scholarly journals Echocardiographically-Derived Septal Positional Angle (EDSPA) as a Measure of Elevated Right Ventricular Systolic Pressure

2021 ◽  
Author(s):  
Jennifer Huang ◽  
Zach Hutchinson ◽  
Grant Burch ◽  
Brendan Kelly ◽  
Erin Madriago
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Atrial Septal Defect ◽  
Correlation Coefficient ◽  
Cardiac Catheterization ◽  
Septal Defect ◽  
Pearson Correlation ◽  
Observer Variability ◽  
Non Invasive ◽  
Positional Angle

Background: Pulmonary hypertension is a significant yet rare disease that can have many long-term consequences, including death. Cardiac catheterization is the gold standard for measuring pulmonary artery mean pressures (PAMP), but is invasive and risks potentially serious complications. This study aimed to create a semi-quantitative, non-invasive measure of PAMP using septal positioning. Methods: This study was a retrospective study of patients with and without pulmonary hypertension who had a transthoracic echocardiogram and cardiac catheterization. Patients undergoing atrial septal defect closure represented controls. Two blinded readers calculated the “Echocardiographically-Derived Septal Positional Angle (EDSPA)” which was compared to corresponding catheterization data including mean pulmonary artery pressures. Results: A total of 159 children were included, of which 151 had useable echocardiographic data. 40 children were identified as having pulmonary hypertension while 111 children had an atrial septal defect. Patient age ranged from a minimum of 54 days and maximum of 19 years [mean 7.1 years (SD=5.30)]. Inter-observer variability between two readers [Pearson correlation coefficient of 0.939 (p <0.001)] and intra-observer variability were low [intraclass correlation coefficient (ICC) of 0.95 and 0.96 for each observer respectively]. An EDSPA of ≤39° predicted a PAMP>20 mmHg (as measured by cardiac catheterization) with a 76% sensitivity and 76% specificity (AUC 0.846). Conclusions: EDSPA is a useful, non-invasive, and reproducible echocardiographic measure of PAMP that is easy to perform. With a sensitivity and specificity near 80%, it has significant utility in screening for pulmonary hypertension and determining which patients should undergo further invasive diagnostic testing.

scholarly journals Pulmonary Artery Pressure Profile in Atrial Septal Defect (ASD) Patients

2016 ◽  
Vol 30 (1) ◽  
pp. 27-28 ◽  
Author(s):  
Md Serajul Haque ◽  
HI Lutfur Rahman Khan ◽  
Razia Sultana Mahmud ◽  
Md Faruq ◽  
Abdul Wadud Chowdury ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Atrial Septal Defect ◽  
Pulmonary Artery Pressure ◽  
Cardiac Catheterization ◽  
Septal Defect ◽  
Age Distribution ◽  
Pressure Profile ◽  
Mean Pressure ◽  
Age Range

The objective of this study was to see the incidence of pulmonary hypertension and its age distribution in atrial septal defect (ASD) patients in our population. A total of 58 ASD (secundum type) patients were included in the study. The diagnosis was done with echocardiography. Subsequently patients under went cardiac catheterization and their pulmonary artery (PA) mean pressure was measured. It was seen that pulmonary pressure increases with age. Severe PA hypertension (mean pressure > 40 mm Hg) was found in 14 patients (24.14%), age range was 10-55 years but most of them were more than 20 years old.Bangladesh Heart Journal 2015; 30(1) : 27-28

Relationship between Invasive and Non-Invasive Hemodynamic Measures in Experimental Pulmonary Hypertension

2020 ◽  
Vol 16 (1) ◽  
pp. 47-53
Author(s):  
Vicente Benavides-Córdoba ◽  
Mauricio Palacios Gómez
Keyword(s):  
Heart Rate ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Right Ventricle ◽  
Correlation Coefficient ◽  
Pearson Correlation ◽  
Systolic Pressure ◽  
Control Group ◽  
Pearson Correlation Coefficient ◽  
Non Invasive

