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Background: The molecular mechanisms underlying aortic valve calcification are poorly understood. Here, we aimed to identify the master regulators of calcification by comparison of genes in valve interstitial cells (VICs) with calcified and noncalcified aortic valves., Methods: Calcified aortic valves were surgically excised from patients with aortic valve stenosis who required aortic valve replacements. Noncalcified and calcified sections were obtained from aortic valve leaflets. Collagenase-digested tissues were seeded into dishes, and VICs adhering to the dishes were cultured for 3 weeks, followed by comprehensive gene expression analysis. Functional analyses of identified proteins were performed by in vitro calcification assays. Tissue localization was determined by immunohistochemical staining for normal (n = 11) and stenotic valves (n = 30)., Results: We found 87 genes showing greater than a twofold change in calcified tissues. Among these genes, 68 were downregulated and 19 were upregulated. Cyclooxygenase-1 (COX1) messenger RNA and protein levels were upregulated in VICs from calcified tissues. The COX1 messenger RNA and protein levels in VICs were also strongly increased by stimulation with osteoblast differentiation medium. These were VIC-specific phenotypes and were not observed in other cell types. Immunohistochemical staining revealed that COX1-positive VICs were specifically localized in the calcified area of aortic valve tissues., Conclusions: The VIC-specific COX1 overexpression played a crucial role in calcification by promoting osteoblast differentiation in aortic valve tissues., (Copyright © 2020 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

We describe 4 patients with postinfarction inferoposterior ventricular septal defect treated by the two-patch technique for infarct exclusion operation. The ventricular septal defects were closed using two bovine pericardial patches as follows. The septal patch was sutured to the noninfarcted septum covering the defect, and the free wall patch was sutured to the endocardium adjacent to the posterior papillary muscle. The two patches were sutured together and all infarcted areas were excluded from the left ventricular pressure. This technique seems to be useful in specific circumstances, such as when the ventricular defect is located in the inferoposterior septum.

In 3 patients previously undergoing one and one-half ventricular repair, right ventricular dysfunction progressed for more than 10 years. Their clinical features resembled those seen in patients undergoing the atriopulmonary Fontan procedure, and reoperation was carried out for conversion to total cavopulmonary connection. Hemodynamics improved subsequent to the circulatory renewal. In 2 patients having atrial arrhythmia before conversion, the resected right atrial wall illustrated grossly abnormal histopathology. These patients suffered from persistent sinus nodal dysfunction and eventually needed pacemaker implantation. The third patient died of sepsis 4 months later.

Three patients with ventricular septal defect, obstructed aortic arch, and valvular aortic stenosis underwent a modification of the Yasui procedure (the Norwood type aortic reconstruction, intraventricular rerouting from the left ventricle to the dual arterial valves, and reconstruction of the right ventricular outflow tract by the Lecompte maneuver). With a follow-up of up to 60 months, the outcome is excellent without progressive lesions or reoperation.