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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histopathologic examination of six, adult human eyes revealed "rosette-like" structures in the retina which appear to have developed after maturation of the retina. These structures resemble dysplastic rosettes which are generally interpreted as a sign of maldevelopment of the retina (retinal dysplasia). The underlying lesions in the eyes of these patients were ocular ischemia, sickle-cell retinopathy, diabetic retinopathy, central retinal vein occlusion, and trauma. It is suggested that a distinction should be made between these degenerative-regressive changes and dysplastic rosettes which represent an abortive attempt of regeneration by germinal cells.
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PMID:Light and electron microscopic study of dysplastic rosette-like structures occurring in the disorganized mature retina. 16

Ultrastructural characteristics of 20 dysplastic human renal arteries were documented. Loss of smooth muscle with collection of fibrous connective tissue predominated in medical fibrodysplasia, whereas excessive accumulations of elastic fibrils typified perimedial dysplasia. Myofibroblasts were a unique feature of both forms of arterial dysplasia. These modified smooth muscle cells seemed to be the source of abnormal connective tissue synthesis. Transformation of medial smooth muscle cells to myofibroblasts represented a morphologic continuum. Intramedial vasa vasorum were often isolated from surrounding cellular elements by unusual amounts of mural ground substances. The results of this study lend further support to the hypothesis that ischemia and direct physical forces effect hormonally altered cells in the pathogenesis of arterial dysplasia.
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PMID:Ultrastructure of medial smooth muscle and myofibroblasts in human arterial dysplasia. 70 49

Five patients with acute posterior myocardial infarction developed varying degrees of atrioventricular (A-V) block prior to rupture of their interventricular septums (IVS). In three of these five the times of septal rupture coincided with the resumption of conduced synus rhythm. During the period of A-V block, the only stable escape rhythm appeared to originate in the A-V junctional region, and in two patients early in their course there was evidence of enhanced A-V junctional automaticity. Although the A-V node contained extensive infarction in all five hearts, its distal part, and the entire His bundle and proximal branches appeared to be spared. The anatomical pattern of dissection within the ruptured IVS was similar in three hearts, extending upward to the crest of the IVS and penetrating into the interatrial septum in two of these. Multiple major coronary narrowing were present in all five hearts, especially of a dominating right coronary artery; recent thrombosis was present in the right coronary artery in four of the five cases. The A-V node artery was markedly narrowed by focal fibromuscular dysplasia in three hearts, compounding the ischemia for the A-V node and eliminating one important source of collateral circulation to the interventricular septum.
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PMID:De subitaneis mortibus. XXIV. Ruptured interventricular septum and heart block. 87 Feb 49

Postmortem findings within the cardiac conduction system are described from the case of a black woman with sarcoid heart disease who died suddenly. Her clinical course had been characterized by recurring ventricular arrhythmias and bouts of syncope. Both the sinus node artery and the atrioventricular (A-V) node artery were sites of focal fibromuscular dysplasia, which thickened slightly the wall of the former but markedly narrowed the lumen of the latter. Small foci of sarcoid infiltration were present in the sinus node and the A-V node. Fatty replacement within the His bundle was attributable to the probable ischemia caused by narrowing of the A-V node artery. Sarcoid granulomata and infiltration with epithelioid cells were present throughout the ventricular myocardium, but were conspicuously less prevalent in the atria. All the large coronary arteries were normal. Many small coronary arteries in the ventricular myocardium were involved by the sarcoidosis and their lumen were narrowed. These findings and analogous ones reported by others are discussed relative to the pathogenesis of syncopal attacks and sudden death which seem to peculiarly prevalent in sarcoid heart disease.
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PMID:Clinicopathologic correlations. De subitaneis mortibus. XXV. Sarcoid heart disease. 87 28

