摘要
The annual meeting of the Heart Failure Association of ESC in Lisbon, in June 2005, was exceptionally successful. There were many very interesting presentations and workshops with the unique rifle： Statins in heart failureCholesterol-lowering is not the only goal. Heart failure （HF） is a progressive disease with coronary artery disease （CAD） as the most often underlying etiology. Treatment to prevent progression of heart failure has been targeted to reverse the consequences of HF and to a less extent the cause - the atherosclerotic plaque itself. On the average 50% of patients with heart failure are treated with lipid intervention. Lipid-lowering treatment with statins clearly reduces morbidity and mortality of patients with documented CAD. Since the prevalent etiology of heart failure is CAD, its prevention may reduce heart failure progression. However, recent studies suggest that pleiotropic effects of statins are more important than the influence related to their cholesterol lowering mechanism. Furthermore it is suggested that low levels of circulating lipoproteins and cholesterol may be independent predictors of impaired outcome in patients with heart failure. There are some possible explanations for this finding. High levels of cholesterol can be beneficial to heart failure patients; cholesterol-rich serum lipoproteins are able to modulate inflammatory immune function because they bind and detoxify bacterial lipopolysaccharide, a very strong stimulator of the release of proinflammatory cytokines that promote heart failure progression and death. So current recommendations strongly emphasize that the aim of treatment of HF is not to lower cholesterol. Cellular ＆ Molecular Immunology. 2005;2（6）：433-437.
The annual meeting of the Heart Failure Association of ESC in Lisbon, in June 2005, was exceptionally successful. There were many very interesting presentations and workshops with the unique rifle： Statins in heart failureCholesterol-lowering is not the only goal. Heart failure （HF） is a progressive disease with coronary artery disease （CAD） as the most often underlying etiology. Treatment to prevent progression of heart failure has been targeted to reverse the consequences of HF and to a less extent the cause - the atherosclerotic plaque itself. On the average 50% of patients with heart failure are treated with lipid intervention. Lipid-lowering treatment with statins clearly reduces morbidity and mortality of patients with documented CAD. Since the prevalent etiology of heart failure is CAD, its prevention may reduce heart failure progression. However, recent studies suggest that pleiotropic effects of statins are more important than the influence related to their cholesterol lowering mechanism. Furthermore it is suggested that low levels of circulating lipoproteins and cholesterol may be independent predictors of impaired outcome in patients with heart failure. There are some possible explanations for this finding. High levels of cholesterol can be beneficial to heart failure patients; cholesterol-rich serum lipoproteins are able to modulate inflammatory immune function because they bind and detoxify bacterial lipopolysaccharide, a very strong stimulator of the release of proinflammatory cytokines that promote heart failure progression and death. So current recommendations strongly emphasize that the aim of treatment of HF is not to lower cholesterol. Cellular ＆ Molecular Immunology. 2005;2（6）：433-437.
