The clinical utility of spirometric screening of asymptomatic smokers for early signs of air flow limitation has recently come under review. The current authors propose that reduced forced expiratory volume in one second (FEV1) is more than a measure of airflow limitation, but a marker of premature death with broad utility in assessing baseline risk of chronic obstructive pulmonary disease (COPD), lung cancer, coronary artery disease and stroke, collectively accounting for 70-80% of premature death in smokers.Reduced FEV1 identifies undiagnosed COPD, has comparable utility to that of serum cholesterol in assessing cardiovascular risk and defines those smokers at greatest risk of lung cancer. As such, reduced FEV1 should be considered a marker that identifies smokers at greatest need of medical intervention.Smoking cessation has been shown to attenuate FEV1 decline and, if achieved before the age of 45-50 yrs, may not only preserve FEV1 within normal values but substantially reduce cardiorespiratory complications of smoking.Recent findings suggest inhaled drugs (bronchodilators and corticosteroids), and possibly statins, may be effective in reducing morbidity and mortality in patients with chronic obstructive pulmonary disease. The current authors propose that spirometry has broad utility in identifying smokers who are at greatest risk of cardiorespiratory complications and greatest benefit from targeted preventive strategies, such as smoking cessation, prioritised screening and effective pharmacotherapy.

Chronic obstructive pulmonary disease (COPD) is characterised by minimally reversible airflow limitation and features of systemic inflammation. Current therapies for COPD have been shown to reduce symptoms and infective exacerbations and to improve quality of life. However, these drugs have little effect on the natural history of the disease (progressive decline in lung function and exercise tolerance) and do not improve mortality. The anti-inflammatory effects of statins on both pulmonary and systemic inflammation through inhibition of guanosine triphosphatase and nuclear factor-kB mediated activation of inflammatory and matrix remodelling pathways could have substantial benefits in patients with COPD due to the following. 1) Inhibition of cytokine production (tumour necrosis factor-a, interleukin (IL)-6 and IL-8) and neutrophil infiltration into the lung; 2) inhibition of the fibrotic activity in the lung leading to small airways fibrosis and irreversible airflow limitation; 3) antioxidant and anti-inflammatory (IL-6 mediated) effects on skeletal muscle; 4) reduced inflammatory response to pulmonary infection; and 5) inhibition of the development (or reversal) of epithelial-mesenchymal transition, a precursor event to lung cancer. This review examines the pleiotropic pharmacological action of statins which inhibit key inflammatory and remodelling pathways in COPD and concludes that statins have considerable potential as adjunct therapy in COPD.

Studies show reduced forced expiratory volume in 1 s (FEV 1

We read with great interest the recent review article by BARNES and CELLI [1] outlining the systemic manifestation of chronic obstructive pulmonary disease (COPD) and the potential benefits of statin therapy in the management of COPD. In this article, the authors propose that statins may have a dual role in reducing pulmonary and systemic inflammation, through inhibition of cell signalling molecules (Ras, Rho and Rac). Attenuation of pulmonary inflammation would result from inhibition of inflammatory cell migration and associated cytokine release into lung tissue. Attenuation of systemic inflammation would result from a reduction in pulmonary inflammation (reduced ''spill over'' into the systemic circulation) and inhibition of interleukin (IL)-6 and C-reactive protein synthesis from the liver and other tissues [2]. We suggest the pharmacological and clinical benefits of statins in COPD [3] may be even greater than described in this review.