Segmental mediolytic arteritis is a rare, noninflammatory arteriopathy that involves the splanchnic arteries of adults with shock and the coronary arteries of neonates with hypoxemia. We report the first case (to our knowledge) of segmental mediolytic arteritis involving the hepatic arteries. The lesion begins with cytoplasmic vacuolar degeneration of the arterial smooth-muscle cells, which then progresses to coalescence of vacuoles, leading to disruption of the media, intramural hemorrhage, and periadventitial fibrin deposition. Segmental mediolysis results in arterial wall defects, which can lead to dissecting aneurysms or hemorrhage due to arterial rupture. The intima and internal elastica are spared from the lytic process, and there is minimal periadventitial inflammation. Segmental mediolytic arteritis is not a true arteritis; therefore, segmental mediolytic arteriopathy may be a preferable term. Morphological similarities exist between segmental mediolytic arteritis and arterial fibromuscular dysplasia. In our case, hepatic ischemia correlated with mediolysis involving the hepatic arterial branches. Segmental mediolytic arteritis is thought to be due to an inappropriate vasospastic response, developing in the setting of hypoperfusion and hypoxemia.
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PMID:Segmental mediolytic arteritis involving hepatic arteries. 158 Jul 59

Ventricular tachycardia arising from the right ventricle usually has a left bundle branch morphology and occurs in a variety of disorders. Uhl's anomaly and right ventricular dysplasia may represent a spectrum of one disorder and are a cause of right heart dilatation, failure, and premature sudden death due to ventricular arrhythmias. Familial forms of the disorder may account for focal clustering in some geographic areas. Management should involve aggressive stratification of arrhythmia risk and may include medical, surgical, or device therapy. In contrast, the syndrome of right ventricular outflow tract tachycardia, including nonischemic exercise-induced and repetitive monomorphic ventricular tachycardia, is a more benign entity. Management often involves beta- and calcium channel blocking drugs or type IC antiarrhythmic drugs. Catheter ablation of the arrhythmia focus in the right ventricular outflow tract has been used in selected patients. In this syndrome the right ventricle is normal, and noninvasive testing as well as electrophysiologic studies can be helpful in distinguishing it from the more malignant right ventricular dysplasia. Ventricular arrhythmias may also be seen after right ventricular incision, as in surgical repair of tetralogy of Fallot and ventricular septal defects. Significant ventricular ectopy associated with an abnormal right ventricle (enlarged or depressed systolic function) is associated with an increased risk for sustained arrhythmia and sudden cardiac death in this group. The optimal indicator(s) of highest risk in these patients remains under investigation but will likely include electrophysiologic testing. Bifascicular block occurs commonly after repair of tetralogy of Fallot, but is usually benign. Isolated right ventricular infarction is rare. Most right ventricular arrhythmias associated with ischemia occur in the setting of iatrogenic catheter manipulation for pacing or hemodynamic monitoring. In conclusion, right ventricular arrhythmias involve an unusual and interesting group of clinical entities and appear to span the spectrum of arrhythmias mechanisms. A macroreentrant activation ring around the ventriculotomy scar may account for the arrhythmias following repair of tetralogy of Fallot. Microreentry at sites of morphologic abnormalities results in the arrhythmias associated with right ventricular dysplasia and ischemia. Triggered activity related to DADs or, less likely, abnormal automaticity, produce repetitive monomorphic ventricular tachycardia and nonischemic exercise-induced ventricular tachycardia, both of which usually originate from the right ventricular outflow tract. Iatrogenic ventricular tachycardia associated with catheter manipulation is especially likely to occur in the presence of right ventricular ischemia and infarction. It is important to recognize these clinical entities because treatment is specific.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tachycardias of right ventricular origin. 173 56

A 74-year-old woman was admitted to the hospital with sudden onset of a blue, painful right index finger, and the condition progressed to digital ulceration. The ulcer gradually healed over a period of 2 months. Peripheral pulses, Doppler-derived brachial and radial systolic pressures, and results of an echocardiogram were normal. Digital pulse volume recordings showed obstructive waveforms in all digits of the right hand. Arteriography showed a normal arch and normal innominate, subclavian, and axillary arteries. The midbrachial artery was markedly abnormal and had alternating areas of stenosis and aneurysm formation. Multiple occlusions involved the palmar arch and proper digital arteries. The abnormal brachial artery segment was excised and replaced with an autogenous reversed saphenous-vein conduit. Histologic examination confirmed the lesion to be medial fibromuscular dysplasia. Fibromuscular dysplasia that involves upper extremity arteries is extremely uncommon and rarely presents with digital artery embolization. This case emphasizes the importance of exclusion of proximal reconstructible arterial occlusive disease by means of complete arteriographic examination of patients who were admitted with unilateral finger or hand ischemia.
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PMID:Digital artery embolization as a result of fibromuscular dysplasia of the brachial artery. 186 35

