrouped into good- and poor-responder status according to their potential to react to increasing doses of LPS (delta TNFα secretion). The optimal cut-off value was calculated by receiver–operator characteristic curve (ROC) analysis.ResultsA total of 56 patients with chronic HF died from any cause during follow-up. At 24 months, cumulative mortality was 16.4% (95% confidence interval 16.0–16.7%). The delta TNFα value representing the optimal cut-off for the prediction of mortality was 1522 pg/mL (24 months) with a sensitivity of 49.3% (95% confidence interval 37.2–61.4%) and specificity of 81.5% (95% confidence interval 61.9–93.6%). LPS responder status remained an independent predictor of death after multivariable adjustment (hazard ratio 0.09 for good- vs. poor-responders, 95% confidence interval 0.01–0.67, p < 0.05).ConclusionsLPS responsiveness in patients with chronic HF is an independent predictor of death. |
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