Ongoing Statin Therapy Lowers Risk for Delirium in ICU

Abstract

Statins are not only lipid lowering drugs by inhibiting the hydroxy-methyl-glutaryl-CoA (HMG-CoA) reductase enzyme, the rate limiting enzyme in cholesterol biosynthesis,Statins also have diverse effects on the cellular mediatorsof inflammation that may be partially responsible for their efficacy in preventing neuroinflammatorydiseases , statins have potential anti-inflammatory effects which is interpreted through reducing plasma levels of inflammatory markers.(Pasterkamp & Lammeren,2010).

Desirable pharmacologic characteristics of a statin include selectivity of effect or uptake in hepatic cells to increase inhibitory activity and reduce activity in non-hepatic cells, lower systemic bioavailability to minimize systemic adverse effects, prolonged elimination half-life, and absence of or minimal metabolism via the CYP 3A4 system (Beaird.2000).

The pathophysiologic mechanisms of delirium remains elusive despite improved diagnosis and potential treatments. Thereare however numerous hypotheses and it seems likely that delirium pathophysiology is multifactorial. Several theories have been proposed to explain the pathophysiologyof delirium, the focus here is on the following six components: (1) neuroanatomic correlates of delirium, (2) sedatives and analgesics, (3) sepsis, (4) biomarkers and neurotransmitters, (5) surgical factors and postoperative cognitive dysfunction (POCD), and (6) future directions such as molecular genetics.Advances in the understanding of how these mechanisms impact brain function appear to be promising for the prevention of ICU delirium and its long-term neurologic sequelae. (Girard et al.,2008).