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Tetralogy of Fallot was repaired previously in a preschooler through right ventriculotomy, providing excellent exposure for ventricular septal defect closure and right ventricular outflow tract obstruction relief. Herein, we describe the preschooler as a 50-year-old man with untreated atrial septal defect found at pulmonary valve replacement in the remote period after tetralogy of Fallot repair. It was inferred intraoperatively that the previous tetralogy of Fallot was repaired only through right ventriculotomy, and atrial septal defect closure was performed together with pulmonary valve replacement. [ABSTRACT FROM AUTHOR]

Background: Aortic aneurysm is a common but life-threatening disease among the elderly, for which no effective medical therapy is currently available. Activation of prostaglandin E2 (PGE2) is known to increase the expression of matrix metalloproteinase (MMP) and the release of inflammatory cytokines, and may thus exacerbate abdominal aortic aneurism (AAA) formation. We hypothesized that selective blocking of PGE2, in particular, EP4 prostanoid receptor signaling, would attenuate the development of AAA. Methods and Findings: Immunohistochemical analysis of human AAA tissues demonstrated that EP4 expression was greater in AAA areas than that in non-diseased areas. Interestingly, EP4 expression was proportional to the degree of elastic fiber degradation. In cultured human aortic smooth muscle cells (ASMCs), PGE2 stimulation increased EP4 protein expression (1.4±0.08-fold), and EP4 stimulation with ONO-AE1-329 increased MMP-2 activity and interleukin-6 (IL-6) production (1.4±0.03- and 1.7±0.14-fold, respectively, P<0.05). Accordingly, we examined the effect of EP4 inhibition in an ApoE-/- mouse model of AAA infused with angiotensin II. Oral administration of ONO-AE3-208 (0.01-0.5 mg/kg/day), an EP4 antagonist, for 4 weeks significantly decreased the formation of AAA (45-87% reduction, P<0.05). Similarly, EP4+/-/ApoE-/- mice exhibited significantly less AAA formation than EP4+/+/ApoE-/- mice (76% reduction, P<0.01). AAA formation induced by periaortic CaCl2 application was also reduced in EP4+/- mice compared with wild-type mice (73% reduction, P<0.001). Furthermore, in human AAA tissue organ cultures containing SMCs and macrophages, doses of the EP4 antagonist at 10-100 nM decreased MMP-2 activation and IL-6 production (0.6±0.06- and 0.7±0.06-fold, respectively, P<0.05) without increasing MMP-9 activity or MCP-1 secretion. Thus, either pharmacological or genetic EP4 inhibition attenuated AAA formation in multiple mouse and human models by lowering MMP activity and cytokine release. Conclusion: An EP4 antagonist that prevents the activation of MMP and thereby inhibits the degradation of aortic elastic fiber may serve as a new strategy for medical treatment of AAA. [ABSTRACT FROM AUTHOR]

A 5-year-old girl has a history of epicardial VVI-pacemaker implantation due to congenital heart block at the age of 2 months. Five years later, she developed heart failure at the same time of battery depletion. The chest X-ray indicated the loop formation of the epicardial leads and the echocardiogram demonstrated paradoxical movement of ventricles. The 3-dimensional computed tomography finally revealed strangulation of biventricular apex caused by loop of the leads. She underwent reoperation. Cardiac strangulation was relieved by total removal of the loop and repositioning of right atrial and ventricular electrodes in a gentle curve of the leads. She was discharged and doing well. Cardiac strangulation is a rare, but it can be lethal. Therefore epicardial pacemaker leads should not be positioned around the ventricle with excessive redundancy.

To avoid stenotic conduit events, 2 modifications were added to Norwood reconstruction with a right ventricle-to-pulmonary artery conduit: open-square insertion of a proximal conduit end and use of a pre-cuffed, spiral-ringed conduit. Three consecutive patients treated with this technique successfully underwent bidirectional Glenn with no stenotic events. These modifications are beneficial and safe., (© The Author 2017. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)