Enlarged Central Pulmonary Artery Did Not Correlate With the Presence of OSA

Abstract

SESSION TITLE: Pulmonary Hypertension SESSION TYPE: Original Investigation Poster PRESENTED ON: Wednesday, November 1, 2017 at 01:30 PM - 02:30 PM PURPOSE: Central pulmonary artery diameters (PAD) ≥3.2 cm on computed tomography (CT) have been shown to correlate with the presence of pulmonary hypertension (PH) [1]. Radiologists routinely document PAD ≥3.2 cm as indicative of possible PH. Anecdotally, we have seen enlarged PAD in patients with obstructive sleep apnea (OSA) who do not have PH. The relationship between OSA and enlarged PAD has not been defined [2]. This study evaluates for an association between PAD and moderate or severe OSA. In addition, the utility of using PAD to predict PH in the setting of OSA is investigated. METHODS: A retrospective chart review examined patients who underwent polysomnography (PSG) at an academic sleep disorder center between 1/1/2015-12/31/2016. We evaluated patients who were over age 18, had CT imaging of PAD and ascending aorta diameter (AD) within 90 days of a PSG. PAD and AD were measured by a radiologist. Enlarged PAD was defined as ≥3.2 cm, abnormal PAD:AD ratio was defined as >1.0. From the PSG, the Apnea-Hypopnea Index (AHI) and Body Mass Index (BMI) were collected. If available, echocardiograms were reviewed for evidence suggestive of PH (defined as right ventricle diameter ≥3.8 cm and/or estimated pulmonary artery systolic pressure ≥30 mmHg). Statistical analysis was done with SPSS version 24 to analyze the relationship between PAD and AHI using ANOVA regression. A second analysis used Fisher's exact test to assess correlation between PAD or PAD:AD with PH on echocardiogram. ROC curves were used to characterize PAD metrics on CT for predicting PH in OSA patients. RESULTS: In the study period, 1652 patients had a PSG. 52 patients had available CT scans (52% male, mean age 54 (SD=15), BMI 33.8 (SD=8.2)). The mean AHI was 25.2 (SD=25.7) and the mean PAD was 2.7 cm (SD=0.5). 46 patients had PSG-diagnosed OSA. Statistical analysis showed no correlation between PAD and AHI (p=0.37). Of the 11 patients with enlarged PAD, 6 had an AHI >20 (mean 25.9, range 20.9-36.5). In patients with PAD <3.0 cm, 15/37 patients had an AHI >20 (mean 50.8, range 21.9-126.5). In patients with a PAD:AD >1.0, 7/12 had an AHI >20 (mean 38.8, range 20.9-126.5). Of the 52 PSG patients, 27 had echocardiograms with assessment of right heart function. 14 patients had sonographic evidence of PH (of which 10 had AHI >20, 4 had PAD ≥3.2 cm). Analysis showed no relationship between enlarged PAD and PH (p=0.4), nor between large PAD:AD ratio and PH (p=1.0). Among OSA patients, PAD ≥3.2 cm predicted PH with a sensitivity of 22% and specificity of 80%. The area under the ROC curve was 0.5 (SD=0.1). CONCLUSIONS: The presence of a PAD >3.2 cm or a PAD:AD ratio >1.0 did not predict the presence of moderate or severe OSA (AHI >20). In addition, there was no statistically significant relationship found between PAD or PAD:AD and echocardiographic evidence of PH among the patient pool studied. Larger sample sizes are needed to confirm these conclusions. CLINICAL IMPLICATIONS: Central PAD and PAD:AD as measured on CT has limited utility to predict OSA or PH in the setting of OSA.