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Cross-sectional echocardiographic diagnosis of unruptured right sinus of Valsalva aneurysm dissecting into the interventricular septum discount finasteride hair loss cure ayurveda. Diagnosis of ruptured sinus of Valsalva aneurysms: potential value of transesophageal echocardiography cheap finasteride 5 mg online hair loss specialist nyc. Sixteen-slice computed tomography, transthoracic real-time 3- dimensional echocardiography and magnetic resonance imaging assessment of a long-term survivor of rupture of sinus of valsalva aneurysm. Percutaneous closure of ruptured sinus of Valsalva aneurysm using an Amplatzer occluder device. Penny Introduction It can be challenging to develop an adequate understanding of the three-dimensional interrelationships of the thoracic vessels and their embryologic predecessors. We encourage the reader to use the three-dimensional models which accompany this chapter to understand the normal development of the great arteries and how each lesion develops. Classically, anomalies of the great arteries have been described with the aid of the totipotential diagram, a two- dimensional depiction of the great arteries and their branches. The totipotential diagrams are depicted for each lesion discussed, but the chapter will focus on the three-dimensional models to elucidate the anatomy. While aortic arch anomalies have been documented as early as the 18th century (3), much remains unknown about these lesions. While some anomalies of the aortic arch effect as many as 1% of the population, others are quite rare. In the absence of a vascular ring, few result in symptoms, leading to underestimation of their prevalence. Though the anatomy of most lesions has been well documented (1), the proposed development of each lesion has largely remained theoretical. It is only recently that we have been able to document the embryologic underpinnings of aortic arch development (4) and in the absence of direct visualization of the development of the many abnormalities, it is not possible to be definitive about their exact origins. Normal Anatomy The normal aorta extends superiorly from the center of the heart, posterior to the pulmonary trunk (Fig. Because the ventricular outflow tracts cross each other, the aortic valve is to the right of the pulmonary valve. The ascending aorta continues as the transverse arch, which courses almost directly posterior, and only slightly leftward, abutting the left side of the trachea, and coursing over the left mainstem bronchus (Fig. It then turns downward to continue as the descending thoracic aorta just leftward and anterior to the spine. The arterial duct, extending from the origin of the left pulmonary artery, inserts into the aortic P. The first branch is the brachiocephalic artery, which courses rightward and superiorly for a short distance before dividing into the right subclavian artery and right common carotid artery. The right subclavian artery proceeds directly rightward toward the right arm, while the right common carotid artery proceeds superiorly and slightly rightward, toward the right side of the neck. The second branch of the aortic arch is the left common carotid artery, which proceeds superiorly and slightly leftward, toward the left side of the neck. The third branch is the left subclavian artery, which proceeds superiorly for a short distance before making a sharp turn leftward to continue directly toward the left arm. The subclavian arteries give rise to two important branches at their proximal end. The vertebral arteries arise from the superior aspect of the subclavian artery and proceed superiorly toward the head. The internal thoracic arteries (mammary arteries) proceed directly inferiorly along the ipsilateral side of the sternum, and connect with the anterior intercostal arteries. The descending thoracic aorta gives rise to the posterior intercostal arteries at each vertebral level, which connect to the corresponding anterior intercostal arteries. C: The normal pulmonary arteries—superior view with the distal aortic arch and branches cut away. Color coding for all figures: yellow, third aortic arch derivative; orange, fourth aortic arch derivative; pink, fifth aortic arch derivative (not depicted in current figure); blue, sixth aortic arch derivative; green, seventh intersegmental artery derivative; purple truncus arteriosus and/or aortic sac derivative; red, dorsal aorta and descending aorta derivative; salmon, foregut derivative; gray, trachea. In the neck, there are two pairs of arteries that proceed superiorly to insert into the circle of Willis. The vertebral arteries course along the right and left aspect of the spine, within the spinal column, before joining together to form the basilar artery which inserts into the posterior aspect of the circle of Willis. The common carotid arteries divide into the external carotid arteries, which supply the face and ear, and the internal carotid arteries, which insert into the anterolateral aspects of the circle of Willis, through which they communicate with the vertebral arteries. This connection is important during certain pathologic states as it allows for “steal” from the circle of Willis to supply an isolated subclavian artery via the vertebral artery (see below). The right brachiocephalic artery arises together with left common carotid artery, via a common brachiocephalic trunk. In addition to