Good fences make good neighbors: How an iatrogenic atrial septal defect can impact the pulmonary circulation.

Document Type

Conference Proceeding

Publication Date


Publication Title

Am J Respir Crit Care Med


We present a case of pulmonary arterial hypertension (PAH) worsened by the iatrogenic creation of an atrial septal defect (ASD) during an interventional cardiac procedure. Case Report A 77-year-old female presented for dyspnea associated with hypoxemia that had worsened two years after a left atrial appendage (LAA) ablation done for atrial fibrillation with inability to tolerate anticoagulation. Historically she had mild emphysema, hypertension, mitral valve regurgitation (MVR) and a known small patent foramen ovale (PFO) with left-to-right shunting. Current echocardiogram now showed bidirectional shunting; with new right-to-left shunting across the PFO and a large degree of left-to-right shunting across the persistent ASD created during the ablation procedure. The patient underwent right heart catheterization (RHC) and was found to have both precapillary and postcapillary pulmonary hypertension (PH) in the setting of left-to-right shunt. Postcapillary PH improved with the administration of nitroprusside with an associated increment in cardiac output (table). Due to concern for worsening of the precapillary PH component by significant left-to-right shunting, decision was made to close the ASD with a GORE Cardioform Septal Occluder device, resulting also in closure of the PFO due to close proximity. The procedure was well-tolerated, however, she had minimal relief of symptoms in the following months despite efforts at optimizing blood pressure and volume status. Repeat RHC done four months later showed severe precapillary PH with complete resolution of postcapillary PH (table), likely the result of vascular remodeling due to longstanding postcapillary PH, further worsened by former ASD. Given New York Heart Association (NYHA) Functional Class (FC) IV symptoms, intravenous treprostinil was initiated with marked improvement in NYHA FC, brain natriuretic peptide, normalization of pulmonary artery pressure on echocardiogram and decreased oxygen requirements. Discussion PAH is well described in cases of congenital heart disease, including ASD. In the case of our patient, iatrogenically created ASD led to significant left-to-right shunting. This likely worsened pulmonary vasculopathy and remodeling resulting in severe PAH improved by parenteral pulmonary vasodilator therapy. With advances in minimally invasive cardiac procedures requiring transseptal puncture, iatrogenically created PAH due to this mechanism may increase in incidence. Conclusion Our case illustrates an iatrogenic cause of PAH due to left-to-right shunting accentuated by an ASD created during LAA ablation. This phenomenon was treatable by closure of the shunt and initiation of parenteral pulmonary vasodilators. As minimally invasive cardiac interventional procedures become more common, surveillance for this iatrogenic cause of PAH will be needed. [Table Presented].



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