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Closure of a Patent Foramen Ovale (PFO): An Intervention Sequence
Published on: December 23, 2022
Haemodynamic effects of patent foramen ovale and atrial septal defect closure: a comparison during percutaneous shunt
Justin G L M Luermans1, Willem J W Bos, Martijn C Post
1Department of Cardiology, St Antonius Hospital, Nieuwegein, the Netherlands.
Insights
Percutaneous closure of atrial septal defects (ASD) in adults significantly increases blood pressure and stroke volume. Patent foramen ovale (PFO) closure showed no significant short-term hemodynamic changes.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Hemodynamics
Background:
- Percutaneous closure of patent foramen ovale (PFO) and atrial septal defect (ASD) is common.
- Limited data exist on immediate hemodynamic changes post-closure.
Purpose of the Study:
- To investigate the acute hemodynamic effects of percutaneous intra-atrial shunt closure.
- To compare changes between PFO and ASD closure.
Main Methods:
- Non-invasive finger pressure measurements (Finometer) in 25 patients undergoing PFO (n=15) or ASD (n=10) closure.
- Modelflow methodology used to calculate systolic, mean, diastolic pressures, heart rate, stroke volume, cardiac output, and total peripheral resistance.
Main Results:
- ASD closure led to significant increases in systolic (7.1 mmHg), mean (3.8 mmHg) pressures, and stroke volume (8.5 ml, 13.5%).
- Heart rate decreased by 5.1 bpm after ASD closure.
- PFO closure did not result in significant hemodynamic alterations.
Conclusions:
- Percutaneous ASD closure in adults acutely increases systolic blood pressure and stroke volume.
- Percutaneous PFO closure has no immediate hemodynamic impact.
Summary Objectives:
We investigated the haemodynamic effect of percutaneous closure of an intra-atrial shunt, using non-invasive finger pressure measurements.
Background:
Percutaneous closure of both patent foramen ovale (PFO) and atrial septal defect (ASD) is widely practised. Currently no data are available on short-term haemodynamic changes induced by closure.
Methods:
Twenty-five consecutive patients (mean age 49 +/- 17 years, 10 men) who underwent a percutaneous closure of a PFO (n = 15) or ASD (n = 10) were included in this study. During the procedure blood pressure and heart rate (HR) were monitored continuously with a Finometer. Changes in systolic, mean, and diastolic pressure, stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were computed from the pressure registrations using Modelflow methodology.
Results:
Baseline characteristics were similar for the PFO and ASD patients. After PFO closure none of the haemodynamic parameters changed significantly. After ASD closure the systolic, mean, and diastolic pressures increased 7.1 +/- 5.4 (P = 0.003), 3.8 +/- 3.5 (P = 0.007) and 2.0 +/- 3.0 mmHg (P = ns) respectively. HR decreased 5.1 +/- 5.3 beats per minute (P = 0.01). SV, CO and TPR increased 8.5 +/- 6.4 ml (13.5%; P = 0.002), 0.21 +/- 0.45 l min(-1) (5.6%; P = ns) and 0.02 +/- 0.14 dynes (4.1%; P = ns) respectively. The changes in SV differ between the PFO and ASD patients (P = 0.009).
Conclusions:
Using non-invasive finger pressure measurements, we found that SV, mean and systolic blood pressure increased immediately after percutaneous closure of an ASD in adults, whereas the percutaneous PFO closure had no effect on haemodynamic characteristics.