the usual blood vessels, the left vertebral artery arises directly from the aortic arch, between the left common carotid artery and left subclavian artery, instead of arising from the left subclavian artery. Both of these findings are considered normal variants, but must be kept in mind when evaluating patients for other, pathologic arch anomalies (5). The pulmonary trunk arises anterior to the aorta and proceeds leftward and posteriorly, spiraling along the left aspect of the ascending aorta (see Fig. The right pulmonary artery courses rightward, underneath the aortic arch, but remains anterior to the trachea and bronchus. The left pulmonary artery proceeds leftward and posteriorly, toward the midaxillary line. The arterial duct originates at the branching point, closer to the left pulmonary artery, and proceeds in an anterosuperior and leftward direction to insert into the proximal descending aorta, immediately distal to the aortic isthmus. Normal Embryology The developing heart forms within the pharyngeal mesoderm, in the region that develops into the neck, and migrates into the thorax over time. The heart tube is located ventral (anterior) to the pharyngeal pouches, a series of structures that give rise to the head and neck components (Fig. It is immediately ventral to the developing gut tube, which gives rise to the bronchial tree and lung buds. The truncus arteriosus is a channel that connects the ventricular mass to the aortic sac. It develops into the ventricular outflow tracts, and the aortic sac develops into the proximal great arteries. Dorsally (posteriorly) there are two parallel arteries, the dorsal aortae, which course caudally (inferiorly), on either side of the neural tube, before joining medially to form the descending aorta (Fig. The aortic sac is connected to each dorsal aorta via a series of paired aortic arches that course along the left and right aspect of the gut tube in a ventral to dorsal (anterior to posterior) direction. Rather, they form sequentially before either regressing or developing into their final structures. Dorsal (posterior) to the dorsal aortae are the vertebral arteries, which course cranially (superiorly) toward the brain, eventually joining together to form the basilar artery which enters the posterior aspect of the circle of Willis, through which they will communicate with the internal carotid arteries. At each segmental level, the dorsal aortae give off intersegmental arteries that connect to the ipsilateral vertebral artery. The most important of the intersegmental arteries is the seventh intersegmental artery as it develops into the subclavian artery. This is why the vertebral arteries connect to the subclavian arteries in the mature embryo. The dorsal aortae course posteriorly and connect medially to form the descending aorta.

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Surgical management of the patent ductus arteriosus: with summary of four surgically treated cases buy finasteride master card hair loss cure 90. Outcomes following neonatal patent ductus arteriosus ligation done by pediatric surgeons: a retrospective cohort analysis 1 mg finasteride free shipping hair loss curezone. A comparison of on-site and off-site patent ductus arteriosus ligation in premature infants. Unilateral vocal fold paralysis after congenital cardiothoracic surgery: a meta-analysis. Percutaneous closure of the small patent ductus arteriosus using occluding spring coils. Safety of percutaneous patent ductus arteriosus closure: an unselected multicenter population experience. Percutaneous closure of patent ductus arteriosus in small infants with significant lung disease may offer faster recovery of respiratory function when compared to surgical ligation. Prevention of infective endocarditis: Guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Outcomes for patients with an aortopulmonary window, and the impact of associated cardiovascular lesions. Early and late results after repair of aortopulmonary septal defect and associated anomalies in infants <6 months of age. Congenital Heart Surgery Nomenclature and Database Project: aortopulmonary window. Transcatheter closure of an aortopulmonary window with a modified double umbrella occluder system. Paul Matherne Coronary and aortic root anomalies represent a relatively small but interesting group of malformations that may occur alone or in association with structural heart disease (1,2,3). Recognizing and identifying these anomalies has become an important part of the evaluation of complex congenital heart disease. In the absence of structural heart disease, coronary anomalies are also important in certain clinical situations such as dilated cardiomyopathy (4), hypertrophic cardiomyopathy (5), and sudden cardiac events in older children (6). This chapter will review coronary artery development and anatomy, coronary anomalies in the absence of structural heart disease, coronary anomalies in the presence of structural heart disease, and aortic root anomalies. Coronary Vascular Anomalies Embryology The cells of the developing myocardium initially receive nourishment directly from circulating blood in the ventricular cavity. As the myocardium thickens and develops, the presence of multiple trabeculations allows close proximity of the myocardial cells to the ventricular cavity. These trabeculations then develop into a sinusoidal system that continues to minimize diffusion distance