Lung ventilation–perfusion imbalance in pulmonary emphysema: assessment with automated V/Q quotient SPECT

Suga, Kazuyoshi; Kawakami, Yoshiyuki; Koike, Hideo; Iwanaga, Hideyuki; Tokuda, Osamu; Okada, Munemasa; Matsunaga, Naofumi

doi:10.1007/s12149-010-0369-7

Cited by 22 publications

(12 citation statements)

References 34 publications

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“…Previously in clinical studies, Jogi et al have demonstrated that V/Q SPECT is sensitive to COPD-related pathologies (13), and Suga et al have quantified the V/Q mismatch due to emphysema in a per-voxel manner (14). Our results affirm that V/Q methodologies, being functional measurements, are sensitive to early pathologic changes that lead to COPD but may not be apparent, even at a higher resolution, with anatomic imaging systems such as CT. Because V/Q imaging is a common nuclear medicine technique and SPECT/CT systems are increasingly used (21), V/Q measurement could play an important role in the diagnosis, treatment, and further understanding of COPD (13,22,23).…”

Section: Discussionsupporting

confidence: 76%

“…V/Q SPECT imaging, on the other hand, is a well-established nuclear medicine technique that provides spatial information regarding the 2 core processes of respiratory gas exchange, ventilation of alveolar units and perfusion of the pulmonary capillary beds (11), and the results of this technique correlate well with those derived from MIGET (12). SPECT V/Q is commonly used in the diagnosis of pulmonary embolism but has been shown to be sensitive to early indicators of COPD in addition to being capable of identifying comorbid disease and distinguishing pathophysiologic changes (13,14). Furthermore, coregistration of nuclear imaging data to CT images allows for greater insight into the anatomic position of lung dysfunction and structural information such as the distribution of emphysema.…”

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confidence: 99%

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Detection of Lung Dysfunction Using Ventilation and Perfusion SPECT in a Mouse Model of Chronic Cigarette Smoke Exposure

et al. 2013

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Chronic obstructive pulmonary disease is a leading cause of morbidity and mortality worldwide. Exposure to cigarette smoke (CS) is a major risk factor for developing this chronic airflow impairment, but the early progression of disease is not well defined or understood. Ventilation/perfusion (V/Q) SPECT provides a noninvasive assessment of lung function to further our current understanding of how CS affects the lung. Methods: BALB/c mice were imaged with V/Q SPECT and CT after 8 and 24 wk of whole-body exposure to mainstream CS. Bronchoalveolar lavage was collected and cell differentials produced to determine inflammatory patterns. Histologic lung sections were collected, and a semiautomated quantitative analysis of airspace enlargement was applied to whole histology slices. Results: Exposure to CS induced an inflammatory response that included increases in the numbers of both mononuclear cells and neutrophils. Airspace enlargement was also significantly increased at 8 wk of CS exposure and was still more pronounced at 24 wk. Ventilation and perfusion correlation at the voxel level depicted a significant decrease in matching at 8 wk of CS exposure that was also apparent after 24 wk. The standard deviation (SD) of the log(V/Q) curve, a basic measure of heterogeneity, was increased from 0.44 6 0.02 in age-matched controls to 0.62 6 0.05 with CS exposure at 24 wk, indicating an increase in V/Q mismatching between 8 and 24 wk of CS exposure. CT, however, was not capable of discriminating control from CS-exposed animals at either time point, even with greater resolution and respiratory gating. Conclusion: This study demonstrated that, before CT detection of structural changes, V/Q imaging detected changes in gas-exchange potential. This functional impairment corresponded to increased lung inflammation and increased airspace enlargement. In vivo V/Q imaging can detect early changes to the lung caused by CS exposure and thus provides a noninvasive method of longitudinally studying lung dysfunction in preclinical models. In the future, these measures could be applied clinically to study and diagnose the early stages of chronic obstructive pulmonary disease.

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Section: Discussionsupporting

confidence: 76%

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confidence: 99%

Detection of Lung Dysfunction Using Ventilation and Perfusion SPECT in a Mouse Model of Chronic Cigarette Smoke Exposure

et al. 2013

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“…HRCT imaging detects early emphysema by identifying pulmonary tissue with radiologic attenuation below a predetermined threshold, findings that roughly correlate with a low DL CO and pathologic evidence of emphysema (74)(75)(76)(77)(78)(79)(80). Although several studies have shown that a significant proportion of asymptomatic smokers have HRCT evidence of emphysema (78,(81)(82)(83), early HRCT findings of ''emphysema'' are not proven to be correlated directly with lung destruction (84)(85)(86)(87)(88)(89)(90). Hyperpolarized gas diffusion-weighted magnetic resonance imaging has also been used to identify emphysema, with a correlation of elevated levels of the apparent diffusion coefficient with decreased DL CO (91).…”

Section: Early Detection Of Lung Destructionmentioning

confidence: 99%

Circulating Endothelial Microparticles as a Measure of Early Lung Destruction in Cigarette Smokers

