1/104. Disseminated intravascular meconium in a newborn with meconium peritonitis.A 3-day-old premature infant with meconium peritonitis, periventricular leukomalacia, and pulmonary hypertension died with respiratory insufficiency. An autopsy disclosed intravascular squamous cells in the lungs, brain, liver, pancreas, and kidneys. Numerous pulmonary capillaries and arterioles were occluded by squamous cells, accounting for pulmonary hypertension. brain parenchyma surrounding occluded cerebral vessels showed infarct and gliosis. A mediastinal lymph node filled with squamous cells alluded to the mechanism by which these cells from the peritoneal cavity likely entered the bloodstream--namely, via diaphragmatic pores connecting with lymphatics. Thus, disseminated intravascular meconium rarely may complicate meconium peritonitis and have devastating consequences.- - - - - - - - - - ranking = 1keywords = hypertension (Clic here for more details about this article) |
2/104. Complex vascular lesions at autopsy in a patient with phentermine-fenfluramine use and rapidly progressing pulmonary hypertension.Anorectic agents, such as aminorex and fenfluramine derivatives, have been associated previously with the development of primary pulmonary hypertension. The combination diet drug phentermine-fenfluramine (or "phen-fen") was recently marketed in the united states. We describe a case of a 39-year-old woman with rapidly progressing, fatal pulmonary hypertension following administration of phentermine-fenfluramine. autopsy was remarkable for complex pulmonary vascular lesions most consistent with thrombotic arteriopathy.- - - - - - - - - - ranking = 3keywords = hypertension (Clic here for more details about this article) |
3/104. Segmental portal hypertension due to splenic vein obstruction: imaging findings and diagnostic pitfalls in four cases.Segmental portal hypertension due to isolated splenic vein obstruction is a rare but important entity as it is the only curable cause of portal hypertension by splenectomy. Four cases are presented illustrating the radiological features of splenic vein obstruction, and the diagnostic pitfalls that arose in patients with complicated clinical presentations.- - - - - - - - - - ranking = 3keywords = hypertension (Clic here for more details about this article) |
4/104. Respiratory distress due to tracheal compression by the dilated innominate artery.The case reported is of an 88 yr old female with hypertension and respiratory distress. A chest radiograph revealed a widening of the upper mediastinum. Computed tomographic scanning revealed tracheal compression by the innominate artery, which was elongated and curved. After intubation, she was treated with antihypertensive drugs. This resulted in the remarkable recovery of the patient from respiratory distress. To the authors' knowledge, this is the first reported case of respiratory distress owing to tracheal compression by elongation and curvature of the innominate artery.- - - - - - - - - - ranking = 0.5keywords = hypertension (Clic here for more details about this article) |
5/104. Clinical significance of azygos vein enlargement: radiographic recognition and etiologic analysis.azygos vein enlargement can be detected in congestive heart failure, portal hypertension, inferior vena cava thrombosis, right atrial mural thrombosis, a pulmonary embolism, congenital azygos continuation to the inferior vena cava, and the arteriovenous fistula. radiography, particularly computed tomography (CT), is very useful, not only in recognition of azygos vein enlargement, but also in evaluation of its etiology for the institution of the appropriate treatment of the diseases.- - - - - - - - - - ranking = 0.5keywords = hypertension (Clic here for more details about this article) |
6/104. Pulmonary hypertension associated with pulmonary occlusive vasculopathy after allogeneic bone marrow transplantation.BACKGROUND: Pulmonary vasculature abnormalities, including pulmonary veno-occlusive disease, have been demonstrated in marrow allograft recipients. However, it is often difficult to make a correct diagnosis of pulmonary lesions. methods: An open lung biopsy was performed on a patient who developed severe pulmonary hypertension after bone marrow transplantation for T-cell lymphoma. RESULTS: An open lung biopsy specimen demonstrated pulmonary arterial occlusion due to intimal fibrosis and veno-occlusion. The most striking alteration was partial to complete occlusion of the small arteries by fibrous proliferation of the intima. CONCLUSION: High-dose preparative chemotherapy and radiation before transplantation are thought to have contributed to the development of vasculopathy in this patient, because arterial occlusion by intimal fibrosis and atypical veno-occlusion are often associated with lung injury due to chemoradiation. An open lung biopsy is essential for diagnosing pulmonary vascular disease presenting signs compatible with posttransplantation pulmonary hypertension.- - - - - - - - - - ranking = 3keywords = hypertension (Clic here for more details about this article) |
7/104. Spontaneous cerebral haemorrhage without hypertension in non-mosaic 45X Turner's syndrome.Cerebral haemorrhage without hypertension, arteriosclerosis or clotting defect has not been reported in patients with Turner's syndrome before. In a 51 year old female patient with non-mosaic Turner's syndrome, acute aphasia and right-sided hemiplegia occurred, due to left-sided basal ganglia haemorrhage. The history for hypertension was negative, blood pressure was normal throughout hospitalisation as well as during 24 h monitoring, and all tests for secondary hypertension were negative. There was no indication of arteriosclerosis or a clotting defect. Since there were hypermobile joints, hyperextensible skin and ectatic ascending aorta and brachiocephalic trunk on angiography, a general connective tissue defect was assumed, making arteries more vulnerable to physiologically increased blood pressure and rupture of intracerebral arteries with consecutive bleeding.- - - - - - - - - - ranking = 3.5keywords = hypertension (Clic here for more details about this article) |
