Key result
Poor subpleural perfusion on dual-energy computed tomography was associated with significantly higher pulmonary vascular resistance (879 vs 574 dynes-s/cm5) in patients with CTEPH.
Why the study?
The existence of microvasculopathy in patients with chronic thromboembolic pulmonary hypertension has been suggested, but its pathophysiological impact required evaluation.
Does microvasculopathy assessed by dual-energy computed tomography correlate with worse hemodynamics in patients with chronic thromboembolic pulmonary hypertension?
Observational (n=93)
No
Does microvasculopathy assessed by dual-energy computed tomography correlate with worse hemodynamics in patients with chronic thromboembolic pulmonary hypertension?
Microvasculopathy identified by dual-energy CT is present in over half of treatment-naïve CTEPH patients and is associated with more severe hemodynamics independent of pulmonary vascular obstruction.
Answers are grounded in this paper and cite their sources.
May signal more severe hemodynamics in CTEPH; hypothesis-generating for DECT microvasculopathy assessment, needs prospective validation.
The existence of microvasculopathy in patients with chronic thromboembolic pulmonary hypertension has been suggested. Recently, dual‐energy computed tomography has been used to produce a sensitive iodine distribution map in lung fields to indicate microvasculopathy according to poor subpleural perfusion. Our aim was to evaluate the impact of microvasculopathy on pathophysiology in chronic thromboembolic pulmonary hypertension. According to the extent of poor subpleural perfusion, ninety‐three interventional treatment‐naïve patients were divided into poorly perfused ( n = 49) or normally perfused group ( n = 44). We assessed cardiopulmonary exercise test, right heart catheterization, and dual‐energy computed tomography parameters for quantitative evaluation of lung perfusion of blood volume score. Lung perfusion of blood volume score in normally perfused group was significantly inversely correlated with pulmonary vascular resistance (pulmonary vascular resistance = 6816.1 × lung perfusion of blood volume score −0.793 , R 2 = 0.225, p < 0.01), but lung perfusion of blood volume score in poorly perfused group was not. Poorly perfused group had higher pulmonary vascular resistance (879 ± 409 dynes‐s/cm 5 vs. 574 ± 279 dynes‐s/cm 5 , p < 0.01) and lower lung perfusion of blood volume score (22.1 ± 5.4 vs. 26.4 ± 6.6, p < 0.01) and % diffusing capacity for carbon monoxide divided by the alveolar volume (59.9 ± 15.4% vs. 78.8 ± 14.2%, p < 0.01). Perfusion of blood volume score in the normally perfused group showed an inverse correlation with pulmonary vascular resistance; however, that in poorly perfused group did not. Microvasculopathy might contribute to severe hemodynamics, apart from pulmonary vascular obstruction. In our experience, more than half of treatment‐naïve chronic thromboembolic pulmonary hypertension patients have microvasculopathy.
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Onishi et al. (2020) conducted an observational in Chronic thromboembolic pulmonary hypertension (n=93). Poor subpleural perfusion on dual-energy computed tomography (indicating microvasculopathy) vs. Normal subpleural perfusion was evaluated on Pulmonary vascular resistance (dynes-s/cm5) (p=<0.01). Poor subpleural perfusion on dual-energy computed tomography was associated with significantly higher pulmonary vascular resistance (879 vs 574 dynes-s/cm5) in patients with CTEPH.
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