Chest
Volume 138, Issue 1, July 2010, Pages 47-51
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ORIGINAL RESEARCH
COPD
The Effects of Hypoxia on Markers of Coagulation and Systemic Inflammation in Patients With COPD

https://doi.org/10.1378/chest.09-2764Get rights and content

Background

It has been demonstrated that there is an increased risk of venous thromboembolism (VTE) during air travel on flights of long duration. Patients with COPD are also at increased risk of VTE, particularly during exacerbations, possibly because of a hypercoagulable state secondary to hypoxia and/or heightened systemic inflammation. We investigated the effects of hypoxia on indices of coagulation and systemic inflammation in patients with COPD.

Methods

Twenty clinically stable patients with mild COPD were recruited. Patients were randomized to receive either medical air or 100% nitrogen through a 40% venturi mask at a flow rate of 10 L/min for 2 h. Blood was sampled for thrombin-antithrombin complex (TAT), prothrombin activation fragments 1 + 2 (F1 + 2), von Willebrand factor antigen (VWF:Ag), D-dimer, and interleukin-6 (IL-6) at baseline and after 2 h.

Results

Patients in the hypoxia and control groups were similar in terms of age, sex, pack-years smoked, and severity of airflow obstruction. There was no difference in baseline TAT, F1 + 2, VWF:Ag, D-dimer, or IL-6 levels between groups. In the control group, there was no change in markers of coagulation or systemic inflammation over the 2-h study. In patients who underwent hypoxic challenge, there was an increase in TAT (P < .001), F1 + 2 (P < .01), and IL-6 (P < .01), whereas D-dimer and VWF:Ag levels were unchanged.

Conclusions

This study demonstrates that a 2-h hypoxic challenge in patients with COPD results in coagulation activation in conjunction with an increase in systemic inflammation.

Section snippets

Materials and Methods

Twenty patients with confirmed COPD19 were recruited from primary and secondary care. All patients had an FEV1 > 50% predicted and were studied when clinically stable, defined as no requirement for antibiotic or oral corticosteroid therapy and no change in respiratory symptoms beyond normal day-to-day variation in the preceding month.20 Patients were excluded from the study if they had known heart disease, malignancy, or any other condition associated with a hypercoagulable state or increased

Results

All 20 recruited patients completed the study. No patients became unwell or had a decrease in oxygen saturation < 88% during the hypoxic challenge period, and no test was abandoned. Patients in the hypoxic challenge and control groups were similar in terms of age, sex, and smoking history (Table 1). Resting baseline heart rate, respiratory rate, and oxygen saturations were similar between groups, as were measures of baseline TAT, VWF:Ag, D-dimer, and IL-6. Although patients in the control group

Discussion

The results of this single-blind placebo-controlled study suggest that a normobaric hypoxic challenge in patients with COPD results in an increase in markers of coagulation activation in association with an increase in a marker of systemic inflammation. Both TAT complex and F1 + 2 are measures of thrombin formation, and are widely used as general markers of coagulation activation.10 The increase in both TAT and F1 + 2 in patients undergoing hypoxic challenge and not those receiving medical air

Acknowledgments

Author contributions: Dr Sabit: contributed to the development and design of this study; collection, analysis, and interpretation of the data; drafting and revision of the manuscript; and approval of the submitted manuscript.

Mr Thomas: contributed to the design of the study and revision of the manuscript.

Dr Shale: contributed to the analysis of data, revision of the manuscript, and generation of funding for the study.

Dr Collins: contributed to development and design of this study and revision

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    Funding/Support: This study was supported by a Cardiff and Vale Lung Function Fund and GlaxoSmithKline Global. Dr Sabit was a Cardiff and Vale NHS Trust Clinical Research Fellow.

    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestpubs.org/site/misc/reprints.xhtml).

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