Perfusion imaging heterogeneity during NO inhalation distinguishes pulmonary arterial hypertension (PAH) from healthy subjects and has potential as an imaging biomarker
Abstract Background Without aggressive treatment, pulmonary arterial hypertension (PAH) has a 5-year mortality of approximately 40%. A patient’s response to vasodilators at diagnosis impacts the therapeutic options and prognosis. We hypothesized that analyzing perfusion images acquired before and du...
| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2022-12-01
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| Series: | Respiratory Research |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12931-022-02239-8 |
| _version_ | 1797985495063461888 |
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| author | Tilo Winkler Puja Kohli Vanessa J. Kelly Ekaterina G. Kehl Alison S. Witkin Josanna M. Rodriguez-Lopez Kathryn A. Hibbert Mamary T. Kone David M. Systrom Aaron B. Waxman Jose G. Venegas Richard N. Channick R. Scott Harris |
| author_facet | Tilo Winkler Puja Kohli Vanessa J. Kelly Ekaterina G. Kehl Alison S. Witkin Josanna M. Rodriguez-Lopez Kathryn A. Hibbert Mamary T. Kone David M. Systrom Aaron B. Waxman Jose G. Venegas Richard N. Channick R. Scott Harris |
| author_sort | Tilo Winkler |
| collection | DOAJ |
| description | Abstract Background Without aggressive treatment, pulmonary arterial hypertension (PAH) has a 5-year mortality of approximately 40%. A patient’s response to vasodilators at diagnosis impacts the therapeutic options and prognosis. We hypothesized that analyzing perfusion images acquired before and during vasodilation could identify characteristic differences between PAH and control subjects. Methods We studied 5 controls and 4 subjects with PAH using HRCT and 13NN PET imaging of pulmonary perfusion and ventilation. The total spatial heterogeneity of perfusion (CV2 Qtotal) and its components in the vertical (CV2 Qvgrad) and cranio-caudal (CV2 Qzgrad) directions, and the residual heterogeneity (CV2 Qr), were assessed at baseline and while breathing oxygen and nitric oxide (O2 + iNO). The length scale spectrum of CV2 Qr was determined from 10 to 110 mm, and the response of regional perfusion to O2 + iNO was calculated as the mean of absolute differences. Vertical gradients in perfusion (Qvgrad) were derived from perfusion images, and ventilation-perfusion distributions from images of 13NN washout kinetics. Results O2 + iNO significantly enhanced perfusion distribution differences between PAH and controls, allowing differentiation of PAH subjects from controls. During O2 + iNO, CV2 Qvgrad was significantly higher in controls than in PAH (0.08 (0.055–0.10) vs. 6.7 × 10–3 (2 × 10–4–0.02), p < 0.001) with a considerable gap between groups. Qvgrad and CV2 Qtotal showed smaller differences: − 7.3 vs. − 2.5, p = 0.002, and 0.12 vs. 0.06, p = 0.01. CV2 Qvgrad had the largest effect size among the primary parameters during O2 + iNO. CV2 Qr, and its length scale spectrum were similar in PAH and controls. Ventilation-perfusion distributions showed a trend towards a difference between PAH and controls at baseline, but it was not statistically significant. Conclusions Perfusion imaging during O2 + iNO showed a significant difference in the heterogeneity associated with the vertical gradient in perfusion, distinguishing in this small cohort study PAH subjects from controls. |
| first_indexed | 2024-04-11T07:19:08Z |
| format | Article |
| id | doaj.art-b72092f0ebae45b79c5c838832f9ffbc |
| institution | Directory Open Access Journal |
| issn | 1465-993X |
| language | English |
| last_indexed | 2024-04-11T07:19:08Z |
| publishDate | 2022-12-01 |
| publisher | BMC |
| record_format | Article |
| series | Respiratory Research |