Gordon

Gudi

Krause

et al. 2011

Am J Respir Crit Care Med

203

173

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Rationale: There is increasing evidence that emphysema is associated with primary loss of pulmonary capillary endothelium. Plasma levels of endothelial microparticles (EMPs), small vesicles released from activated or apoptotic endothelial cells, are elevated in vascularrelated disorders. Objectives: To evaluate whether plasma EMP levels are elevated in smokers with early lung destruction as assessed by normal spirometry but reduced diffusing capacity of the lung for carbon monoxide (DL CO ). Methods: Lung health was assessed by pulmonary function tests (PFTs: spirometry, total lung capacity, DL CO ) and chest X-ray; smoking status was assessed by urine nicotine and cotinine. EMP levels (CD42b 2 CD31 1 microparticles) were quantified as activated or apoptotic. The initial cohort (n 5 92) included healthy nonsmokers (normal PFTs), healthy smokers (normal PFTs), and smokers with early evidence of lung destruction (normal spirometry, low DL CO ). Two prospective cohorts were then tested: a group similar to the initial cohort and an HIV1 1 cohort. Measurements and Main Results: Healthy smokers had mildly increased levels of EMPs. Strikingly, 95% of smokers with normal spirometry, low DL CO had increased EMPs, with reduced CD62 1 / CD31 1 ratios (P , 10 24 ) and elevated CD42b 2 CD31 1 annexin V 1 EMPs (P , 10 24 ), suggesting derivation from endothelial apoptosis. Most elevated EMPs were angiotensin-converting enzyme positive, suggesting derivation from pulmonary capillaries. Both prospective cohorts confirmed the initial cohort data. Conclusions: Plasma EMPs with apoptotic characteristics are elevated in smokers with normal spirometry but reduced DL CO , consistent with the concept that emphysema is associated, in part, with capillary endothelium apoptosis, suggesting that the early development of emphysema might be monitored with plasma EMP levels.

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“…Jogi et al [10] have shown the ability of this technique to identify early disease and stage disease severity in COPD patients. Further, Suga et al [11] have quantified the impact of emphysema on V/Q in the lungs of COPD patients.…”

Section: Introductionmentioning

confidence: 99%

Impact of inflammation, emphysema, and smoking cessation on V/Q in mouse models of lung obstruction

et al. 2014

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BackgroundChronic obstructive pulmonary disease (COPD) is known to greatly affect ventilation (V) and perfusion (Q) of the lung through pathologies such as inflammation and emphysema. However, there is little direct evidence regarding how these pathologies contribute to the V/Q mismatch observed in COPD and models thereof. Also, little is known regarding how smoking cessation affects V/Q relationships after inflammation and airspace enlargement have become established. To this end, we have quantified V/Q on a per-voxel basis using single photon emission computed tomography (SPECT) in mouse models of COPD and lung obstruction.MethodsThree distinct murine models were used to investigate the impact of different pathologies on V/Q, as measured by SPECT. Lipopolysaccharide (LPS) was used to produce neutrophilic inflammation, porcine pancreatic elastase (PPE) was used to produce emphysema, and long-term cigarette smoke (CS) exposure and cessation were used to investigate the combination of these pathologies.ResultsCS exposure resulted in an increase in mononuclear cells and neutrophils, an increase in airspace enlargement, and an increase in V/Q mismatching. The inflammation produced by LPS was more robust and predominantly neutrophilic, compared to that of cigarette smoke; nevertheless, inflammation alone caused V/Q mismatching similar to that seen with long-term CS exposure. The emphysematous lesions caused by PPE administration were also capable of causing V/Q mismatch in the absence of inflammation. Following CS cessation, inflammatory cell levels returned to those of controls and, similarly, V/Q measures returned to normal despite evidence of persistent mild airspace enlargement.ConclusionsBoth robust inflammation and extensive airspace enlargement, on their own, were capable of producing V/Q mismatch. As CS cessation resulted in a return of V/Q mismatching and inflammatory cell counts to control levels, lung inflammation is likely a major contributor to V/Q mismatch observed in the cigarette smoke exposure model as well as in COPD patients. This return of V/Q mismatching to control values also took place in the presence of mild airspace enlargement, indicating that emphysematous lesions must be of a larger volume before affecting the lung significantly. Early smoking cessation is therefore critical before emphysema has an irreversible impact on gas exchange.

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Lung ventilation–perfusion imbalance in pulmonary emphysema: assessment with automated V/Q quotient SPECT

Cited by 22 publications

References 34 publications

Detection of Lung Dysfunction Using Ventilation and Perfusion SPECT in a Mouse Model of Chronic Cigarette Smoke Exposure

Detection of Lung Dysfunction Using Ventilation and Perfusion SPECT in a Mouse Model of Chronic Cigarette Smoke Exposure

Circulating Endothelial Microparticles as a Measure of Early Lung Destruction in Cigarette Smokers

Impact of inflammation, emphysema, and smoking cessation on V/Q in mouse models of lung obstruction

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