scholarly journals ‘End-stage’ heart failure therapy: potential lessons from congenital heart disease: from pulmonary artery banding and interatrial communication to parallel circulation

Heart ◽  
2016 ◽  
Vol 103 (4) ◽  
pp. 262-267 ◽  
Author(s):  
Dietmar Schranz ◽  
Hakan Akintuerk ◽  
Norbert F Voelkel
Keyword(s):  
Heart Failure ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Congenital Heart ◽  
Pulmonary Artery Banding ◽  
Heart Failure Therapy ◽  
Interatrial Communication ◽  
End Stage Heart Failure ◽  
End Stage

Polymorphisms in cytokine genes do not predict progression to end-stage heart failure in children

2002 ◽  
Vol 12 (5) ◽  
pp. 461-464 ◽  
Author(s):  
Steven A. Webber ◽  
Gerard J. Boyle ◽  
Steven Gribar ◽  
Yuk Law ◽  
Pamela Bowman ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Inflammatory Cytokines ◽  
Congenital Heart ◽  
Healthy Children ◽  
Ventricular Failure ◽  
Cytokine Genes ◽  
End Stage Heart Failure ◽  
End Stage

A number of cytokines have been implicated in the pathophysiology of congestive heart failure. Genetic polymorphisms of several cytokine genes are known to result in altered gene expression, enabling us to characterize patients as "high" or "low" producers of specific cytokines. We speculate that the cytokine genotypes for a population of children who underwent heart transplantation for end-stage ventricular failure due to cardiomyopathy or congenital heart disease would be enriched for "high producers" of pro-inflammatory cytokines and "low producers" of anti-inflammatory cytokines. Methods: Cytokine genotyping was performed for the following cytokines on 94 transplanted children using polymerase chain reaction-sequence specific technique: tumor necrosis factor-α (−308), interleukin 10 (−1082, −819, −592), interleukin 6 (−174), transforming growth factor-β1(codons 10 & 25), and interferon-γ (+874). Patients with ventricular failure after transplantation for dilated cardiomyopathy, numbering 37, or for congenital heart disease, numbering 34, were compared to 15 children transplanted for structural disease, such as hypoplastic left heart syndrome, without ventricular failure, and to data from healthy children. An additional 8 children with restrictive or hypertrophic cardiomyopathy were also studied. Results: No differences in genotypic distribution were seen between the groups, and all patients were comparable to genotypic distributions as assessed from published normal data. Conclusion: No evidence is found to support the hypothesis that these polymorphisms for cytokine genes influence progression to end-stage heart failure in children undergoing transplantation because of cardiomyopathy or congenital heart disease.

scholarly journals Left Ventricular Noncompaction and Congenital Heart Disease Increases the Risk of Congestive Heart Failure

2020 ◽  
Vol 9 (3) ◽  
pp. 785 ◽  
Author(s):  
Keiichi Hirono ◽  
Yukiko Hata ◽  
Nariaki Miyao ◽  
Mako Okabe ◽  
Shinya Takarada ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Congenital Heart ◽  
Left Ventricular ◽  
Pulmonary Artery Banding ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
Septal Defects

Background: Left ventricular noncompaction (LVNC) is a hereditary cardiomyopathy that is associated with high morbidity and mortality rates. Recently, LVNC was classified into several phenotypes including congenital heart disease (CHD). However, although LVNC and CHD are frequently observed, the role and clinical significance of genetics in these cardiomyopathies has not been fully evaluated. Therefore, we aimed to evaluate the impact on the perioperative outcomes of children with concomitant LVNC and CHD using next-generation sequencing (NGS). Methods: From May 2000 to August 2018, 53 Japanese probands with LVNC (25 males and 28 females) were enrolled and we screened 182 cardiomyopathy-associated genes in these patients using NGS. Results: The age at diagnosis of the enrolled patients ranged from 0 to 14 years (median: 0.3 months). A total of 23 patients (43.4%) were diagnosed with heart failure, 14 with heart murmur (26.4%), and 6 with cyanosis (11.3%). During the observation period, 31 patients (58.5%) experienced heart failure and 13 (24.5%) developed arrhythmias such as ventricular tachycardia, supraventricular tachycardia, and atrioventricular block. Moreover, 29 patients (54.7%) had ventricular septal defects (VSDs), 17 (32.1%) had atrial septal defects, 10 had patent ductus arteriosus (PDA), and 7 (13.2%) had Ebstein’s anomaly and double outlet right ventricle. Among the included patients, 30 underwent surgery, 19 underwent biventricular repair, and 2 underwent pulmonary artery banding, bilateral pulmonary artery banding, and PDA ligation. Overall, 30 genetic variants were identified in 28 patients with LVNC and CHD. Eight variants were detected in MYH7 and two in TPM1. Echocardiography showed lower ejection fractions and more thickened trabeculations in the left ventricle in patients with LVNC and CHD than in age-matched patients with VSDs. During follow-up, 4 patients died and the condition of 8 worsened postoperatively. The multivariable proportional hazards model showed that heart failure, LV ejection fraction of < 24%, LV end-diastolic diameter z-score of > 8.56, and noncompacted-to-compacted ratio of the left ventricular apex of > 8.33 at the last visit were risk factors for survival. Conclusions: LVNC and CHD are frequently associated with genetic abnormalities. Knowledge of the association between CHD and LVNC is important for the awareness of clinical implications during the preoperative and postoperative periods to identify the populations who are at an increased risk of additional morbidity.