between the myocytes and the circulation. While previously these sinusoids were thought to be the forerunners of the coronary vascular system, but new data have provided evidence for an epicardial origin of the coronary vascular system (7). The new model of coronary vascular development (7) begins with formation of a proepicardial profusion by cells from the primordial liver. These cells establish the proepicardium and epicardial cells and then migrate over the surface of the heart. The epicardial cells invade the forming subepicardial matrix and form the coronary vascular plexus. The epicardial cells then undergo epithelial mesenchymal transformation by an as yet undefined mechanism that probably involves multiple growth factors. Nascent capillaries then are associated with subepicardial mesenchymal cells to form mature vessels, which fuse and grow inward to penetrate the aorta rather than coronary buds from the aortic sinuses fusing with the coronary vessels (8). The new experimental data on the development of the coronary system implicate multiple growth factors as well as adhesion molecules and chemotactic factors in this complicated coordinated migration and transformation of cells to form coronary vessels. The presence of congenital anomalies of coronary arteries suggests abnormalities in these signaling pathways or alterations in local factors that direct coronary vessel development. The entire blood flow to the myocardium is derived from two main coronary arteries arising from the right and left aortic sinuses of Valsalva (Fig. The left main coronary artery is of variable length in adults (average 13 mm long, range 2 to 40 mm) and gives rise to the circumflex branch, which courses posteriorly in the atrioventricular groove; the left main coronary then continues as a left anterior descending branch. The right coronary artery gives rise to a small conal branch and then courses posteriorly in the opposite direction along the atrioventricular groove. There is no separate septal branch, the septum being supplied by perforating branches that enter the septum from the anterior and posterior descending coronary arteries. In 69% of the population, the right coronary artery is dominant (10), giving rise to the posterior descending coronary artery, which extends to the apex and supplies the posterior part of the ventricular septum, the inferior wall of the left ventricle, and the atrioventricular node (11). Interestingly, a significant number of patients with bicuspid aortic valves or aortic stenosis (20% to 57%) have left dominant systems and a short left main coronary artery (10,12,13). Within the myocardium, small arteries branch repeatedly until they reach the endocardium. Normally, there are connections between coronary arterial branches that are 25 to 200 μm in diameter and are known as collaterals. They may be superficial or subendocardial, and they are capable of enlarging if pressure gradients develop between branches. These collateral arteries become significant in cases of primary arterial occlusion, in which cases they may allow reperfusion of affected myocardium. Cardiac Veins The coronary sinus arises from the proximal portion of the left sinus horn and the common cardinal vein. The great cardiac vein begins at the apex and runs up the anterior interventricular groove to enter the coronary sinus before running around the left edge of the heart in the posterior atrioventricular groove until it enters the right atrium near the atrioventricular node. The middle cardiac vein runs up in the posterior atrioventricular groove to enter the coronary sinus. The posterior ventricular vein drains the free wall of the left ventricle up to the coronary sinus. The small cardiac vein runs with the right coronary artery in the right posterior part of the atrioventricular groove; it drains into the coronary sinus or directly into the right atrium, as do the small veins draining the right ventricular free wall (14,15). Anomalies of Coronary Arteries in the Absence of Structural Heart Disease Normal Variations The right and left coronary arteries arise from the right and left aortic sinuses of Valsalva (see Fig. Usually they come from the middle of the sinuses, but they may arise from the sinotubular junction or even above it. The arteries are usually perpendicular to the aortic wall; that is, they are radially arranged relative to the center of the aorta. Separate origin of the conus branch of the right coronary artery occurs commonly (11). The corresponding anomaly on the left side—separate origins of the left anterior descending and left circumflex coronary arteries— occurs in about 1% of people and is more frequent with bicuspid aortic valves (11). Abnormal Origin of Right or Left Coronary Artery from Inappropriate Sinus Anomalous Origin of Left Coronary Arterial Branches from Right Sinus of Valsalva The most common anomaly, accounting for about one-third of all major coronary arterial anomalies, is origin of the left circumflex coronary artery from the right main coronary artery (Fig. The left circumflex coronary artery passes behind the aorta to reach its normal territory of supply. This anomaly has no general clinical significance in the pediatric population, but the artery may be compressed if both mitral and aortic prosthetic valves or annuloplasty rings are implanted. These anomalous arteries may have an unusually high incidence of coronary atheroma (2).

