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Prognostic Significance of Computed Tomography Findings in Pulmonary Vein Stenosis(1) Pulmonary vein stenosis (PVS) can be a severe, progressive disease with lung involvement. We aimed to characterize findings by computed tomography (CT) and identify factors associated with death; (2) Veins and lung segments were classified into five locations: right upper, middle, and lower; and left upper and lower. Severity of vein stenosis (0-4 = no disease-atresia) and lung segments (0-3 = unaffected-severe) were scored. A PVS severity score (sum of all veins + 2 if bilateral disease; maximum = 22) and a total lung severity score (sum of all lung segments; maximum = 15) were reported; (3) Of 43 CT examinations (median age 21 months), 63% had bilateral disease. There was 30% mortality by 4 years after CT. Individual-vein PVS severity was associated with its corresponding lung segment severity (p < 0.001). By univariate analysis, PVS severity score > 11, lung cysts, and total lung severity score > 6 had higher hazard of death; and perihilar induration had lower hazard of death; (4) Multiple CT-derived variables of PVS severity and lung disease have prognostic significance. PVS severity correlates with lung disease severity.
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Pulmonary Edema: A Pictorial Review of Imaging Manifestations and Current Understanding of Mechanisms of DiseasePulmonary edema is a common clinical entity caused by the extravascular movement of fluid into the pulmonary interstitium and alveoli. The four physiologic categories of edema include hydrostatic pressure edema, permeability edema with and without diffuse alveolar damage (DAD), and mixed edema where there is both an increase in hydrostatic pressure and membrane permeability. As radiographic manifestations and etiologies are varied, an appreciation for both the common and uncommon manifestations and causes of pulmonary edema is essential for accurate diagnosis.
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Pulmonary artery hypertension in severe aortic stenosis: incidence and mechanismWe investigated the incidence and mechanism of pulmonary artery hypertension (PAH) in a consecutive series of patients with aortic stenosis who were undergoing diagnostic cardiac catheterization. Forty-five patients with severe aortic stenosis were divided into two groups: group 1 comprised 13 patients (29%) with PAH (pulmonary artery systolic pressure > 50 mm Hg); group 2 comprised 32 patients (71%) without PAH. Group 1 patients had a higher incidence of congestive heart failure, a lower left ventricular ejection fraction and cardiac index, and more mitral regurgitation as compared with group 2 patients. Of the 13 group 1 patients, 8 had a transpulmonary gradient (pulmonary artery mean pressure--pulmonary capillary wedge pressure) > or = 10 mm Hg, consistent with reactive PAH. We conclude that PAH frequently accompanies aortic stenosis and is often reactive.
