Percent emphysema, airflow obstruction, and impaired left ventricular filling

Abstract

Background: Very severe chronic obstructive pulmonary disease causes cor pulmonale with elevated pulmonary vascular resistance and secondary reductions in left ventricular filling, stroke volume, and cardiac output. We hypothesized that emphysema, as detected on computed tomography (CT), and airflow obstruction are inversely related to left ventricular end-diastolic volume, stroke volume, and cardiac output among persons without very severe lung disease.

Methods: We measured left ventricular structure and function with the use of magnetic resonance imaging in 2816 persons who were 45 to 84 years of age. The extent of emphysema (expressed as percent emphysema) was defined as the percentage of voxels below -910 Hounsfield units in the lung windows on cardiac computed tomographic scans. Spirometry was performed according to American Thoracic Society guidelines. Generalized additive models were used to test for threshold effects.

Results: Of the study participants, 13% were current smokers, 38% were former smokers, and 49% had never smoked. A 10-point increase in percent emphysema was linearly related to reductions in left ventricular end-diastolic volume (-4.1 ml; 95% confidence interval [CI], -3.3 to -4.9; P<0.001), stroke volume (-2.7 ml; 95% CI, -2.2 to -3.3; P<0.001), and cardiac output (-0.19 liters per minute; 95% CI, -0.14 to -0.23; P<0.001). These associations were of greater magnitude among current smokers than among former smokers and those who had never smoked. The extent of airflow obstruction was similarly associated with left ventricular structure and function, and smoking status had similar modifying effects on these associations. Percent emphysema and airflow obstruction were not associated with the left ventricular ejection fraction.

Conclusions: In a population-based study, a greater extent of emphysema on CT scanning and more severe airflow obstruction were linearly related to impaired left ventricular filling, reduced stroke volume, and lower cardiac output without changes in the ejection fraction.

Conflict of interest statement

Dr. Enright reports receiving consulting fees from Pfizer and Gilead; Dr. Hoffman, having equity ownership in and being a founder of VIDA Diagnostics and receiving lecture fees from Sanofi-Aventis, AstraZeneca, and Chiesi Pharmaceuticals; Dr. Kawut, receiving grant support from Pfizer; Dr. Lima, receiving grant support from Toshiba Medical Systems and General Electric; and Dr. Smith, receiving consulting fees from Merck and KarmelSonix. No other potential conflict of interest relevant to this article was reported.

2010 Massachusetts Medical Society

Figures

Figure 1. Relationship between Percent Emphysema and Left Ventricular (LV) End-Diastolic and Stroke Volumes

Results of multivariate analyses of the relationship between percent emphysema and left ventricular end-diastolic volume (Panel A) and stroke volume (Panel B) are shown. Solid lines indicate smoothed regression lines adjusted for age, race or ethnic group, sex, body-surface area, number of pack-years of smoking, urinary cotinine level, educational level, presence or absence of diabetes mellitus, fasting plasma glucose level, body-mass index, presence or absence of hypertension, systolic and diastolic blood pressure, C-reactive protein level, fibrinogen level, CT scanner type, and tube current in milliamperes. Dashed lines indicate 95% confidence intervals. Dots represent predicted plus residual values. The smoothing functions did not improve the model fit as compared with linear terms for LV end-diastolic volume or LV stroke volume, which implies that thresholds in the relationship of percent emphysema to LV end-diastolic volume and to stroke volume could not be demonstrated.

Figure 2. Relationship between the Ratio of Forced Expiratory Volume in 1 Second to Forced Vital Capacity and Left Ventricular (LV) End-Diastolic and Stroke Volumes

Results of multivariate analyses of the relationship between the ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1:FVC) and left ventricular end-diastolic volume (Panel A) and stroke volume (Panel B) are shown. Solid lines indicate smoothed regression lines adjusted for age, race or ethnic group, sex, body-surface area, number of pack-years of smoking, urinary cotinine level, educational level, height, presence or absence of diabetes mellitus, fasting plasma glucose level, presence or absence of hypertension, systolic and diastolic blood pressure, C-reactive protein level, and fibrinogen level. Dashed lines indicate 95% confidence intervals. Dots represent predicted plus residual values. The smoothing function improved the model fit as compared with the linear term for LV end-diastolic volume (P = 0.003) but not for LV stroke volume. Differences in smoking status accounted for this nonlinearity (Fig. 3 in the Supplementary Appendix).