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Pulmonary Artery Endovascular Device to Improve Vascular Compliance in Pulmonary Hypertension
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A7593 - Pulmonary Artery Endovascular Device to Improve Vascular Compliance in Pulmonary Hypertension
Author Block: I. M. Lang1, K. Vollmers2, C. Gerges3, M. Pritzker4, J. Gainor5, J. Scandurra5, E. Weir6, I. M. Lang7; 1Internal Medicine II, Cardiology, AKH-Vienna, Medical University of Vienna, Vienna, Austria, 2Aria CV, Saint Paul, MN, United States, 3Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Vienna, Austria, 4University of Minnesota, St. Paul, MN, United States, 5Aria CV, Minneapolis, MN, United States, 6VA Medical Center, Wayzata, MN, United States, 7Medical University of Vienna, Vienna, Austria.
Deadline for abstract submission: Wednesday 1 November 2017
Current word count: 232 (limit 400, not including, title, author’s info, institutions, tables, images and spaces)
Title:
Karl Vollmers1, Christian Gerges2, Marc Pritzker3, John Gainor1, John Scandurra1, Kenneth Weir3, Irene M Lang2
Affiliations: 1) Aria CV, Saint Paul Minnesota, 2) Medical University of Vienna, 3) University of Minnesota
This abstract was funded by Aria CV.
Rationale: Pulmonary arterial hypertension (PAH) is associated with an early and progressive loss of pulmonary arterial compliance (CPA). Low CPA is a sensitive prognostic indicator for mortality in PAH (1).
Methods: Following routine right heart catheterization, we determined whether a balloon, placed percutaneously in the main pulmonary artery, connected through a catheter to a reservoir outside the body, could acutely improve CPA. We hypothesized that the movement of gas from the balloon to the reservoir in systole may compensate for the loss of CPA.
Results: In seven patients with severe PAH on stable multidrug therapy, percutaneous activation of the device for approximately 10 minutes increased CPA by 0.4ml/mmHg (22%) and increased direct Fick cardiac output by 0.6L/min (7%). Exercise in five patients, after activation of the device for 10 minutes, increased CPA by 0.6ml/mmHg (47%), and increased cardiac output by 1.6 L/min (20%), relative to control exercise. There were no complications.
Conclusions: Because a difference in baseline CPA of 0.4ml/mmHg between groups of PAH patients has been reported to be associated with a marked difference in long-term mortality (2), we conclude that the activation of our pulmonary artery balloon device on top of combination PAH-specific treatment may enable a sustained increase of CPA during chronic use, thus potentially improving long-term mortality.
1.
Thenappan T et al, Ann Am Thorac Soc 2016 13: 276-284
2. McGoon MD et al, JACC 2006 47: 799-8032.
Author Block: I. M. Lang1, K. Vollmers2, C. Gerges3, M. Pritzker4, J. Gainor5, J. Scandurra5, E. Weir6, I. M. Lang7; 1Internal Medicine II, Cardiology, AKH-Vienna, Medical University of Vienna, Vienna, Austria, 2Aria CV, Saint Paul, MN, United States, 3Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Vienna, Austria, 4University of Minnesota, St. Paul, MN, United States, 5Aria CV, Minneapolis, MN, United States, 6VA Medical Center, Wayzata, MN, United States, 7Medical University of Vienna, Vienna, Austria.
Deadline for abstract submission: Wednesday 1 November 2017
Current word count: 232 (limit 400, not including, title, author’s info, institutions, tables, images and spaces)
Title:
Karl Vollmers1, Christian Gerges2, Marc Pritzker3, John Gainor1, John Scandurra1, Kenneth Weir3, Irene M Lang2
Affiliations: 1) Aria CV, Saint Paul Minnesota, 2) Medical University of Vienna, 3) University of Minnesota
This abstract was funded by Aria CV.
Rationale: Pulmonary arterial hypertension (PAH) is associated with an early and progressive loss of pulmonary arterial compliance (CPA). Low CPA is a sensitive prognostic indicator for mortality in PAH (1).
Methods: Following routine right heart catheterization, we determined whether a balloon, placed percutaneously in the main pulmonary artery, connected through a catheter to a reservoir outside the body, could acutely improve CPA. We hypothesized that the movement of gas from the balloon to the reservoir in systole may compensate for the loss of CPA.
Results: In seven patients with severe PAH on stable multidrug therapy, percutaneous activation of the device for approximately 10 minutes increased CPA by 0.4ml/mmHg (22%) and increased direct Fick cardiac output by 0.6L/min (7%). Exercise in five patients, after activation of the device for 10 minutes, increased CPA by 0.6ml/mmHg (47%), and increased cardiac output by 1.6 L/min (20%), relative to control exercise. There were no complications.
Conclusions: Because a difference in baseline CPA of 0.4ml/mmHg between groups of PAH patients has been reported to be associated with a marked difference in long-term mortality (2), we conclude that the activation of our pulmonary artery balloon device on top of combination PAH-specific treatment may enable a sustained increase of CPA during chronic use, thus potentially improving long-term mortality.
1.
Thenappan T et al, Ann Am Thorac Soc 2016 13: 276-284
2. McGoon MD et al, JACC 2006 47: 799-8032.
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