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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In man a close interrelationship exists between hyperadrenergic states, myocardial ischemia, necrosis, infarction and sudden cardiac death. Persistent high catecholamine levels may also be associated with increased vascular endothelial turnover and permeability to calcium and lipoproteins, increased blood velocity, abnormal blood flow patterns and atheroma formation. There are thus good reasons to predict a cardiovascular protective effect of beta-blockers. Animal data indicate that in spite of apparently adverse plasma lipoprotein changes beta-blockers retard atheromatous plaque formation under conditions of high cholesterol diet with or without stress. A slow heart rate, as well as a reduction in calcium influx and inhibition of both esterification of arterial wall cholesterol (by ACAT) and endothelial permeability to lipoproteins, may be central to this process. Beta-blockers benefit a spectrum of conditions related to the atheromatous process and myocardial necrosis. These are silent ischemia; stable (including mixed), unstable and preinfarction angina; periinfarction events (including myocardial rupture and dissection of the ascending aorta); and myocardial necrosis associated with stress conditions such as head injuries and subarachnoid hemorrhage. In one study coronary deaths in hypertensive men, particularly in smokers, were significantly reduced by metoprolol (a beta 1-selective blocker) compared to a diuretic. In contrast in the MRC study of mild hypertension only nonsmoking men with mild to moderate hypertension who received a nonselective beta-blocker appeared to experience fewer myocardial infarctions. Recent clinical data showed that moderate-severe hypertensives who were optimally controlled by atenolol-based treatment over a 10-year period were less likely to die from myocardial infarction than those suboptimally controlled, irrespective of a rise in serum triglyceride levels. Thus the net effect of acute beta-blockade in hyperadrenergic states, including myocardial infarction, is to limit cardiovascular damage. Chronic beta-blockade inhibits atheroma formation (in animals) and beneficially modifies the incidence of stroke and myocardial infarction, which in man are the long-term consequences of hypertension.
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PMID:The beta-receptor, atheroma and cardiovascular damage. 257 Apr 26

The mechanism by which atherosclerotic plaque causes stroke and transient ischemic attack is not fully understood. One possibility is that the plaque stenosis may set up hemodynamic conditions causing local arterial wall collapse. Arterial wall collapse may, in turn, affect the integrity of the plaque. This study was designed to define the effects of stenosis on the production of arterial wall collapse using a latex tube model. Stenoses ranging up to 81% by diameter were tested in a Starling resistor chamber under pulsatile pressure conditions upstream of the tube. Increasing the degree of stenosis progressively decreased the external pressure necessary to produce collapse, from 37 mm Hg with the 0% stenosis to 24 mm Hg for the 81% stenosis. The stenoses greater than 70% produced a new phenomenon of "systolic wall collapse" just distal to the stenosis. The maximum diameter decrease was 2.83 mm from the baseline diameter of 6.41 mm. Cyclic wall motion just downstream of the stenosis increased with the increased degree of stenosis from 0.34 mm at 0% stenosis to -1.28 mm at 75% stenosis. The phenomena are discussed in terms of simplified Bernoulli pressure drops. We conclude that local arterial stenosis can produce conditions favorable for wall collapse and increased wall motion at physiologic pressure and flow. This collapse may be important in the development of atherosclerotic plaque fracture and subsequent thrombosis or distal embolization.
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PMID:Effect of stenosis on wall motion. A possible mechanism of stroke and transient ischemic attack. 259 63

Duplex ultrasound (US) scans of 110 carotid arteries ipsilateral to hemispheric strokes were compared with scans of 90 asymptomatic vessels in the same patients to determine the relative prevalence of stenotic lesions. In addition, scans of paired carotid arteries in patients with stroke involving only one cerebral hemisphere were compared to determine whether the incriminated side demonstrated a greater degree of stenosis than the asymptomatic side. The duplex US findings demonstrated a positive correlation between stenosis and hemispheric stroke. However, only 20% of carotid arteries ipsilateral to hemispheric stroke showed a reduction in diameter greater than 70%, compared with 5% of asymptomatic vessels. A minimal difference was demonstrated between the symptomatic and asymptomatic groups with respect to lesser degrees of stenosis. In paired carotid arteries, the degree of stenosis of the symptomatic vessel exceeded that of the asymptomatic vessel in only 43% of cases. These results suggest that the prevalence of severe carotid stenosis in stroke patients has been previously overestimated. The findings also emphasize the need for further investigation of other plaque-related risk factors that may enhance stroke prevention through improved selection of surgical or medical therapy. Factors currently under investigation include plaque ulceration, intraplaque hemorrhage, plaque echogenicity, and the effects of sequential stenoses.
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PMID:Degree of cervical carotid artery stenosis and hemispheric stroke: duplex US findings. 264 47

