In 120 patients with severe emphysema evaluated for participation in the National Emphysema Treatment Trial, pulmonary hemodynamics and ventricular function were assessed. Pulmonary function tests were (%predicted): FEV(1) = 27%; residual volume = 224.6%; diffusion capacity = 26.7%. In 90.8% of patients, end-expiratory pulmonary artery mean pressure was > 20 mm Hg; in 61.4%, end-expiratory wedge pressure was > 12 mm Hg. Cardiac index was normal. Mean pulmonary artery pressure correlated inversely with arterial PO(2), and severity of emphysema, and directly with wedge pressure. Multiple stepwise regression revealed that arterial PO(2) was not an independent predictor of mean pulmonary artery pressure. No correlation was found between indices of emphysema severity and PA pressures. Diastolic ventricular pressures were increased without evidence of systolic dysfunction. We conclude that (1) elevations of pulmonary vascular pressures are common, (2) pulmonary hypertension may be related to factors other than hypoxia, (3) pulmonary hypertension does not impair resting systemic O(2) delivery, and (4) elevated cardiac diastolic pressures do not represent systolic dysfunction.
The reduced tidal volume strategy used in this study was safe. Failure to observe beneficial effects of small tidal volume ventilation treatment in important clinical outcome variables may have occurred because a) the sample size was too small to discern small treatment effects; b) the differences in tidal volumes and plateau pressures were modest; or c) reduced tidal volume ventilation is not beneficial.
Rationale: Vascular alteration of small pulmonary vessels is one of the characteristic features of pulmonary hypertension in chronic obstructive pulmonary disease. The in vivo relationship between pulmonary hypertension and morphological alteration of the small pulmonary vessels has not been assessed in patients with severe emphysema. Objectives: We evaluated the correlation of total cross-sectional area of small pulmonary vessels (CSA) assessed on computed tomography (CT) scans with the degree of pulmonary hypertension estimated by right heart catheterization. Methods: In 79 patients with severe emphysema enrolled in the National Emphysema Treatment Trial (NETT), we measured CSA less than 5 mm 2 (CSA ,5 ) and 5 to 10 mm 2 (CSA 5210 ), and calculated the percentage of total CSA for the lung area (%CSA ,5 and %CSA 5-10 , respectively). The correlations of %CSA ,5 and %CSA 5-10 with pulmonary arterial mean pressure (Ppa) obtained by right heart catheterization were evaluated. Multiple linear regression analysis using Ppa as the dependent outcome was also performed. Measurements and Main Results: The %CSA ,5 had a significant negative correlation with Ppa (r 5 20.512, P , 0.0001), whereas the correlation between %CSA 5-10 and Ppa did not reach statistical significance (r 5 20.196, P 5 0.083). Multiple linear regression analysis showed that %CSA ,5 and diffusing capacity of carbon monoxide (DL CO ) % predicted were independent predictors of Ppa (r 2 5 0.541): %CSA ,5 (P , 0.0001), and DL CO % predicted (P 5 0.022). Conclusions: The %CSA ,5 measured on CT images is significantly correlated to Ppa in severe emphysema and can estimate the degree of pulmonary hypertension.Keywords: chronic obstructive pulmonary disease; emphysema; pulmonary hypertension; CT Pulmonary hypertension is an important predictor of mortality in chronic obstructive pulmonary disease (COPD) (1-3). Various factors, including endothelial dysfunction, inflammation, and hypoxia, have been recognized as potential contributors to the development of secondary pulmonary hypertension in emphysema, but its pathogenesis has not been fully clarified. Nevertheless, it is generally recognized that vascular remodeling of small pulmonary arteries is an essential morphological feature of pulmonary hypertension; narrowing and diminution of the small pulmonary vessels have been shown on conventional angiography in emphysema (4-6). However, to our knowledge, the in vivo relationship between pulmonary hypertension and the magnitude of small pulmonary vessel morphological change has not been quantitatively assessed in severe emphysema.A recent histological study suggested that vascular remodeling leads to reduced distensibility of small pulmonary vessels and that this remodeling is closely related to pulmonary hypertension (7). Such a decrease in distensibility of small pulmonary vessels may lead to increased pulmonary vascular resistance and elevated pulmonary vascular pressure. Therefore, we hypothesized that measurements of the total cross-sectional area of small ...
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