Study: CT perfusion may pinpoint emphysema susceptibility in smokers
The study, published online in the April early edition of the Proceedings of the National Academy of Sciences, sought to confirm recent evidence that suggests that that endothelial dysfunction and pathology of pulmonary vascular responses may serve as a precursor to smoking-associated emphysema.
“Although it is known that emphysematous destruction leads to vasculature changes, less is known about early regional vascular dysfunction which may contribute to and precede emphysematous changes,” wrote lead author Eric Hoffman, PhD, professor of radiology, internal medicine and biomedical engineering at the University of Iowa Carver College of Medicine in Iowa City, and colleagues.
Working under the assumption that all smokers have a consistent inflammatory response, the researchers believed that increased perfusion heterogeneity in emphysema-susceptible smokers may have the inability to block hypoxic vasoconstriction in patchy, small regions of inflammation. Hoffman and colleagues employed multidetector row CT perfusion imaging to compare smokers showing early signs of emphysema susceptibility to emphysema-free smokers and individuals who had never smoked.
The researchers selected 17 nonsmokers, 12 smokers with normal CT imaging studies and 12 smokers with subtle CT findings of centrilobular emphysema for inclusion in their study. Each participant underwent dynamic ECG-gated multidetector CT perfusion scans with a central bolus contrast injection.
Quantitative image analysis was used to determine regional perfusion parameters, pulmonary blood flow and mean transit time. Hoffman and colleagues calculated the mean and coefficient of variation and assessed the statistical differences for the smokers with subtle CT findings compared to nonsmokers and smokers with normal CT findings.
The findings of the study showed that the 12 individuals with subtle CT findings had the most disrupted patterns of blood flow compared to the other participants and also suggested that abnormal blood flow occurs before emphysema develops.
"Our study suggests that some smokers have an abnormal response to inflammation in their lungs; instead of sending more blood to the inflamed areas to help repair the damage, blood flow is turned off and the inflamed areas deteriorate," said Hoffman.
Lung inflammation caused by smoking can be repaired by increased blood flow, which brings oxygen to the site of damage, explained the authors. However, the findings suggest that the ability to distinguish when to turn off or when to increase blood flow can be defective in some individuals and likely due to genetics. The authors said that should this genetic difference be coupled with smoking, which increases lung inflammation, the risk of developing emphysema could greatly increase.
Hoffman and colleagues concluded that the results of their study could help physicians “understand the underlying causes of this disease and help distinguish this type of emphysema from other forms of chronic obstructive pulmonary disease.” In addition, they said that multidetector row CT perfusion imaging may be a tool to test the effectiveness of new therapies by looking at the changes in lung blood flow.