Pulmonary Arterial Hypertension in Patients With Transcatheter Closure of Secundum Atrial Septal Defects

Abstract

Background— Pulmonary arterial hypertension (PAH) may develop in patients with atrial septal defects (ASD); however, little is known about associated risk factors and its evolution after transcatheter ASD closure. Methods and Results— We conducted a cohort study on 215 adults with attempted transcatheter ASD closure from 1999 to 2006. Patients were classified according to baseline systolic pulmonary artery pressures as having no (I, <40 mm Hg), mild (II, 40 to 49 mm Hg), moderate (III, 50 to 59 mm Hg), or severe (IV, ≥60 mm Hg) PAH. Independent predictors of moderate or severe PAH were older age (odds ratio [OR], 1.10 per year; P <0.0001), larger ASD (OR, 1.13 per millimeter; P =0.0052), female sex (OR, 3.9; P =0.0313), and at least moderate tricuspid regurgitation (OR, 3.6; P =0.0043). At 15 (interquartile range, 8 to 43) months post–ASD closure, patients with higher baseline pressures were more likely to experience a ≥5-mm Hg decrease (33.7%, 73.9%, 79.2%, and 100.0% in groups I to IV, P <0.0001), with a larger magnitude of reduction (0, 8, 17, and 22 mm Hg; P <0.0001). However, normalization of pressures (<40 mm Hg) occurred less frequently in patients with more advanced PAH (90.2%, 71.7%, 66.7%, and 23.5%, P <0.0001). Among patients with moderate or severe PAH, independent predictors of normalization were lower baseline pressures (OR, 0.91 per mm Hg; P =0.0418) and no more than mild tricuspid regurgitation (OR, 0.14; P =0.0420). Conclusion— In adults with ASDs, severity of PAH is modulated by age, sex, defect size, and degree of tricuspid regurgitation. Patients with moderate or severe PAH may benefit from substantial reductions in pulmonary artery pressures after transcatheter ASD closure, although the PAH values remain elevated in a sizeable proportion.

Pediatric Pulmonary Hypertension

“…The incidence of PH in patients with an ASD is 6% to 17% 395 ; PAH persisting after ASD closure is more likely in older patients with larger defects. 396 Infants with an ASD or a VSD with concomitant chronic lung disease are at an increased risk for the early development of severe PVD and complications after cardiac surgery. 397 The presence of resting cyanosis (oxygen saturation <90%) is worrisome because it predicts risk of elevated PVR and death after closure of the defect.…”

Pulmonary Vascular Resistance as Assessed by Bicycle Stress Echocardiography in Patients With Atrial Septal Defect Type Secundum

“…Indeed, age at repair is known as an independent predictor of late outcome, 20 and late closure is associated with incomplete remodeling. [5][6][7] Bicycle stress echocardiography may identify patients with altered pulmonary vascular hemodynamics that could not be detected at rest. A steeper PAP-flow plot may be related to limitations in exercise capacity as indicated by the relation with peak VO 2 .…”

“…3,4 When occlusive fibrotic lesions have developed, closure of the ASD later in life, although still feasible, may not result in complete normalization of pulmonary artery pressures and has been shown to be associated with worse outcome. [5][6][7] Studies have suggested that an abnormal increase in pulmonary artery pressures during exercise reflects mild pulmonary vascular disease and limits exercise capacity. 8 -11 However, pulmonary artery pressures are defined by both cardiac output and PVR.…”

Clinical Evaluation and Management of Pulmonary Hypertension in the Adult With Congenital Heart Disease

“…This situation is commonly encountered following ASD repair; despite favorable overall prognosis, echocardiography suggests a high prevalence of PH. 9 Elevated PASP in this situation may be attributable to (1) high PVR (ie, true PAH-CHD); (2) a spurious finding, because echocardiographic and invasive PAP correlate only moderately (r≈0.7) with wide limits of agreement 9,10 ; (3) elevated pulmonary venous pressure, which is common after ASD closure owing to noncompliant atria or septal patch/device; or (4) high pulse pressure due to stiff, noncompliant pulmonary arteries secondary to chronic pulmonary overcirculation.…”