Introduction: Animal models have been used to understand the pathophysiology of pulmonary hypertension, to describe the mechanisms of action and to evaluate promising active ingredients. The monocrotaline-induced pulmonary hypertension model is the most used animal model. In this model, invasive and non-invasive hemodynamic variables that resemble human measurements have been used. Aim: To define if non-invasive variables can predict hemodynamic measures in the monocrotaline-induced pulmonary hypertension model. Materials and Methods: Twenty 6-week old male Wistar rats weighing between 250-300g from the bioterium of the Universidad del Valle (Cali - Colombia) were used in order to establish that the relationships between invasive and non-invasive variables are sustained in different conditions (healthy, hypertrophy and treated). The animals were organized into three groups, a control group who was given 0.9% saline solution subcutaneously (sc), a group with pulmonary hypertension induced with a single subcutaneous dose of Monocrotaline 30 mg/kg, and a group with pulmonary hypertension with 30 mg/kg of monocrotaline treated with Sildenafil. Right ventricle ejection fraction, heart rate, right ventricle systolic pressure and the extent of hypertrophy were measured. The functional relation between any two variables was evaluated by the Pearson correlation coefficient. Results: It was found that all correlations were statistically significant (p <0.01). The strongest correlation was the inverse one between the RVEF and the Fulton index (r = -0.82). The Fulton index also had a strong correlation with the RVSP (r = 0.79). The Pearson correlation coefficient between the RVEF and the RVSP was -0.81, meaning that the higher the systolic pressure in the right ventricle, the lower the ejection fraction value. Heart rate was significantly correlated to the other three variables studied, although with relatively low correlation. Conclusion: The correlations obtained in this study indicate that the parameters evaluated in the research related to experimental pulmonary hypertension correlate adequately and that the measurements that are currently made are adequate and consistent with each other, that is, they have good predictive capacity.

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.

Massive Pulmonary Artery Thrombosis, Pulmonary Hypertension and Untreated Atrial Septal Defect

Cardiology ◽  
2002 ◽  
Vol 97 (1) ◽  
pp. 53-54 ◽  
Author(s):  
Nobukazu Ishizaka ◽  
Norihide Kage ◽  
Haruko Iida ◽  
Shinsuke Mutoh ◽  
Yasunobu Hirata ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Artery Thrombosis

scholarly journals Non-invasive pulmonary artery pressure estimation by electrical impedance tomography in a controlled hypoxemia study in healthy subjects

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Martin Proença ◽  
Fabian Braun ◽  
Mathieu Lemay ◽  
Josep Solà ◽  
Andy Adler ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Healthy Volunteers ◽  
Correlation Coefficient ◽  
Electrical Impedance Tomography ◽  
Pulmonary Artery Pressure ◽  
Electrical Impedance ◽  
Impedance Tomography ◽  
Artery Pressure ◽  
Non Invasive

AbstractPulmonary hypertension is a hemodynamic disorder defined by an abnormal elevation of pulmonary artery pressure (PAP). Current options for measuring PAP are limited in clinical practice. The aim of this study was to evaluate if electrical impedance tomography (EIT), a radiation-free and non-invasive monitoring technique, can be used for the continuous, unsupervised and safe monitoring of PAP. In 30 healthy volunteers we induced gradual increases in systolic PAP (SPAP) by exposure to normobaric hypoxemia. At various stages of the protocol, the SPAP of the subjects was estimated by transthoracic echocardiography. In parallel, in the pulmonary vasculature, pulse wave velocity was estimated by EIT and calibrated to pressure units. Within-cohort agreement between both methods on SPAP estimation was assessed through Bland–Altman analysis and at subject level, with Pearson’s correlation coefficient. There was good agreement between the two methods (inter-method difference not significant (P > 0.05), bias ± standard deviation of − 0.1 ± 4.5 mmHg) independently of the degree of PAP, from baseline oxygen saturation levels to profound hypoxemia. At subject level, the median per-subject agreement was 0.7 ± 3.8 mmHg and Pearson’s correlation coefficient 0.87 (P < 0.05). Our results demonstrate the feasibility of accurately assessing changes in SPAP by EIT in healthy volunteers. If confirmed in a patient population, the non-invasive and unsupervised day-to-day monitoring of SPAP could facilitate the clinical management of patients with pulmonary hypertension.

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

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.

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

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.

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