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Mechanism of Statin-Associated Mortality Reduction in COPDResponse FREE TO VIEW

John R. Hurst, MD; Gerry Hagan, MD; Jadwiga A. Wedzicha
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Affiliations: Academic Unit of Respiratory Medicine, University College, London, UK,  GlaxoSmithKline, Greenford, UK,  Academic Unit of Respiratory Medicine, University College, London, UK,  Lovelace Respiratory Research Unit, Albuquerque, NM

Correspondence to: John R. Hurst, MD, Academic Unit of Respiratory Medicine, University College, London, UK; e-mail: jrhurst@lineone.net



Chest. 2007;132(4):1409-1410. doi:10.1378/chest.07-1435
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We read with interest the article by Frost et al (April 2007)1reporting reduced mortality in COPD patients prescribed statins. The antiinflammatory properties of these drugs hold exciting promise in respiratory disease, especially COPD, in which there is heightened systemic inflammation associated with increased cardiovascular morbidity.2There are currently no randomized trials of statins in COPD, and the mechanism underlying any mortality benefit remains unexplained. We recently performed a study3 of systemic biomarkers in patients with COPD, and have now analyzed these data with respect to the presence of cardiovascular disease (CVD) and prescription of statins on plasma interleukin (IL)-6 and C-reactive protein (CRP).

Plasma biomarkers were assayed in samples from 90 patients with stable COPD (mean age, 70.1 years [SD, 8.2 years]; median FEV1, 1.00 L (range, 0.74 to 1.33 L); median FEV1, 43.9% of predicted (range, 27.5 to 56.8% of predicted).3 Self-reported CVD (angina, myocardial infarction, cerebrovascular disease, and/or peripheral vascular disease) and prescription of statins were recorded at clinic visits within 6 months of the samples (available in 87 of 90 patients).

Sixteen patients (18%) had CVD, of whom 7 patients (44%) were receiving statins. Of the 71 patients (82%) without CVD, 12 patients (17%) were receiving statins. Age, FEV1, exacerbation frequency, and inhaled steroid dose did not vary between patients with and without CVD, or who were and were not prescribed statins.

As expected, in COPD patients not receiving statins, those with CVD had a higher plasma IL-6 concentration than those without CVD: median, 3.02 pg/mL vs 1.49 pg/mL (p = 0.022). Furthermore, patients with COPD and CVD who were prescribed statins had lower plasma IL-6 concentrations than those not receiving these drugs: 1.43 pg/mL vs 3.02 pg/mL (p = 0.031). However, plasma IL-6 concentrations were not significantly different in COPD patients without CVD in the presence or absence of statins: 1.11 pg/mL vs 1.49 pg/mL (p = 0.187). There were no differences with respect to CRP.

In conclusion, while statins were associated with reduced plasma IL-6 concentration in patients with COPD and comorbid CVD, this may not be true in patients without CVD. This observation may be important in the interpretation of clinical trials of statins in patients with COPD.

Dr. Hurst has no conflict of interest to declare. Dr. Hagan is employed by GlaxoSmithKline. Dr. Wedzicha has received honoraria and research funding from GlaxoSmithKline.

The author has no conflict of interest to disclose.

Frost, FJ, Petersen, H, Tollestrup, K, et al (2007) Influenza and COPD mortality protection as pleiotropic, dose-dependent effects of statins.Chest131,1006-1012. [PubMed] [CrossRef]
 
Hothersall, E, McSharry, C, Thomson, NC, et al Potential therapeutic role for statins in respiratory disease.Thorax2006;61,729-734. [PubMed]
 
Hurst, JR, Donaldson, GC, Perera, WR, et al Use of plasma biomarkers at exacerbation of chronic obstructive pulmonary disease.Am J Respir Crit Care Med2006;174,867-874. [PubMed]
 
To the Editor:

We very much appreciate the additional data presented by Hurst et al that may be relevant to our previously published article.1 They present a very interesting hypothesis that should be testable. We found no evidence of reduced influenza-related morbidity among statin users, even though there was a reduced risk of death. We did not, however, stratify by whether the patients had preexisting cardiovascular disease (CVD). We are currently evaluating whether statin users and nonusers have similar comorbidities and mortality risks prior to initiation of statin therapy. Using these additional data, we may be able to examine whether people with or without a history of diagnosed CVD were differentially affected by statin therapy, as suggested by Hurst et al. Unfortunately, perhaps because statins are used to reduce CVD risks, statin users commonly have CVD comorbidities.

References
Frost, FJ, Petersen, H, Tollestrup, K, et al Influenza and COPD mortality protection as pleiotropic, dose-dependent effects of statins.Chest2007;131,1006-1012. [PubMed] [CrossRef]
 

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References

Frost, FJ, Petersen, H, Tollestrup, K, et al (2007) Influenza and COPD mortality protection as pleiotropic, dose-dependent effects of statins.Chest131,1006-1012. [PubMed] [CrossRef]
 
Hothersall, E, McSharry, C, Thomson, NC, et al Potential therapeutic role for statins in respiratory disease.Thorax2006;61,729-734. [PubMed]
 
Hurst, JR, Donaldson, GC, Perera, WR, et al Use of plasma biomarkers at exacerbation of chronic obstructive pulmonary disease.Am J Respir Crit Care Med2006;174,867-874. [PubMed]
 
Frost, FJ, Petersen, H, Tollestrup, K, et al Influenza and COPD mortality protection as pleiotropic, dose-dependent effects of statins.Chest2007;131,1006-1012. [PubMed] [CrossRef]
 
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