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It is identical to the short-axis method used in clinical imaging and represents the most common method of cardiac dissection used at our institution for the evaluation of acquired heart disease 5 mg finasteride otc hair loss prevention shampoo. In addition to the short-axis method buy discount finasteride 5 mg line hair loss in menopause, the long-axis and four-chamber planes represent other tomographic sections commonly obtained clinically and may be correlated with anatomic features in normal hearts. Other planes, parallel to the standard anatomic directions, also have been used clinically, not only for transesophageal echocardiography but also for magnetic resonance imaging (31). These include frontal (coronal), parasagittal (lateral), and horizontal (transverse) planes of section. In cardiac specimens, any of the aforementioned tomographic planes can be applied not only to normal hearts but also to acquired and congenital forms of heart disease (Figs. Although the tomographic method of cardiac dissection has been used by anatomists and pathologists for more than a century, it has not been widely accepted, probably because it is time consuming and requires prior fixation (preferably perfusion fixation). For congenitally malformed hearts, tomographic sections are particularly well suited for demonstrating not only the primary anomalies and various interventions but also their secondary effects on the heart. Thus, photographs of specimens dissected tomographically provide clarity as teaching tools and correlate well with current clinical imaging modalities. A and B: Long-axis views show inflow and outflow tracts of right ventricle (A) and left ventricle (B). C: Long-axis view of thoracic aorta shows left bronchus and right pulmonary artery traveling beneath aortic arch. A–C: Four-chamber views, at levels of coronary sinus (A), fossa ovalis (B), and aortic valve (C). D–F: Horizontal (transverse) views at levels of ventricular inflow (D) and outflow (E) tracts and pulmonary artery (F). A: Short-axis view of common atrioventricular valve in complete atrioventricular septal defect. B: Four-chamber view of hypoplastic right ventricle in tricuspid atresia C: Long-axis view of hypoplastic left ventricle in aortic atresia. Moreover, after one section has been made and documented photographically, the specimens can be glued back together and resectioned along another tomographic plane. For this purpose, any of the readily available cyanoacrylate glues (such as Krazy Glue or Super Glue) will suffice. The best results are attained with smooth dry surfaces; roughened surfaces (such as those produced by using scissors) may adhere poorly. Photography of Cardiac Specimens It is difficult to overestimate the role of photography in the teaching of congenital heart disease. Although schematic diagrams are helpful, the visualization of actual specimens is often necessary for an appreciation of three-dimensional features. In this regard, the well-planned dissection and photography of a classic lesion may be remembered far longer than written words (33). However, having access to the most expensive photographic equipment does not guarantee good results. For example, to increase the depth of field of focus, the aperture should be as small as possible (achieved by setting the f-stop as large as possible, preferably 16 or greater). One of the simplest yet most important factors for attaining high-quality photographs is the initial focusing of the camera. Few things can ruin a photograph as quickly and irreversibly as failure to attend to sharp focusing. The use of black or white backgrounds is favored over backlighting through translucent sheets of colored plastic. In this regard, it is important to note that standard black poster board, available from art supply stores, is generally made with water-soluble ink and will stain the specimens. Because fresh specimens have shiny surfaces that produce extensive glare, tissues should be fixed before being photographed. Maintenance of lifelike colors can be achieved by fixation in formalin for only brief periods (5 to 15 minutes) or in nonformalin fixatives such as Kaiserling or Jores (32). For perfusion-fixed specimens that have been in formalin less than a week, colors may be partially restored by soaking the tissues in 80% ethanol for 15 to 30 minutes. Specimens are then thoroughly dried with paper towels to eliminate reflective glare. In some cases, pins are necessary to hold thin or collapsible structures in position. From a technical perspective, a piece of black cardboard is placed on a piece of similarly sized corkboard, and the specimen is placed on the cardboard. Pins of various sizes are then used to stabilize the specimen, and the heads of the pins are removed with cutting pliers so they will not be visible in the photograph (32). Probes, arrows, transillumination, and normal specimens (for comparison) also may be used to highlight specific morphologic features. Part I (Growth): A quantitative anatomic study of 200 specimens from subjects from birth to 19 years old. Venous valves in subclavian and internal jugular veins: Frequency, position, and structure in 100 autopsy cases. Incidence and size of patent foramen ovale during the first 10 decades of life: An autopsy study of 965 normal hearts. Quantitative morphology of normal human tricuspid valve: Autopsy study of 24 cases. Mitral valve apparatus: A spectrum of normality relevant to mitral valve prolapse. The tricuspid valve annulus: Study of size and motion in normal subjects and in patients with tricuspid regurgitation. Normal variations in the relationship of the tricuspid valve to the membranous septum in the human heart. Comparison of echocardiographic and necropsy measurements of left ventricular wall thickness in patients with coronary artery disease. Standardized nomenclature of the ventricular septum and ventricular septal defects, with applications for two-dimensional echocardiography. Anterolateral muscle bundle of the left ventricle in atrioventricular septal defect: Left ventricular outflow tract and subaortic stenosis. The morphology of the human newborn ductus arteriosus: A reappraisal of its structure and closure with special reference to prostaglandin E1 therapy. Aortic origin of conus coronary artery: Evidence of postnatal coronary development. Clinical significance of isolated coronary bridges: Benign and frequent condition involving the left anterior descending artery. Multiplane transesophageal echocardiography: Image orientation, examination technique, anatomic correlations, and clinical applications. Photography of medical specimens: Experiences from teaching cardiovascular pathology. Edwards Perspectives on Nomenclature Through 5,000 years of recorded human history, only during the past 60 have treatments become available to substantially improve the quality of life and increase the longevity of children with cardiac anomalies. Within these 60 years, diagnostic and interventional procedures have been developed that have defined the frontiers of medical technology and creativity.

