Abstract

BackgroundThe ratio of the diameter of the pulmonary artery (PA) to the diameter of the aorta (PA:A) on computed tomography (CT) imaging is associated with both COPD exacerbation and pulmonary hypertension. The mechanisms of PA enlargement in COPD are poorly understood.MethodsIn this retrospective, single center study we evaluated pulmonary function, CT scans, right heart catheterizations, and echocardiography in 88 subjects with mild-to-moderately severe COPD. A sensitivity analysis was performed in 43 subjects in whom CT scan and echocardiogram were performed within 50 days of each other. To evaluate the association between PA:A ratio and echocardiographic parameters and hemodynamics, we performed simple correlations and multivariable linear regression analysis adjusting for lung function, age, sex, race, and diastolic function.ResultsAll subjects had preserved left ventricular (LV) systolic function (LV ejection fraction 62.7%±5.5%). Among them, 56.8% had evidence of diastolic dysfunction. There was no association between PA:A ratio and the presence of diastolic dysfunction. In a multivariable model, PA:A ratio was associated with right ventricular (RV) chamber size (β=0.015; P<0.003), RV wall thickness (β=0.56; P<0.002), and RV function (−0.49; P=0.05). In the subgroup of subjects with testing within 50 days, the association with RV chamber size persisted (β=0.017; P=0.04), as did the lack of association with diastolic function. PA:A ratio was also associated with elevated PA systolic pressures (r=0.62; P=0.006) and pulmonary vascular resistance (r=0.46; P=0.05), but not pulmonary arterial wedge pressure (r=0.17; P=0.5) in a subset of patients undergoing right heart catheterization.ConclusionIn patients with mild-to-moderately severe COPD and preserved LV function, increased PA:A ratio occurs independent of LV diastolic dysfunction. Furthermore, the PA:A ratio is associated with right heart structure and function changes, as well as pulmonary hemodynamics. These findings indicate that PA:A ratio is a marker of intrinsic pulmonary vascular changes rather than impaired LV filling.

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