Axillary artery access for stenting of aortic coarctation in a 1.2 kg premature newborn with malignant systemic hypertension: a case report.

Background: Axillary artery access is rarely used for demanding percutaneous transcatheter interventions. However, there are many clear advantages.

Case Summary: We describe this attractive approach in a 3-week-old premature neonate (bodyweight of 1.

Fulminant cytomegalovirus myocarditis in an infant with concomitant large atrial and ventricular septal defects: medical intervention strategy for functional cardiac regeneration.

A cytomegalovirus-associated heart failure in a young infant with atrial and ventricular septal defects is reported in this case report. The patient recovered by an anti-congestive and anti-viral therapy with an extra percutaneous transcatheter treatment strategy. In the context of bi-ventricular predominant right heart failure associated with supra-systemic pulmonary hypertension, the already closed arterial duct was re-opened and stented to unload the right ventricle and thereby augment the systemic blood flow.

Percutaneous closure of perimembranous ventricular septal defects utilizing almost ideal Amplatzer Duct Occluder II: Why limitation in sizes?

Aim: The purpose of this study is to describe the special aspects of perimembranous ventricular septal defects (pmVSD) closure by utilizing Amplatzer Duct Occluder II (ADO II) devices with a rational request for bigger ADO-II sizes, based on our experience in transcatheter device closure of pmVSD.

Methods And Results: At our institution, placement of an ADO II device was used in 15 patients with pmVSD; the patients' age ranged between 6 months and 20 years. The indications for closure were CHF (n = 4), hemodynamically significant shunt (n = 7), tricuspid regurgitation (n = 3), and high risk for infective endocarditis (n = 2), respectively.

Ataxia telangiectasia alters the ApoB and reelin pathway.

Autosomal recessive ataxia telangiectasia (A-T) is characterized by radiosensitivity, immunodeficiency, and cerebellar neurodegeneration. A-T is caused by inactivating mutations in the ataxia telangiectasiamutated (ATM) gene, a serine-threonine protein kinase involved in DNA damage response and excitatory neurotransmission. The selective vulnerability of cerebellar Purkinje neurons (PN) to A-T is not well understood.