Background: Chronic inflammation and immune system activation underlie a variety of seemingly
unrelated cardiac conditions including not only atherosclerosis and the subsequent coronary artery disease but
also peripheral artery disease, hypertension with target organ damage and heart failure. The beneficial effects of
HMG-CoA reductase inhibitors or statins are mainly attributed to their ability to inhibit hepatic cholesterol biosynthesis.
Beyond their lipid lowering activity, ample evidence exists in support of their potent anti-inflammatory
properties which initiate from the inhibition of GTPase isoprenylation, activating a cataract of secondary pathways
and extend to the inhibition and blocking of immune cell activation and interaction.
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Objective: To summarize the anti-inflammatory mechanisms of statins in clinical and experimental settings in
cardiovascular disease.
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Methods: A systematic search of PubMed and the Cochrane Database was conducted in order to identify the
majority of trials, studies, current guidelines and novel articles related to the subject.
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Results: In vitro, statins have immuno-modulatory and anti-inflammatory effects, and they can exert antiatherosclerotic
effects independently of their hypolipidemic actions. In addition, positive results have emerged
from mechanistic and experimental studies on the active role of HMG-CoA reductase inhibitors in HF. By extrapolating
those data in clinical setting, we further understand how HMG-CoA reductase inhibitors can beneficially
affect not only systolic but also diastolic HF.
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Conclusion: In this review article, we present the basic pathophysiologic data supporting the anti-inflammatory
actions of statins in clinical and experimental settings and we link these mechanisms with confirmatory clinical
data on the potent non lipid lowering effects of HMG-CoA reductase inhibitors.
MEVALONIC ACIDURIA: IMPAIRED UBIQUINON BIOSYNTHESIS AND MODEL FOR SIDE EFFECTS OF HMG-COA REDUCTASE INHIBITORS
