Analysis of arterial intimal hyperplasia: review and hypothesis

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Despite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology? Hypothesis: I argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it "benign intimal hyperplasia". However, normal or "benign " intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates earl

The role of echocardiography in transcatheter closure of atrial septal defects

Closure of so-called "secundum" atrial septal defects with a device inserted on a catheter necessitates precise delineation of their morphology. Echocardiography is the diagnostic method of choice to demonstrate this morphology, and to differentiate such defects located within the oval fossa from the other variants producing an interatrial communication. Precordial echocardiography usually allows selection of cases likely to be suitable for closure in this fashion. This selection is based on the localisation and the size of the deficiency in the oval fossa, the length of the interatrial septum, and the adequacy of the infolded rims surrounding the defect. Suitability for closure is reevaluated by transesophageal echocardiography: either as a separate investigation or at the start of the interventional catheterisation. This investigation requires a multiplane transesophageal echocardiographic probe, since only oblique planes will demonstrate the entrance of the systemic and pulmonary veins and their relationship to the defect. Transesophageal echocardiography sen es as an important monitoring tool during the interventional procedure. As such, it is a necessary adjunct to fluoroscopy. The stretched diameter of the defect measured with a balloon is the main determinant of the choice of the type and size of the device. This diameter can be measured fluoroscopically, as well as on echo. Colorflow mapping serves to rule out residual shunting during the occlusion of the defect with the balloon. During deployment of the device, constant echocardiographic visualisation of the device and its position relative to the atrial septum facilitates proper placement. Such constant visualisation can only be provided by repeated quick acquisitions of multiple planes. Once the device is released, the investigator should continue to record the position of the device, and assess the potential for residual shunting. Most of the devices show some subtle change in position during the first 20 minutes after implantation

The role of echocardiography in transcatheter closure of atrial septal defects

Closure of so-called "secundum" atrial septal defects with a device inserted on a catheter necessitates precise delineation of their morphology. Echocardiography is the diagnostic method of choice to demonstrate this morphology, and to differentiate such defects located within the oval fossa from the other variants producing an interatrial communication. Precordial echocardiography usually allows selection of cases likely to be suitable for closure in this fashion. This selection is based on the localisation and the size of the deficiency in the oval fossa, the length of the interatrial septum, and the adequacy of the infolded rims surrounding the defect. Suitability for closure is reevaluated by transesophageal echocardiography: either as a separate investigation or at the start of the interventional catheterisation. This investigation requires a multiplane transesophageal echocardiographic probe, since only oblique planes will demonstrate the entrance of the systemic and pulmonary veins and their relationship to the defect. Transesophageal echocardiography sen es as an important monitoring tool during the interventional procedure. As such, it is a necessary adjunct to fluoroscopy. The stretched diameter of the defect measured with a balloon is the main determinant of the choice of the type and size of the device. This diameter can be measured fluoroscopically, as well as on echo. Colorflow mapping serves to rule out residual shunting during the occlusion of the defect with the balloon. During deployment of the device, constant echocardiographic visualisation of the device and its position relative to the atrial septum facilitates proper placement. Such constant visualisation can only be provided by repeated quick acquisitions of multiple planes. Once the device is released, the investigator should continue to record the position of the device, and assess the potential for residual shunting. Most of the devices show some subtle change in position during the first 20 minutes after implantation

THE RESTRICTED SURGICAL RELEVANCE OF MORPHOLOGIC CRITERIA TO CLASSIFY SYSTEMIC-PULMONARY COLLATERAL ARTERIES IN PULMONARY ATRESIA WITH VENTRICULAR SEPTAL-DEFECT

Now that systemic-pulmonary collateral arteries are used for unifocalization in patients with pulmonary atresia and ventricular septal defect, the question arises whether morphologic criteria of these collateral arteries could help to provide better results. In an attempt to classify the morphologic features of systemic-pulmonary collateral arteries, we studied 31 heart-lung autopsy specimens with pulmonary atresia and ventricular septal defect. The course of the systemic-pulmonary collateral arteries (origin, branching pattern, and connections with systemic and central pulmonary arteries) was related to their histologic characteristics. The results show that systemic-pulmonary collateral arteries cannot be classified according to their course related to the trachea and the main branches of the bronchi. The histologic features of these collateral arteries vary along their course to the lungs. Nearly all systemic-pulmonary collateral arteries contain a muscular or a musculoelastic segment. One type of collateral artery (complex loop anastomoses) is completely muscular and resembles a bronchial artery. Nutritive branches (bronchial arteries) arise from all histologic types of systemic-pulmonary collateral artery segments. The size and number of intimal proliferations in muscular, elastic, and musculoelastic segments did not differ significantly. In 29 of 31 cases a ductus arteriosus did not coexist with large collateral arteries (two cases unknown). It is concluded that a classification of large systemic-pulmonary collateral arteries based on morphologic features results in a highly variable system, which does not facilitate decisions for the suitability of these arteries for unifocalization procedures. The variability of the systemic-pulmonary collateral arteries corresponds with the recent embryologic finding that during development, collateral artery formation is possible during extended periods