Pulmonary edema after device closure of ASD

Pulmonary edema after device closure of ASD

Device closure of atrial septal defect (ASD) is almost replacing surgical ASD closure in all cases with suitable morphology. Percutaneous ASD closure is usually well tolerated. One of the rarest complications in literature following device closure of atrial septal defect is the occurrence of pulmonary edema after device closure of ASD. Acute pulmonary edema is well reported after surgical closure of ASD, especially in the elderly, when a sudden increase in the preload to a poorly compliant and small left ventricle leads to diastolic heart failure.

One of the earliest reports of left heart failure after device closure of ASD was in a 78 year old female who had a left ventricular ejection fraction of 65% [1]. She developed acute left ventricular failure and pulmonary edema two hours after device closure of ASD, with left ventricular ejection fraction of 20%. She needed mechanical ventilation, catecholamine support and high dose diuretics. She had to be in hospital for two weeks after the procedure. Low preload which was there due to ASD for decades would have predisposed for left ventricular failure with sudden increase in preload after device closure of ASD.

Similar episodes have been reported by other workers as well [2,3]. In a large series of 529 patients undergoing ASD device closure between 1998 and 2008, Tomar M et al had three patients with transient pulmonary edema. They needed intensive care for two days post procedure [4].

Left ventricular conditioning to prevent pulmonary edema after device closure of ASD

Schubert S and colleagues successfully used left ventricular conditioning to prevent acute left ventricular failure in patients aged above 60 years, undergoing device closure of ASD [5]. They assessed the response to balloon occlusion of atrial septal defect and if the mean atrial pressures rose over 10 mm Hg, the device closure was deferred and left ventricular conditioning applied. Left ventricular conditioning was with dopamine, milrinone and furosemide for 48-72 hours prior to definitive ASD closure. This was needed in one fourth of their elderly patients. Device closure was done uneventfully in after conditioning in all but two who were given fenestrated device because the atrial pressures remained above 10 mm Hg even after pre-treatment.


  1. Ewert P, Berger F, Nagdyman N, Kretschmar O, Lange PE. Acute left heart failure after interventional occlusion of an atrial septal defect. Z Kardiol. 2001 May;90(5):362-6.
  2. Singhi AK, Mahesh K, Kumar RK. Pulmonary edema following transcatheter closure of atrial septal defect. Ann Pediatr Cardiol. 2010 Jan;3(1):90-1.
  3. Viaene D, Vermeersch P, Van den Branden F. Pulmonary oedema after percutaneous ASD-closure. Acta Cardiol. 2010 Apr;65(2):257-60.
  4. Tomar M, Khatri S, Radhakrishnan S, Shrivastava S. Intermediate and long-term followup of percutaneous device closure of fossa ovalis atrial septal defect by the Amplatzer septal occluder in a cohort of 529 patients. Ann Pediatr Cardiol. 2011 Jan;4(1):22-7.
  5. Schubert S, Peters B, Abdul-Khaliq H, Nagdyman N, Lange PE, Ewert P. Left ventricular conditioning in the elderly patient to prevent congestive heart failure after transcatheter closure of atrial septal defect. Catheter Cardiovasc Interv. 2005 Mar;64(3):333-7.