Abstract
PURPOSE The patent foramen ovale (PFO) is a source of intracardiac right-to-left shunt and is present in ~1/3rd of the adult population. Deficits in pulmonary gas exchange efficiency associated with PFO have been well-documented (Lovering et al, J Appl Physiol 2016). However, changes in pulmonary artery pressure and total pulmonary resistance (TPR) following closure have not previously been reported. METHODS Four candidates (3F, 1M) for closure of PFO were identified by local cardiologists and referred to our laboratory as subjects. 3 subjects (3F) received physician clearance to participate in the exercise trials. 1 subject (1M) was not cleared for exercise so only resting measures were taken. Presence and size of PFO was confirmed utilizing transthoracic saline contrast echocardiography (TTSCE). A radial arterial catheter was placed utilizing aseptic technique. Subjects exercised at 4 sub-maximal workloads (25%, 50%, 75% and 90% of pre-closure VO2Max), with arterial blood drawn anaerobically during the last 30 seconds of each workload and immediately analyzed in duplicate for gas content. Transthoracic ultrasound measures of cardiac output (QT) and pulmonary arterial systolic pressure (PASP) were taken prior to exercise and during the final minute of each workload. TPR was calculated as PASP/ QT. Subjects then underwent percutaneous closure of PFO utilizing a commercially available closure device (Amplatzer PFO Occluder, Abbott, Illinois; Cardioform Septal Occluder, GORE, Arizona). All measures were repeated in the laboratory 3-6 months after closure of PFO following confirmation of endothelialization of the closure device with TTSCE. RESULTS Data were analyzed by a 2-way (Closure x Workload) RMANOVA. There was a main effect of closure on PASP F(1, 11) = 21.05, p = 0.0008, and a main effect of closure on TPR F(1, 11) = 9.899, p = 0.0093, with reductions in both following closure. There was a main effect of workload, but not closure, on cardiac output F(4, 11) = 60.18, p < 0.0001. There were main effects of both workload F(4,11) = 73665, p = .0033 and closure F(1,11) = 28.31, p = .0002 on pulmonary gas exchange efficiency. CONCLUSION Improvements in pulmonary gas exchange efficiency are expected with removal of the intracardiac right-to-left shunt. However, our results demonstrating a significantly reduced pulmonary artery pressure, due to a significantly reduced TPR, are intriguing and deserve more attention to better understand the contributing factors of a PFO to exercise-induced pulmonary hypertension.
Published Version
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