Cystic changes of gastric mucosal glands have been described mainly after gastric operations, and like intestinal metaplasia and dysplasia, they may represent a premalignant condition. Their association with gastritis raises the possibility of their being secondary to the inflammatory process. Enterogastric reflux of duodenal contents, local chronic ischemia, and inflammatory reaction as a result of gastric surgery and suture at gastroenterostomy have been considered responsible for this lesion. In 18 of 157 consecutive patients (11.5%) who underwent endoscopic gastric biopsy within a year we found cystic changes of gastric mucosal glands. Cystic changes were present in 43% of 30 patients after gastric operation for duodenal ulcer disease, within an average of 8.4 years in contrast to only 4% of patients with an intact stomach. This change is statistically significant (Z = 1.97, (p less than 0.05) and suggests that there is a cause-and-effect link between the operation and the development of cystic lesions. In three patients we traced the original operative specimen, and in none did we find cystic changes. All the cases were associated with chronic gastritis; mild dysplasia was found in four (22%). The cystic glands were shown (by alcian blue-periodic acid-schiff staining) to secrete neutral mucin like normal gastric glands, and unlike dysplastic glands or intestinal metaplasia where acid mucin is characteristic. Thus, our findings suggest an inflammatory cause for the cystic glandular change (reactive, hyperplastic change of glands), and suggest that it is probably not a preneoplastic state.
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PMID:Cystic changes in gastric glands after gastric surgery and in the intact stomach. 191 56

An overview is given over etiology and prognosis of cerebral ischemias until the age of 40. In a time period of 19 years, 168 patients were diagnosed with cerebral ischemia until the age of 40 (91 females, 77 males). The most frequent etiology is premature atherosclerosis in patients with vascular risk factors (up to 50%). Cardiogenic embolism is responsible for 1 to 34% of the cases: cardiac valve diseases and endocarditis being the most frequent sources. In 2 to 19% a vasculitis is diagnosed. While infectious arteritis is especially frequent in countries of the third world, immunovasculitides are common in Europe and the USA. Noninflammatory vasculopathies include spontaneous or traumatic dissection, fibromuscular dysplasia and vascular malformations. A migrainous stroke is especially frequent in female smokers with intake of oral contraceptives. During pregnancy both sinus thrombosis and arterial ischemia occur. Hematologic causes for ischemia are polycythemia, thrombocytosis and genetic diseases (sickle cell anemia, AT3-deficiency). Cerebral ischemia may occur in connection with the ingestion of ergot-derivates. The prognosis of cerebral ischemia in young adults is better than in older stroke-patients.
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PMID:[Cerebral ischemia in young adults]. 193 40

The epidermal nevus syndrome (ENS) is a sporadic neurocutaneous disorder that consists of epidermal nevi and congenital anomalies involving the brain and other systems. From among over 60 patients with ENS presenting with neurologic manifestations, we identified 17 who had hemimegalencephaly based on pathologic or radiologic studies. Associated brain and neurologic abnormalities included gyral malformations in 12 of 12, mental retardation in 13 of 14, seizures in 16 of 17 (including 9 with infantile spasms), and contralateral hemiparesis in 7 of 12. All had ipsilateral epidermal nevi of the head, and several had ipsilateral facial hemihypertrophy. We concluded that these abnormalities comprise a recognizable neurologic variant of ENS that we believe represents the full expression of primary brain involvement. Several patients also had evidence of acquired brain lesions such as infarcts, atrophy, porencephaly, and calcifications, which are best explained by prior ischemia or hemorrhage. Given repeated observations of blood vessel anomalies in ENS patients, we hypothesize that underlying vascular dysplasia predisposes to these acquired lesions. The same cause may be invoked to explain the wide variety of neurologic symptoms reported in ENS patients without hemimegalencephaly. While the cause of ENS remains unknown, several observations suggest a somatic mutation.
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PMID:Epidermal nevus syndrome: a neurologic variant with hemimegalencephaly, gyral malformation, mental retardation, seizures, and facial hemihypertrophy. 199 73


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