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Introduction

University of Nebraska Medical Center, Omaha, Nebraska; and University of Colorado Health Sciences Center, Denver, Colorado

Correspondence and requests for reprints should be addressed to Stephen I. Rennard, M.D., Department of Internal Medicine, University of Nebraska Medical Center, 985885 Nebraska Medical Center, Omaha, NE 68198-5885. E-mail: srennard{at}unmc.edu

"Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking" (1). This definition of COPD presented in the American Thoracic Society/European Respiratory Society guidelines represents an evolution from the GOLD definition (2). It highlights the fact that COPD is "preventable and treatable" and that the inflammatory response is largely due to cigarette smoking.

This is the fourth Lund COPD symposium, a series of meetings which have been sponsored by AstraZeneca and which have highlighted specific areas relevant to COPD (3–5). The current symposium "Chronic Obstructive Pulmonary Disease: A Disorder of the Cardiovascular and Respiratory Systems" was based on the concept that COPD affects not only the lungs but other organ systems. Prominent among these is the cardiovascular system. As a result, much of the morbidity and mortality associated with COPD is due to cardiovascular disease, and much of the therapy required is aimed at the cardiovascular system.

Recognizing that COPD is both preventable and treatable begs the question of what can be prevented and what can be treated. Great advances have been made in the prevention and treatment of cardiovascular complications, of hypertension, hyperlipidemias, diabetes, and other conditions. Many patients with COPD also need treatment in this regard.

The revisions in the definition also highlight the importance of cigarette smoking, which is a major risk factor not only for COPD, but also for cardiovascular disease. Interestingly, individuals who smoke and who develop COPD further increase their risk of cardiovascular disease (6).

The concurrence of COPD with cardiovascular disease, therefore, represents more than the simultaneous presence of relatively common conditions. The question of whether similar pathogenic mechanisms and/or shared susceptibilities account for the disease associations becomes a key question and forms the underlying theme addressed throughout the symposium.

Specific topics addressed include the epidemiology of cardiovascular disease in COPD and their interrelationships, the hemodynamic aspects of COPD, implications of systemic inflammation in COPD, the role that hypoxia may play in modulating vascular responses, interactions between COPD and coagulation, and, finally, therapeutic implications of concurrent COPD and cardiovascular disease.

Adequate treatment of patients requires an integrated approach to all of their medical problems. It is the exceptional patient who has a single pathologic process affecting a single organ system. Material presented in the following symposium, therefore, is likely to be of interest both to the investigator seeking shared mechanisms between diseases of different organ systems and the clinician seeking to effectively treat real patients.

	FOOTNOTES

 
Conflict of Interest Statement: S.I.R. has participated as a speaker in scientific meetings and courses under the sponsorship of AstraZeneca, GlaxoSmithKline, and Pfizer and has consulted with several pharmaceutical companies with relevance to the topics noted in the present manuscript (Almiral, Altana, Amersham, Array Biopharma, AstraZeneca, Aventis, Boehringer Ingelheim, Critical Therapeutics, GlaxoSmithKline, Globomax, Intermune, Merck, Novartis, Ono, Otsuka, Roche, Sanofi, Scios, and Wyeth) and serves on Advisory Boards for Altana and Inspire and has been sponsored by GlaxoSmithKline for several clinical trials and has received laboratory support and has also conducted clinical trials for Roche, Pfizer, Sanofi, and Novartis and has conducted both clinical trials and basic studies under the sponsorship of Centocor and has conducted basic studies under the sponsorship of AstraZeneca and a patent is pending on the use of PDE4 inhibitors in repair and is a co-inventor of the patent owned by the University of Nebraska Medical Center; N.V. has an industry-sponsored grant pending for animal research from GlaxoSmithKline.

	REFERENCES

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1. American Thoracic Society/European Respiratory Society. Standards for the Diagnosis and Management of Patients with COPD. Available at www.thoracic.org/copd [Cited 2005 Mar 16].
2. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. 2003. Available at www.goldcopd.com/wr.html.
3. Rennard SI, Farmer SG. Symposium COPD. Into the new millennium. Chest 2002;121:113S–223S.
4. Rennard SI, Farmer SG. COPD 2001: a major challenge for medicine, the pharmaceutical industry, and society. Chest 2002;121:113S–115S.[Free Full Text]
5. Rennard SI, Farmer SG. Exacerbations and progression of disease in asthma and chronic obstructive pulmonary disease. Proc Am Thorac Soc 2004;1:88–92.[Abstract/Free Full Text]
6. Ashley F, Kannel WB, Sorlie PD, Masson R. Pulmonary function: relation to aging, cigarette habit, and mortality. Ann Intern Med 1975;82:739–745.[Medline]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Rennard, S. I. Articles by Voelkel, N. Search for Related Content PubMed Articles by Rennard, S. I. Articles by Voelkel, N.