Self-assessment CME RadioGraphic
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Assess the Pulmonary Vasculature
Pulmonary arterial findings suggestive of pulmonary hypertension include central pulmonary artery enlargement, pulmonary artery–to-aorta ratio greater than 1, and increased segmental artery-to-bronchus ratio.
Although the Framingham Heart Study set a normal cutoff value for pulmonary artery size at 29 mm for men and 27 mm for women (measured as the transverse diameter of the main pulmonary artery on an axial image at the level of the bifurcation of the right pulmonary artery), this isolated value is not specific for pulmonary hypertension, as multiple other factors can affect pulmonary artery size, including body mass index, systemic hypertension, diabetes, age, and underlying cardiovascular disease (46,47). A more accurate measurement is to compare the ratio of the diameter of the main pulmonary artery to that of the ascending aorta (transverse diameter measured on the same axial image as used for the main pulmonary artery measurement), where a ratio greater than 1 is suggestive of pulmonary hypertension (Fig 13) (48,49). In addition to the size of the main pulmonary artery, one should also assess the segmental artery-to-bronchus ratio. If this ratio is greater than 1 in three or more lobes, this finding is also highly specific for pulmonary hypertension (46).
In addition to assessing size of the pulmonary arteries, one should assess the morphology of the pulmonary vasculature. For instance, abruptly tapering or corkscrew vessels are associated with pulmonary hypertension, as are dilated bronchial or other systemic collaterals (50). In cases of CTEPH, which are important to recognize since invasive treatments are possible (51), close inspection of the pulmonary vasculature scans can demonstrate adherent thrombus (Fig 14), abrupt occlusion of pulmonary arteries, luminal irregularities with eccentric wall thickening, abrupt caliber change (often due to recanalization), and webs or bands (21,52,53).
Differentiating between PAH (also known as primary pulmonary hypertension) and CTEPH is not always easy. Classically, patients with mosaic attenuation due to CTEPH often demonstrate a well-demarcated segmental or subsegmental distribution of mosaicism due to the vascular distribution of thrombi, whereas the mosaic pattern in PAH often manifests as focal perivascular hyperattenuation or small scattered areas of low attenuation confined to the secondary pulmonary lobule (20). The perivascular areas of hyperattenuation may mimic discrete centrilobular ground-glass nodules that are of uncertain cause but thought to represent cholesterol granulomas, large plexogenic arterial lesions, or small systemic collateral arteries (Fig 13) (54). In addition, dilated peripheral arteries can have a corkscrew morphology (20). While adherent thrombus is a good clue to the presence of CTEPH, in situ thrombus and/or atherosclerosis may result from severe long-standing PAH and can sometimes be confused for CTEPH, so assessment of the pattern of mosaic attenuation is important for differentiation of these entities (20,55,56).
资料来源 | http://pubs.rsna.org/doi/full/10.1148/rg.2015140308