Information obtained during the past decade suggests the need to reexamine the possibility that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering onset of coronary thrombosis is supported by the findings that 1) the frequencies of onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations with parallel increases in the period from 6:00 AM to noon, 2) transient myocardial ischemia shows a similar morning increase, and episodes are often preceded by mental or physical triggers, 3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi, 4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state or coronary vasoconstriction, are accentuated in the morning, and 5) aspirin and beta-adrenergic blocking agents, which block certain of these processes, have been shown to prevent disease onset. The hypothesis is presented that occlusive coronary thrombosis occurs when 1) an atherosclerotic plaque becomes vulnerable to rupture, 2) mental or physical stress causes the plaque to rupture, and 3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of onset of acute disease suggests the need for pharmacologic protection of patients during vulnerable periods, and provides clues to mechanism, the investigations of which may lead to improved methods of prevention.
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PMID:Circadian variation and triggers of onset of acute cardiovascular disease. 229 45

A method for long-term culture of microvascular endothelial cells from Mongolian gerbil brain and their biologic properties in vitro are described. Microvessels were isolated from Mongolian gerbil brain by a combination of enzymatic treatment, filtration, and centrifugation and were seeded onto a gelatin-coated dish. A morphologically homogeneous cell plaque showing a cobblestone appearance was removed 2 to 3 weeks after the seeding, and the cells were subcultured. The cultured cells grew as monolayers of flat polygonal cells and were carried for more than 20 passages without morphologic change. These cells synthesized prostacyclin and retained an endothelial specific marker, factor VIII-related antigen. When the cells were cultured in a collagen gel, they rapidly formed capillarylike tubular structures without endothelial cell growth factor or special substrata. Long-term culture of purified microvascular endothelial cells derived from Mongolian gerbil brain will facilitate the study of the function of microvascular endothelial cells in human brain under normal and pathologic conditions.
Stroke 1989 Jul
PMID:Long-term culture of microvascular endothelial cells derived from Mongolian gerbil brain. 266 7

Embolization of atherosclerotic material from the ascending aorta resulting from placement of cannulas or vascular clamps is a major cause of stroke during cardiac surgical procedures. In an effort to identify atherosclerotic disease of the ascending aorta which might predispose to embolization, intraoperative B-mode ultrasonography was performed in 50 patients. The aorta was imaged from the aortic annulus to the origin of the innominate artery in transverse and longitudinal views. The results were compared with visual and tactile examination of the aorta for the presence of atherosclerosis. Ultrasonic imaging demonstrated atherosclerotic disease in 29 patients (58%). Visual examination and palpation identified atherosclerosis in 12 patients (24%). The amount and location of plaque was sufficient to require a change in the site of arterial cannulation or the proximal vein graft anastomoses or the technique of cardiopulmonary perfusion in 12 of the 50 patients (24%). All 12 patients were 65 years of age or older. Palpation underestimates the presence of atherosclerotic disease in the ascending aorta. Intraoperative ultrasonography accurately identifies patients with atherosclerotic disease of the ascending aorta. This allows the surgeon to modify cannulation, perfusion, and operative techniques to reduce the risk of perioperative stroke due to the embolization of atherosclerotic debris from the ascending aorta.
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PMID:Intraoperative ultrasonic imaging of the ascending aorta. 267 86