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The pulmonary hypertensive crisis order finasteride paypal hair loss in men 34, as it has been called proven 5mg finasteride hair loss in men 34, is thought to result from interaction of a hypertrophied and perhaps hypercontractile circulation with an injured vascular endothelium, with platelets and leukocytes that were exposed to postcardiopulmonary bypass and hypothermia and may more easily degranulate and release potent vasoconstrictor agents, particularly thromboxanes and leukotrienes. In recent studies, increased density of neuroepithelial bodies has been observed in the airways of patients at risk for this complication (15). The neuroendocrine cells, which are also oxygen sensors, contain bombesin and serotonin, agents known to be potent vasoconstrictors. There is also an increase in vasoconstrictor neuropeptide-containing nerves (16) (Fig. Because most of the pulmonary hypertensive crises occur while weaning from the ventilator, it is tempting to speculate that swings in airway pressure might lead to degranulation of the neuroepithelial cells and release of the vasoconstrictor substances. Moreover, there is a striking decrease in lung compliance accompanying the pulmonary hypertensive crisis. In ultrastructural lung biopsy studies from patients with congenital heart defects and pulmonary hypertension, alterations in endothelial cells support endothelial dysfunction as a cause of heightened pulmonary vascular reactivity and also relate endothelial dysfunction to the pathogenesis of progressive pulmonary vascular disease. On scanning electron microscopy, the endothelial surface of normal thin-walled pulmonary arteries has a “corduroy-like” appearance in that the cells form narrow, even ridges. In contrast, the endothelial surface of hypertensive thick-walled pulmonary arteries has a “cable-like” texture in that the cells form deep, twisted ridges. The hypertensive endothelium may be predisposed to interact abnormally with marginating blood elements, such as platelets and leukocytes. This might result in the release of pulmonary vasoconstrictor substances and smooth muscle mitogens (17). On transmission electron microscopy, the endothelium appeared to show heightened metabolic activity with an increased rough endoplasmic reticulum. The subendothelium of the muscular arteries is also abnormal in that there appears to be degradation and neosynthesis of the internal elastic lamina. This observation provided an important clue related to the discovery of heightened elastolytic activity in the vessel wall associated with the initiation and progression of pulmonary vascular disease. This could indeed account for the development of platelet fibrin microthrombi in the postoperative period and for abnormal release of vasoactive compounds causing increased vascular reactivity. B: Tyrosine hydroxylase immunoreactive perivascular nerve fibers at the advential–medial border of an alveolar duct artery in a child aged 2 1/2. A study of nerves containing peptides in the pulmonary vasculature of healthy infants and children and of those with pulmonary hypertension. There also is evidence that production of the vasoconstrictor endothelin also might be increased in patients with pulmonary hypertension and congenital heart defects (21). Many patients with high-flow congenital heart defects that are operated upon in a timely fashion show a fall in pulmonary artery pressure and return to normal resting hemodynamics, indicating resolution and regression of pulmonary hypertensive structural changes. This is supported by experimental studies and by anecdotal reports of resolution of severe pulmonary vascular disease in the remaining lung after single lung transplant. There are, however, some patients who maintain a high level of pulmonary vascular resistance and are refractory to vasodilator therapy despite what appear to be mild vascular changes on light microscopy (medial hypertrophy), P. For these patients, the prognosis may be not much better than those with unexplained pulmonary hypertension (22). A recent study of outcomes of patients with congenital heart disease (systemic-to-pulmonary shunt lesions) and pulmonary hypertension in the current treatment era demonstrated significantly decreased 20- year survival in patients with residual pulmonary vascular disease following defect closure (36%) relative to patients with Eisenmenger syndrome (87%) or those patients with an unrepaired systemic-to-pulmonary shunt without Eisenmenger syndrome (86%). While preoperative hemodynamics are unknown for the surgically repaired group, the late average age at operation may suggest advanced pulmonary vascular