Congenital Absence of the Left Pericardium in Combination with Left Pulmonary Artery Hypoplasia, Right Aortic Arch, and Secundum Atrial Septal Defect

1992 ◽  
Vol 40 (03) ◽  
pp. 155-157 ◽  
Author(s):  
V. Lonský ◽  
M. Štětina ◽  
P. Habal ◽  
D. Marková
Keyword(s):  
Pulmonary Artery ◽  
Atrial Septal Defect ◽  
Aortic Arch ◽  
Septal Defect ◽  
Left Pulmonary Artery ◽  
Right Aortic Arch ◽  
Congenital Absence ◽  
Secundum Atrial Septal Defect ◽  
Pulmonary Artery Hypoplasia

Isolation of the left brachiocephalic artery associated with right aortic arch and left-sided arterial duct

1996 ◽  
Vol 6 (3) ◽  
pp. 239-241 ◽  
Author(s):  
Sashicanta Kaku ◽  
Fatima Pinto ◽  
Manuela Lima
Keyword(s):  
Ventricular Septal Defect ◽  
Pulmonary Artery ◽  
Aortic Arch ◽  
Septal Defect ◽  
Left Pulmonary Artery ◽  
Right Aortic Arch ◽  
Brachiocephalic Artery ◽  
Caval Vein ◽  
Superior Caval Vein ◽  
The Right

SummaryWe report a case of right aortic arch and isolation of the left brachiocephalic artery. Stenosis of the left pulmonary artery, ventricular septal defect and left superior caval vein draining to the right atrium via the coronary sinus were also present in a 13-month-old asymptomatic girl with Down's syndrome. To our knowledge, this association of lesions has not previously been described.

Hoarseness after pulmonary arterial stenting and occlusion of the arterial duct

2003 ◽  
Vol 13 (3) ◽  
pp. 302-304 ◽  
Author(s):  
Mervat Assaqqat ◽  
Ghassan Siblini ◽  
Fadel Al Fadley
Keyword(s):  
Pulmonary Artery ◽  
Atrial Septal Defect ◽  
Recurrent Laryngeal Nerve ◽  
Septal Defect ◽  
Left Pulmonary Artery ◽  
Laryngeal Nerve ◽  
Arterial Stenosis ◽  
Arterial Duct ◽  
Cardiac Lesions ◽  
Pulmonary Arterial

We report a 12-year-old girl who had multiple congenital cardiac lesions, specifically an arterial duct, left pulmonary arterial stenosis, an atrial septal defect in the oval fossa, and mild Ebstein's malformation of the tricuspid valve. Therapeutic transcatheter intervention was performed to stent the left pulmonary artery, occlude the arterial duct with a coil, and place a device to close the atrial septal defect. Subsequent to the catheterization, she complained of hoarseness, which was shown to be due to entrapment of the left recurrent laryngeal nerve between the coil used to close the arterial duct and the stent placed in the left pulmonary artery. Laryngoscopy confirmed paralysis of the recurrent laryngeal nerve.

scholarly journals Serum soluble suppression of tumorigenicity-2 level associates with severity of pulmonary hypertension associated with uncorrected atrial septal defect

2020 ◽  
Vol 10 (2) ◽  
pp. 204589402091583 ◽  
Author(s):  
Reza S. Pratama ◽  
Anggoro B. Hartopo ◽  
Dyah W. Anggrahini ◽  
Vera C. Dewanto ◽  
Lucia K. Dinarti
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Atrial Septal Defect ◽  
Pulmonary Artery Pressure ◽  
Septal Defect ◽  
Eisenmenger Syndrome ◽  
Secundum Atrial Septal Defect ◽  
Artery Pressure ◽  
Mean 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.

Anomalous Origin of Left Pulmonary Artery from Aorta with Atrial Septal Defect

2008 ◽  
Vol 29 (4) ◽  
pp. 860-861
Author(s):  
Jang Hoon Lee ◽  
Tae Eun Jung ◽  
Young Hwan Lee
Keyword(s):  
Pulmonary Artery ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Left Pulmonary Artery ◽  
Anomalous Origin
Sign in / Sign up

Export Citation Format

Share Document