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Editorials |

Clarion Call for Trials Assessing “Cardiopulmonary” Agents To Reduce Morbidity and Mortality in Inflammatory Lung Diseases

G. B. John Mancini, MD
Author and Funding Information

Affiliations: Vancouver, BC, Canada ,  Dr. Mancini is Professor of Medicine, Director of Continuing Medical Education, University of British Columbia, Department of Medicine, and Director of Cardiovascular Imaging Research Core Laboratory, Division of Cardiology, Vancouver Hospital.

Correspondence to: G. B. John Mancini, MD, Vancouver Hospital, 10209-2775 Laurel St, Vancouver, BC, Canada V5Z 1M9; e-mail: mancini@interchange.ubc.ca



Chest. 2007;131(4):950-951. doi:10.1378/chest.06-2838
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Investigators1 from the University of New Mexico provide in this issue of CHEST (see page 1006) a provocative analysis suggesting novel, lifesaving therapy for patients with COPD and influenza/pneumonia. This work focuses on the potential use of statins in these syndromes, and the conclusions are based on a matched cohort study and two separate case-control studies.

The broadest, mechanistic rationale for this study derives from the fact that the pathogenesis of both diseases involves activation of inflammatory and immune processes that cause progressive lung tissue damage and account for morbidity and mortality. Indeed, diverse forms of pulmonary inflammation lead to systemic inflammatory activation with consequences that are much more widespread than merely in the lungs. For example, animal models of lung inflammation show augmentation of the rate of atherosclerosis accumulation in the coronary vessels and aorta.2 Such observations help to explain the association between pulmonary inflammation and cardiac morbidity and mortality. Thus, medications currently associated with cardiovascular risk reduction might have a substantial impact on the clinical outcome of patients suffering from pulmonary inflammation by at least reducing the cardiovascular component of adverse morbidity and mortality. But in addition, statins, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers, through pleiotropic mechanisms, can directly mitigate lung inflammation and injury, thereby making these agents dual cardiopulmonary protectants.37 These agents present extremely attractive opportunities to simultaneously improve both lung disease and cardiovascular comorbities.

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