Pulmonary Artery Banding Still Has an Important Role in the Treatmant of Congenital Heart Disease: Reply

2005 ◽  
Vol 79 (4) ◽  
pp. 1463-1464
Author(s):  
Hiroo Takayama ◽  
Masahide Chikada ◽  
Shinichi Takamoto ◽  
Akihiko Sekiguchi ◽  
Akira Ishizawa
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Congenital Heart ◽  
Pulmonary Artery Banding

Submitral Aneurysm After Pulmonary Artery Banding—A Case Report

2017 ◽  
Vol 9 (3) ◽  
pp. 364-367
Author(s):  
Abid Iqbal ◽  
Sabarinath Menon ◽  
Baiju S. Dharan ◽  
Kapilamoorthy Tirur Raman ◽  
Jayakumar Karunakaran
Keyword(s):  
Congenital Heart Disease ◽  
Young Adults ◽  
Heart Disease ◽  
Case Report ◽  
Pulmonary Artery ◽  
Congenital Heart ◽  
Interatrial Septum ◽  
Pulmonary Artery Banding ◽  
Complex Congenital Heart Disease ◽  
Unique Case

Submitral aneurysms are rare clinical entities occurring predominantly in young adults of African descent. A host of etiologies have been proposed for this entity. We present a unique case of submitral aneurysm which developed after pulmonary artery banding in a three-year-old girl with complex congenital heart disease. The aneurysmal sac was burrowing into the interatrial septum.

Dilatable Pulmonary Artery Banding Palliation in Congenital Heart Disease

2021 ◽  
Vol 12 (2) ◽  
pp. 213-219
Author(s):  
R. Allen Ligon ◽  
Larry A. Latson ◽  
Mark M. Ruzmetov ◽  
Kak-Chen Chan ◽  
Immanuel I. Turner ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Blood Flow ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Balloon Dilation ◽  
Retrospective Chart Review ◽  
Pulmonary Artery Banding ◽  
Surgical Removal

Background: Surgical pulmonary artery banding (PAB) has been limited in practice because of later requirement for surgical removal or adjustment. The aim of this study is to describe our experience creating a dilatable PAB via transcatheter balloon dilation (TCBD) in congenital heart disease (CHD) patients. Methods: Retrospective chart review of adjustable PAB—outline anatomical variants palliated and patient outcomes. Results: Sixteen patients underwent dilatable PAB—median age 52 days (range 4-215) and weight 3.12 kg (1.65-5.8). Seven (44%) of the patients were premature, 11 (69%) had ventricular septal defect(s) with pulmonary over-circulation, four (25%) atrioventricular septal defects, and four (25%) single ventricle physiology. Subsequent to the index procedure: five patients have undergone intracardiac complete repair, six patients remain well palliated with no additional intervention, and four single ventricles await their next palliation. One patient died from necrotizing enterocolitis (unrelated to PAB) and one patient required a pericardiocentesis postoperatively. Five patients underwent TCBD of the PAB without complication—Two had one TCBD, two had two TCBD, and another had three TCBD. The median change in saturation was 14% (complete range 6-22) and PAB diameter 1.7 mm (complete range 1.1-5.2). Median time from PAB to most recent outpatient follow-up was 868 days (interquartile range 190-1,079). Conclusions: Our institution has standardized a PAB technique that allows for transcatheter incremental increases in pulmonary blood flow over time. This methodology has proven safe and effective enough to supplant other institutional techniques of limiting pulmonary blood flow in most patients—allowing for interval growth or even serving as the definitive palliation.

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