disease at the time of operation and inability of the right ventricle to adapt to the increased workload (23). Therapies for the patient with Eisenmenger syndrome have included chronic oxygen, anticoagulants, and palliative surgical procedures, including atrial septal defect creation and intravenous as well as, more recently, subcutaneous, inhaled, or oral prostacyclin analogs. In some cases, these measures have improved the quality of life and in others they have acted as a bridge to a heart–lung transplant or surgical correction along with lung transplant. More recent addition of phosphodiesterase inhibitors and endothelin receptor antagonists in this group of patients awaits the results of clinical trials, but is discussed later in this chapter, and in the subsequent chapter, with regard to patients with idiopathic pulmonary hypertension. Pathophysiology Based Upon Further Pathologic Assessments Recent immunohistochemical studies have been carried out in lung biopsy tissue from patients with congenital heart defects to elucidate mechanisms that are directly related to enhanced proliferation and migration of cells in the neointima with characteristics of smooth muscle cells. There is a progressive increase in the deposition of two matrix glycoproteins, tenascin and fibronectin, in the media and neointima (Fig. We previously related the increased expression of tenascin to vascular smooth muscle cells P. Fibronectin has been related to increased migration of smooth muscle-like cells in the context of neointimal formation. It is also proposed that endothelial cell proliferation and a form of angiogenesis is observed with plexiform lesions. The plexiform lesions in pulmonary hypertension associated with congenital heart disease appear to be derived from different clonal populations of endothelial cells compared with those observed in unexplained pulmonary hypertension where a single clone is usually found (25). Tenascin-C, proliferation and subendothelial fibronectin in progressive pulmonary vascular disease. Creation of large aortopulmonary shunts in dogs, particularly into a single pulmonary artery, resulted in more rapidly progressive pulmonary vascular changes. There are several other experimental models of high-flow congenital heart defects such as sheep or calves after an aortopulmonary lobar anastomosis. In utero placement of an aortopulmonary shunt most faithfully reproduces the changes that might be expected to occur in the newborn with a left-to-right shunt when the pulmonary vascular resistance falls. Takedown of the shunts during the period of rapid lung growth resulted in regression of both structural changes and pulmonary hypertension (30). There are many common features linking the cellular and molecular pathophysiology of pulmonary vascular disease, regardless of etiology, to elevated elastase activity. S100A4/Mts1 was not detected in all cells and appears to be localized in a subpopulation of intimal cells. Immunoreactivity for S100A4/Mts1 was present in the lung parenchyma at a similar level in all grades of pulmonary vascular disease. S100A4/Mts1 produces murine pulmonary artery changes resembling plexogenic arteriopathy and is increased in human plexogenic arteriopathy. In patients with total anomalous pulmonary venous connection, abnormal muscularization of the small arteries and veins was observed from birth, and more severe structural changes (i. In infants with hypoplastic left heart syndrome, the early presence of severe medial hypertrophy of the small arteries and veins suggests that it developed in utero (33). In both adults and children with rheumatic mitral stenosis, Wagenvoort and Wagenvoort (34) observed increased medial wall thickness of the pulmonary arteries. In postmortem arteriograms of infants and children with congenital heart defects and elevated pulmonary venous pressure, the axial pulmonary arteries have a reduced lumen diameter throughout their lengths. On microscopic examination of the lung, there is severe extension of muscle into peripheral intra-acinar arteries, which are normally nonmuscular, and failure of regression of the fetal musculature of the normally muscular arteries. The vessels, however, appear normal sized and are normal or slightly increased in number. The presence of pulmonary vascular changes in defects with high pulmonary venous pressure and the capacity for these abnormalities to regress with improvement in hemodynamics may be relevant because the Norwood and other various staged surgical procedures for the treatment of hypoplastic left heart syndrome ultimately depend on the success of a cavopulmonary shunt.

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