8/104. Portal venous calcifications 20 years after portosystemic shunting: demonstration by spiral CT with CT angiography and 3D reconstructions.BACKGROUND: Evaluation of the value of spiral computed tomography (SCT), and postprocessing procedures in patients with extensive portal venous calcifications 20 years after portosystemic shunting was performed. methods: In two patients spiral CT (SCT) examinations of the abdomen (slice thickness 3 mm, table feed 6 mm/s) were performed prior and after application of 150 ml of contrast material administered at a flow rate of 4 ml/s. Axial images were reconstructed at 2 mm increments for postprocessing procedures and 6 mm increments for axial source images. Postprocessing was performed with a maximum intensity projection (MIP) and shaded surface display (SSD) imaging program. RESULTS: In both cases preoperative plain film radiography of the chest and abdomen showed large curvilinear calcifications located at the upper quadrant of the abdomen. The calcifications were directed along the expected axis and position of the portal vein and the portosystemic venous anastomosis. Axial CT slices and CTA showed that the calcifications were located in the vessel wall and that the portal vein lumen as well as the portosystemic venous anastomosis were patent. CONCLUSION: Long-standing portal hypertension is capable of causing portal venous calcifications due to mechanical stress to the vessel wall even years after performing portosystemic shunting. Typically, the calcifications are directed along the expected axis and position of the portal vein. SCT of the portal venous system is a reliable method to differentiate between calcifications in a thrombus or in the vessel wall, which may have therapeutic significance.- - - - - - - - - - ranking = 0.5keywords = hypertension (Clic here for more details about this article) |
9/104. Dramatic worsening of vascular calcifications after kidney transplantation in spite of early parathyroidectomy.vascular calcification is a common feature in chronic dialysis patients, but their clinical significance is debated and the role of kidney transplantation (TP) in the natural history of their development has received scanty attention. We will describe a case of dramatic worsening of vascular calcifications during TP in a young patient in spite of early and successful parathyroidectomy (PTX), and will discuss other causes which might be putatively linked to vascular damage during the time of TP. A 37-year-old man on regular dialytic treatment (RDT) for 11 years, received his first cadaveric transplantation in January 1993. He underwent PTX 6 months after TP because of the lack of decreasing in parathyroid hormone values despite normal graft function. Although PTX was effective, a dramatic worsening was evident in large as well as in medium and small-sized arteries during the following three years of TP. In February 1997, few months after starting dialysis again because of the recurrence of his primary membranoproliferative glomerulonephritis (MPGN), the patient experienced myocardial infarction followed by aorto-coronary bypass (right coronary artery and anterior descending coronary artery) and leg "claudicatio". Though a role for parathyroid hormone in vascular disease has been commonly accepted, the case here reported clearly shows that blunting parathyroid gland activity may be unable to avoid the worsening of a process of vascular disease during the time of TP. Many other factors--linked to the time of TP--may be involved in vascular diseases, such as nephrotic syndrome, dyslipidemia, hypertension and drugs. In the case of our patient, a clear cut risk factor for his progressive atherosclerosis can be designated hyperlipidema and other disturbancies secondary to a nephrotic syndrome due to relapse of MPGN, together with persistent hypertension. This is the first case report in the English literature which clearly demonstrates that TP may add fuel to the fire of vascular disease also in young people and even in the absence of parathyroid hyperactivity, perhaps on the basis of a favorable genetic background. Furthermore, the history of our patient demonstrates that vascular calcifcation heralds major cardiovascular diseases.- - - - - - - - - - ranking = 1keywords = hypertension (Clic here for more details about this article) |
10/104. pulmonary artery dissection in patients without underlying pulmonary hypertension.AIMS: pulmonary artery (PA) dissection is a rare event which usually occurs in patients with underlying pulmonary hypertension. We describe two patients who developed PA dissection without pre-existing pulmonary hypertension and present an extensive review of the literature. methods AND RESULTS: In the first patient (a 59-year-old woman), acute-onset dyspnoea was initially thought to have been caused by pulmonary thrombosis, and thromboendarterectomy was performed. Histologically, pulmonary dissection without external rupture was evident, chiefly in the right main PA. In the second patient, an 85-year-old man who had hypergammaglobulinaemia of unknown cause and died from a haemorrhagic gastric ulcer, arterial dissection was detected at autopsy. There was no underlying pulmonary hypertension in either patient. Although the true reason for the development of dissection is unclear, pre-existing inflammation was considered to be related to its formation, at least in the second case. CONCLUSIONS: A literature review indicated that idiopathic and inflammation-related PA dissection is extremely unusual. Since PA dissection is very rare, it is important to be aware of its features in order to make a correct diagnosis.- - - - - - - - - - ranking = 3.5keywords = hypertension (Clic here for more details about this article) |
| | Next -> |