Chest
Volume 144, Issue 4, October 2013, Pages 1143-1151
Journal home page for Chest

Original Research
COPD
Impaired Left Ventricular Filling in COPD and Emphysema: Is It the Heart or the Lungs?: The Multi-Ethnic Study of Atherosclerosis COPD Study

https://doi.org/10.1378/chest.13-0183Get rights and content

Background

COPD and heart failure with preserved ejection fraction overlap clinically, and impaired left ventricular (LV) filling is commonly reported in COPD. The mechanism underlying these observations is uncertain, but may include upstream pulmonary dysfunction causing low LV preload or intrinsic LV dysfunction causing high LV preload. The objective of this study is to determine if COPD and emphysema are associated with reduced pulmonary vein dimensions suggestive of low LV preload.

Methods

The population-based Multi-Ethnic Study of Atherosclerosis (MESA) COPD Study recruited smokers aged 50 to 79 years who were free of clinical cardiovascular disease. COPD was defined by spirometry. Percent emphysema was defined as regions < −910 Hounsfield units on full-lung CT scan. Ostial pulmonary vein cross-sectional area was measured by contrast-enhanced cardiac magnetic resonance and expressed as the sum of all pulmonary vein areas. Linear regression was used to adjust for age, sex, race/ethnicity, body size, and smoking.

Results

Among 165 participants, the mean (± SD) total pulmonary vein area was 558 ± 159 mm2 in patients with COPD and 623 ± 145 mm2 in control subjects. Total pulmonary vein area was smaller in patients with COPD (−57 mm2; 95% CI, −106 to −7 mm2; P = .03) and inversely associated with percent emphysema (P < .001) in fully adjusted models. Significant decrements in total pulmonary vein area were observed among participants with COPD alone, COPD with emphysema on CT scan, and emphysema without spirometrically defined COPD.

Conclusions

Pulmonary vein dimensions were reduced in COPD and emphysema. These findings support a mechanism of upstream pulmonary causes of underfilling of the LV in COPD and in patients with emphysema on CT scan.

Section snippets

Materials and Methods

See e-Appendix 1 for a complete description of the methods. The MESA COPD Study recruited patients with COPD and control subjects predominantly from MESA, a population-based, prospective cohort study of subclinical atherosclerosis,27 and the Emphysema and Cancer Action Project, a separate, nonoverlapping lung cancer screening study,28 and also from the outpatient community at Columbia University Medical Center. Included participants were 50 to 79 years of age with a ≥ 10 pack-year smoking

Results

Of 201 participants enrolled at one site where pulmonary vein quantification was performed, 165 completed spirometry, thoracic CT scans, and cardiac MRI with pulmonary vein quantification (e-Fig 1). Participants enrolled but not completing all components of the pulmonary vein study had lower lung function, smaller LV dimensions, and were less likely to report current smoking (e-Table 1).

The mean age of the study patients was 68 ± 7 years, and 60% were men. Fifty-three percent had COPD, and 32%

Discussion

Participants with predominantly mild to moderate COPD had reduced total pulmonary vein cross-sectional area as assessed by contrast-enhanced MRI compared with control subjects without COPD. In addition, pulmonary vein size was inversely associated with percent emphysema and was significantly reduced among participants with emphysema on CT scan who did not have clinical COPD. These findings suggest reduced LV preload in both clinical COPD and in patients with emphysema on CT scan.

To our

Acknowledgments

Author contributions: Dr Barr had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Dr Smith: contributed to study concept and design; data analysis and interpretation; and drafting, revising, and final approval of the manuscript and served as principle author.

Dr Prince: contributed to study concept and design, data interpretation, and revision and final approval of the manuscript.

Dr Hoffman: contributed to

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    Funding/Support: This study was funded by the National Institutes of Health/National Heart, Lung, and Blood Institute [Grants R01-HL093081, R01-HL077612, R01-HL075476, and N01-HC95159-HC95169]; and Fonds de la recherche en santé Québec.

    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.

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