Management of a Mildly Symptomatic 65-Year-Old Woman with an Atrial Septal Defect in the Setting of Normal Pulmonary Artery Pressure

Uncorrected atrial septal defect undergoes right ventricle chronic volume overload which may lead to pulmonary hypertension and Eisenmenger Syndrome. The soluble suppression of tumorigenicity-2 is a left ventricle strain biomarker; however, its role in right ventricle strain is unclear. This study aimed to investigate the implication of serum soluble suppression of tumorigenicity-2 in adult uncorrected atrial septal defect. This was a cross-sectional study. We enrolled 81 adult uncorrected secundum atrial septal defect patients. Clinical and hemodynamic data were collected. Serum samples were withdrawn from the pulmonary artery during right heart catheterization. Serum soluble suppression of tumorigenicity-2 and NT-proBNP levels were measured. Subjects were divided into three groups based on clinical and hemodynamic severity. The correlation of soluble suppression of tumorigenicity-2 with patients' data and comparison among groups were analyzed. A p value <0.05 was considered statistically significant. Results showed that, there were significant correlations between serum soluble suppression of tumorigenicity-2 and mean pulmonary artery pressure ( r = 0.203, p = 0.035) and right ventricle end-diastolic diameter ( r = 0.203, p <0.05). Median serum soluble suppression of tumorigenicity-2 level was incrementally increased from group I (atrial septal defect and no-pulmonary hypertension), group II (left-to-right atrial septal defect and pulmonary hypertension), to group III (Eisenmenger Syndrome): (17.4 ng/mL, 21.8 ng/mL, and 29.4 ng/mL, respectively). A post-hoc analysis showed that serum soluble suppression of tumorigenicity-2 level was significantly different between groups I and III ( p = 0.01). Serum N terminal pro brain natriuretic peptide (NT-proBNP) level was consistently associated with worse clinical and hemodynamic parameters. No correlation was found between serum soluble suppression of tumorigenicity-2 and NT-proBNP level. In conclusion, serum soluble suppression of tumorigenicity-2 level had significant positive correlation with mean pulmonary artery pressure and right ventricle end-diastolic diameter in uncorrected secundum atrial septal defect patients. Higher serum soluble suppression of tumorigenicity-2 level was associated with the presence of pulmonary hypertension and Eisenmenger Syndrome in uncorrected secundum atrial septal defect patients.

Download Full-text

Atrial septal defect with right to left shunt despite normal pulmonary artery pressure

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(87)80104-3 ◽

1987 ◽

Vol 9 (1) ◽

pp. 221-224 ◽

Cited By ~ 36

Author(s):

James D. Thomas ◽

Burton S. Tabakin ◽

Frank P. Ittleman

Keyword(s):

Pulmonary Artery ◽

Atrial Septal Defect ◽

Pulmonary Artery Pressure ◽

Septal Defect ◽

Artery Pressure

Download Full-text

ATRIAL SEPTAL DEFECT: With special reference to the Electrocardiogram, the Pulmonary Artery Pressure and the Second Heart Sound

Heart ◽

10.1136/hrt.12.3.277 ◽

1950 ◽

Vol 12 (3) ◽

pp. 277-292 ◽

Cited By ~ 103

Author(s):

J. M. Barber ◽

O. Magidson ◽

P. Wood

Keyword(s):

Pulmonary Artery ◽

Atrial Septal Defect ◽

Special Reference ◽

Pulmonary Artery Pressure ◽

Septal Defect ◽

Heart Sound ◽

Artery Pressure ◽

Second Heart Sound

Download Full-text

Atrial flutter: yet another cause of arterial desaturation in atrial septal defect

Cardiology in the Young ◽

10.1017/s104795112100010x ◽

2021 ◽

pp. 1-3

Author(s):

Saurabh Kumar Gupta ◽

Sakshi Sachdeva ◽

Rajnish Juneja

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Atrial Septal Defect ◽

Atrial Flutter ◽

Pulmonary Artery Pressure ◽

Septal Defect ◽

Artery Pressure ◽

Arterial Desaturation ◽

Erroneous Diagnosis ◽

First Time

Abstract Pulmonary hypertension is not the only cause of arterial desaturation in patients with atrial septal defect. Arterial desaturation can also occur with normal pulmonary artery pressure making it mandatory to understand the mechanism to avoid erroneous diagnosis. In this report, for the first time, we demonstrate atrial flutter as the cause of arterial desaturation in a patient with large atrial septal defect despite normal pulmonary artery pressure, which was normalised following successful radiofrequency ablation.

Download Full-text

COMPARISON OF ELECTROCARDIOGRAPHS DATA AND PULMONARY ARTERY PRESSURE IN PATIENTS WITH ATRIAL SEPTAL DEFECT OPERATED IN ADULT AGE

Journal of Hypertension ◽

10.1097/00004872-200406002-00103 ◽

2004 ◽

Vol 22 (Suppl. 2) ◽

pp. S32-S33

Author(s):

L. G. Ambatiello ◽

D. M. Ataullakhanova ◽

E. V. Blinova ◽

T. A. Sakhnova ◽

I. E. Chazova

Keyword(s):

Pulmonary Artery ◽

Atrial Septal Defect ◽

Pulmonary Artery Pressure ◽

Septal Defect ◽

Adult Age ◽

Artery Pressure

Download Full-text

Acute Changes on Pulmonary Pressure Following Percutaneous Closure of Secundum Atrial Septal Defect

ACI (Acta Cardiologia Indonesiana) ◽

10.22146/aci.33553 ◽

2018 ◽

Vol 3 (2) ◽

pp. 106

Author(s):

Jessica Wiryanto ◽

Ingrid M. Pardede ◽

Sunanto Ng

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Atrial Septal Defect ◽

Pulmonary Artery Pressure ◽

Pulmonary Circulation ◽

Septal Defect ◽

Percutaneous Closure ◽

Secundum Atrial Septal Defect ◽

Device Closure ◽

Artery Pressure

Pulmonary hypertension is a common complication of congenital heart disease due to systemic – pulmonary circulation shunt which if left uncorrected leads to increased pulmonary artery pressure, vascular remodeling and further increase of pulmonary vascular resistance. Percutaneous closure of the defect interrupts this shunt thus reducing right heart and pulmonary circulation load and pulmonary artery pressure. In this paper we present two cases of percutaneous secundum atrial septal defect closure complicated by pulmonary hypertension along with echocardiographic evaluation of cardiopulmonary hemodynamic changes before and shortly after device closure. Forty years old and thirty three years old females presented to our clinics with classical symptoms of atrial septal defects, assessment revealed TVG of 37 mmHg and 30 mmHg,shortly after the procedure patient was re-evaluated and revealed TVG of 39 mmHg and 23 mmHg respectively. From these cases we conclude that changes in pulmonary artery pressure is not constantly found after device closure. However both patients display improvements in functional capabilities.

Download Full-text