As many factors and disfunction of several organs contribute to worsen the clinical situation, heart failure progression can be only slowed down, not prevented, with therapies of proven efficacy.

		Since the prevalent etiology of heart failure is coronary artery disease, preventing heart failure progression may be related to the prevention of coronary artery disease. A post-hoc analysis of the 4S study showed that the use of statins in patients with coronary artery disease, but without heart failure, can prevent the occurrence of congestive heart failure.
		Recent sudies suggest that a statin treatment may have other effects besides cholesterol lowering. It has been hypothesized that the inhibition of HMGCoA reductase not only reduces cholesterol but, limiting the synthesis of mevalonate-derived molecules, interferes with the synthesis of anti-inflammatory components, thus down regulating cytokine and chemokine production, which is activated in patients with heart failure due to any etiology. There are some suggestions indicating that high levels of cholesterol can be beneficial in patients with heart failure on the basis of the ability of serum lipoproteins to modulate inflammatory immune function, since cholesterol-rich lipoproteins can bind and detoxify bacterial lipopolysaccharide (LPS), whose production is increased in heart failure patients (endotoxin-lipoprotein hypothesis). LPS is a very strong stimulator of the release of pro-inflammatory cytokines which promote heart failure progression. Therefore, only a clinical trial can clarify how the two effects of statins, apparently conflicting, may modulate the inflammatory immune function.
		Statin treatment can also improve endothelial function which is largely compromised in patients with heart failure, irrespective of the underlying etiology, and it is considered co-responsible of the multi-organ failure.

In this context of conflicting evidences, only post-hoc, non-randomized, underpowered sub-analyses have been performed. In the ELITE-2 trial a lower mortality rate in patients with heart failure of any etiology treated with statins (non randomized comparison) was shown.
On 897 patients with LV dysfunction/failure enrolled in the statin arm of the GISSI-Prevenzione trial, no safety problems were observed in the patients allocated to pravastatin and the favorable trend in total mortality reduction was similar among patients with and without LV dysfunction/failure.

Results of HPS (Heart Protection Study), presented in November 2001 , show that statins are effective in the secondary prevenction of ischemic events irrespective of cholesterol levels, in patients without heart failure.