| spelling | doaj.art-b72092f0ebae45b79c5c838832f9ffbc2022-12-22T04:37:49ZengBMCRespiratory Research1465-993X2022-12-0123111610.1186/s12931-022-02239-8Perfusion imaging heterogeneity during NO inhalation distinguishes pulmonary arterial hypertension (PAH) from healthy subjects and has potential as an imaging biomarkerTilo Winkler0Puja Kohli1Vanessa J. Kelly2Ekaterina G. Kehl3Alison S. Witkin4Josanna M. Rodriguez-Lopez5Kathryn A. Hibbert6Mamary T. Kone7David M. Systrom8Aaron B. Waxman9Jose G. Venegas10Richard N. Channick11R. Scott Harris12Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical SchoolDepartment of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Massachusetts General Hospital and Harvard Medical SchoolAbstract Background Without aggressive treatment, pulmonary arterial hypertension (PAH) has a 5-year mortality of approximately 40%. A patient’s response to vasodilators at diagnosis impacts the therapeutic options and prognosis. We hypothesized that analyzing perfusion images acquired before and during vasodilation could identify characteristic differences between PAH and control subjects. Methods We studied 5 controls and 4 subjects with PAH using HRCT and 13NN PET imaging of pulmonary perfusion and ventilation. The total spatial heterogeneity of perfusion (CV2 Qtotal) and its components in the vertical (CV2 Qvgrad) and cranio-caudal (CV2 Qzgrad) directions, and the residual heterogeneity (CV2 Qr), were assessed at baseline and while breathing oxygen and nitric oxide (O2 + iNO). The length scale spectrum of CV2 Qr was determined from 10 to 110 mm, and the response of regional perfusion to O2 + iNO was calculated as the mean of absolute differences. Vertical gradients in perfusion (Qvgrad) were derived from perfusion images, and ventilation-perfusion distributions from images of 13NN washout kinetics. Results O2 + iNO significantly enhanced perfusion distribution differences between PAH and controls, allowing differentiation of PAH subjects from controls. During O2 + iNO, CV2 Qvgrad was significantly higher in controls than in PAH (0.08 (0.055–0.10) vs. 6.7 × 10–3 (2 × 10–4–0.02), p < 0.001) with a considerable gap between groups. Qvgrad and CV2 Qtotal showed smaller differences: − 7.3 vs. − 2.5, p = 0.002, and 0.12 vs. 0.06, p = 0.01. CV2 Qvgrad had the largest effect size among the primary parameters during O2 + iNO. CV2 Qr, and its length scale spectrum were similar in PAH and controls. Ventilation-perfusion distributions showed a trend towards a difference between PAH and controls at baseline, but it was not statistically significant. Conclusions Perfusion imaging during O2 + iNO showed a significant difference in the heterogeneity associated with the vertical gradient in perfusion, distinguishing in this small cohort study PAH subjects from controls.https://doi.org/10.1186/s12931-022-02239-8Pulmonary circulationVascular physiologyFunctional imagingPositron emission tomographyPerfusion distributionVentilation |
| spellingShingle | Tilo Winkler Puja Kohli Vanessa J. Kelly Ekaterina G. Kehl Alison S. Witkin Josanna M. Rodriguez-Lopez Kathryn A. Hibbert Mamary T. Kone David M. Systrom Aaron B. Waxman Jose G. Venegas Richard N. Channick R. Scott Harris Perfusion imaging heterogeneity during NO inhalation distinguishes pulmonary arterial hypertension (PAH) from healthy subjects and has potential as an imaging biomarker Respiratory Research Pulmonary circulation Vascular physiology Functional imaging Positron emission tomography Perfusion distribution Ventilation |
| title | Perfusion imaging heterogeneity during NO inhalation distinguishes pulmonary arterial hypertension (PAH) from healthy subjects and has potential as an imaging biomarker |
| title_full | Perfusion imaging heterogeneity during NO inhalation distinguishes pulmonary arterial hypertension (PAH) from healthy subjects and has potential as an imaging biomarker |
| title_fullStr | Perfusion imaging heterogeneity during NO inhalation distinguishes pulmonary arterial hypertension (PAH) from healthy subjects and has potential as an imaging biomarker |
| title_full_unstemmed | Perfusion imaging heterogeneity during NO inhalation distinguishes pulmonary arterial hypertension (PAH) from healthy subjects and has potential as an imaging biomarker |
| title_short | Perfusion imaging heterogeneity during NO inhalation distinguishes pulmonary arterial hypertension (PAH) from healthy subjects and has potential as an imaging biomarker |
| title_sort | perfusion imaging heterogeneity during no inhalation distinguishes pulmonary arterial hypertension pah from healthy subjects and has potential as an imaging biomarker |
| topic | Pulmonary circulation Vascular physiology Functional imaging Positron emission tomography Perfusion distribution Ventilation |
| url | https://doi.org/10.1186/s12931-022-02239-8 |
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