PubMed · 13974280
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B ROBERTS. Abdominal aneurysms.. https://pubmed.ncbi.nlm.nih.gov/13974280/
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BACKGROUND: The intracellular bacterium Chlamydia pneumoniae is suspected to play a role in formation and progression of atherosclerosis. Many studies investigated cell death initiation versus inhibition by Chlamydia pneumoniae in established cell lines but nothing is known in primary human aortic smooth muscle cells, a cell type among others known to be involved in the formation of the atherosclerotic plaque. Type of cell death was analyzed by various methods in primary aortic smooth muscle cells after infection with Chlamydia pneumoniae to investigate a possible pathogenic link in atherosclerosis. RESULTS: Chlamydiae were found to be localized up to 72 h post infection in aortic smooth muscle cells either as single bacteria or inside of large inclusions. Quantification of host cell death by lactate dehydrogenase release assay revealed strictly dose and time dependent lysis for all tested isolates of Chlamydia pneumoniae. Phosphatidylserine exposure was detected by flow cytometry in Chlamydia pneumoniae infected cells. Ultrastructure of Chlamydia pneumoniae infected human aortic smooth muscle cells showed extensive membrane- and organelle damage, chromatin condensation but no nuclear fragmentation. DNA fragmentation as well as cell membrane permeability was analyzed by TUNEL and NHS-biotin staining and occurred exclusively in cells carrying Chlamydia pneumoniae spots but not in smooth muscle cells with inclusions. These morphological features of cell death were not accompanied by an activation of caspase-3 as revealed by analysis of enzyme activity but involved mitochondrial membrane depolarization as shown by TMRE uptake and release of cytochrome c from mitochondria. CONCLUSION: This study provides evidence that Chlamydia pneumoniae induce a spot like infection in human aortic smooth muscle cells, which results in a chimeric cell death with both apoptotic and necrotic characteristics. This aponecrotic cell death may assist chronic inflammation in atherosclerotic blood vessels.
OBJECTIVE: To emphasize the diagnostic possibility of the anomalous origin of one pulmonary artery from the ascending aorta in infants with clinically refractory heart failure and no intracardiac structural defect. METHODS: Retrospective study of 4 infants with refractory heart failure undergoing 2-dimensional echocardiographic study with subcostal, suprasternal, and parasternal views, and hemodynamic and angiocardiographic study in the anteroposterior projection. RESULTS: Three of the 4 infants had their right pulmonary artery originating from the ascending aorta as their major diagnosis. In the fourth patient, the left pulmonary artery originated from the ascending aorta in association with a large interventricular septal defect. The pressure level in both pulmonary arteries in all infants was that of the systemic level. All patients underwent surgery, which consisted of translocation of the anomalous pulmonary artery from the aorta. Neither immediate nor late cardiac deaths occurred. CONCLUSION: Once the diagnosis of anomalous origin of the pulmonary artery from the ascending aorta in the isolated form is established, the surgical correction should be immediately performed, not only because of the risk of developing pulmonary vascular disease, but also because of the excellent surgical results currently obtained.
The anomalous origin of the right pulmonary artery (AORPA) from the ascending aorta is a rare congenital malformation. We describe an infant who underwent a surgical correction with direct anastomosis between the right pulmonary artery and the pulmonary trunk. Eighteen months later, the patient remains asymptomatic, and no significant residual stenosis was detected on angioresonance.