Carotid endarterectomy (CE), when performed in patients with previous stable stroke followed by complete or almost complete recovery, seems to be affected by a higher peroperative risk. From January 1982 to March 1988, we performed 230 CE in 207 patients, 188 (81.8%, Group 1) in patients with TIA or an asymptomatic plaque and 42 (18.2%, Group 2) in patients with previous strokes. The need for a temporary indwelling shunt has been evaluated with the measurement of carotid back pressure and, in the last 100 CEE, with the monitoring of somatosensory evoked responses (the shunt has however been used routinely anyway in the very first part of our experience). The incidence of carotid back-pressure values and of positive somatosensory evoked responses were similar in the two groups of C.E., even if the differences in the prealable evaluation were not statistically significant. The shunt has been nevertheless used more frequently in Group 2 (40.5 vs 28.2%). Statistical analysis has been performed with the chi 2 method. The incidence of permanent and transient neurologic deficits and of the peroperative mortality due to neurological and non-neurological causes was, respectively, 0.5, 2.6, 1.6, 0% (Group 1) and 2.4, 7.3, 2.4, 2.4% (Group 2) (non-significant). If we exclude the first 50 operations (in which technical and/or anaesthesiological problems may have influenced the neurological outcome of the patients operated upon), the previous values become, respectively, 0,07*, 0,7, 0% (Group 1) and 0, 5,5*, 0, 2,7% (Group 2) (*p less than 0,01, the only significant difference).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Peroperative morbidity and mortality in thromboendarterectomy of the carotid bifurcation in patients with a previous stabilized stroke. Our results and review of the literature]. 268 26

Contrast-enhanced computed tomography of the neck permits low-risk evaluation of morphologic complications of carotid plaque, including (and foremost) calcification. To investigate the patterns and clinical significance of calcified deposits in the cervical carotid arteries using computed tomography we studied 40 patients with unilateral symptoms of hemispheric ischemia. Calcium deposits observed in the external, internal, and common carotid arteries were oriented in space and individually scored. We found calcified deposits in 39 patients. Stepwise multiple regression of the data provided evidence strongly suggesting a correlation between advancing age and calcium scores. Calcium was more heavily concentrated in the posterior half of arteries (p less than 0.01), in particular of the internal and common carotid arteries, and always in relation to an atheromatous plaque, suggesting a causative link to hemodynamic forces within the arteries. There was no difference in calcification scores between symptomatic and asymptomatic sides, indicating that calcium deposits do not contribute to the development of symptoms.
Stroke 1989 Nov
PMID:Computed tomographic study of cervical carotid calcification. 281 80

We histologically examined specimens from 11 patients with recent occluding thrombi at the carotid bifurcation to study local factors in the vessel wall that precipitated the thrombi. The area of stenosis of the vessel lumen was determined morphometrically. Severe atherosclerotic stenosis was frequent but was not a prerequisite for thrombus formation since specimens from almost one half of the patients had only moderate narrowing of the lumen (less than 60% stenosis). Specimens from three patients showed ulcerations, those from one showed intraplaque hemorrhage, and those from one massive plaque rupture, all of which were thought to be important in thrombogenesis. All such types of plaque complications may thus precipitate thrombi but no single complication was particularly predominant, and specimens from one half of the patients showed no complications at all. Screening of the carotid arteries for stenosis can therefore detect only one half of the individuals who ultimately will develop thrombosis, and the risk caused by plaque complications seems to be moderate in unselected materials.
Stroke 1989 Nov
PMID:Pathogenesis of carotid thrombosis. 281 81

The purpose of our study was to determine the origin and relation of vasa vasorum to atherosclerotic plaque at the bifurcation of the common carotid artery. We randomly selected 12 unembalmed adult human cadavers, 40-96 years of age. We prepared luminal casts of the arteries from eight cadavers and cleared the arteries from the remaining four cadavers. A network of vasa vasorum surrounding atherosclerotic plaque was observed in five luminal casts and in two cleared specimens; the vasa vasorum originated from the superior thyroid and ascending pharyngeal arteries. Three of the five luminal casts also demonstrated vasa vasorum arising directly from the internal carotid artery distal to the plaque. An extensive network of vasa vasorum was not observed in specimens from the five cadavers relatively free of gross atherosclerotic plaque. Our findings demonstrate the importance of the external carotid artery in giving rise to the vasa vasorum that supply the areas of atherosclerotic plaque.
Stroke 1989 Nov
PMID:The origin and distribution of vasa vasorum at the bifurcation of the common carotid artery with atherosclerosis. 281 82


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