Embolus

About: Embolus is a research topic. Over the lifetime, 1619 publications have been published within this topic receiving 25798 citations. The topic is also known as: emboli.

Artificial embolization of cerebral arteries: report of use in a case of arteriovenous malformation

Abstract: It has been the theoretical and technical consideration of one of us (A. J. L.) that certain large arteriovenous malformations of the brain can be treated by artificial embolization. The major feeding arteries are greatly enlarged compared to the arteries to the surrounding brain. 1 Because of the reduced peripheral resistance there is a far greater flow of blood to the malformation than to the surrounding brain. 2 The main arterial feeders arborize into considerably smaller, "arteriole-like" vessels before entrance into the larger channels which constitute the bulk of the lesion. 3 Therefore, an embolus of predetermined size and configuration, introduced even far proximal to the malformation, will always find its way to it. By its size the embolus will be excluded from passage into the smaller branches to the brain and will ultimately come to rest at a site proximal to the malformation where normal and abnormal vessels are

Acute cor pulmonale resulting from pulmonary embolism: its clinical recognition

Abstract: The immediate result of a high degree of occlusion of the pulmonary artery is sudden dilatation of the right ventricle and right auricle, which may best be termed acute cor pulmonale in contrast to the well known cor pulmonale of chronic nature associated with progressive enlargement of the right side of the heart secondary to certain pulmonary diseases. The clinical evidence of the acute cor pulmonale resulting from pulmonary embolism deserves consideration because of the frequency and importance of the condition and of the common difficulty in diagnosis. The growing readiness of surgeons to undertake the operative procedure for the removal of the embolus from the pulmonary artery further emphasizes the importance of establishing the correct diagnosis, and until this can be done the entire procedure must be regarded as extremely hazardous. During the past two years we have encountered several instructive cases of pulmonary embolism which have shown, we

Aortic Atherosclerotic Disease and Stroke

Abstract: In the 1940s, most strokes were attributed to cerebral vasospasm, a mechanism that is not given a great deal of credence today. It was not until the early 1950s that Harvard neurologist C. Miller Fisher1 stressed the importance of carotid artery atherosclerosis as a major cause of cerebral infarction. Later that decade, the importance of atrial fibrillation as a cause of cerebral embolism began to be stressed,2 and the presence of a left atrial thrombus was first seen on angiocardiography in 1965.3 Despite the established importance of these 2 causes of stroke, carotid disease and atrial fibrillation, nearly half of strokes were listed as “of undetermined cause” in a large stroke registry as recently as 1989.4 In this series, 40% of 1273 cerebral infarctions in the Stroke Databank of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) were thought to be cryptogenic (from the Latin crypticus , meaning secret or mysterious). The clinical syndrome in those patients, as well as the angiographic and computed tomographic (CT) findings, could be reclassified as embolic; however, because no source of embolus could be identified, the authors kept these strokes in the undetermined cause category. In 1990, a third leading cause of embolic stroke was identified on transesophageal echocardiography (TEE), namely severe atherosclerotic plaques in the aortic arch.5 The 3 patients described in that initial report were a 68-year-old woman with dysarthria and an embolus to the foot, a 77-year-old woman with a cerebellar infarction after cardiac catheterization, and a 70-year-old man with staggering, diplopia, and a visual field cut. All 3 had severe plaque in the aortic arch on TEE. In addition, freely mobile projections were seen superimposed on the plaques, making it seem likely that these findings were the reason for the patients’ embolic …

Differentiation between different pathological cerebral embolic materials using transcranial Doppler in an in vitro model.

Abstract: The detection of circulating particulate cerebral emboli using transcranial Doppler ultrasonography has been recently reported. It has been suggested that this method might allow discrimination between different embolic materials; this would be very useful for selecting specific pharmacological treatment in individual patients. This study was designed to identify those parameters of the Doppler signal that might prove useful in discriminating between different types and sizes of particulate cerebral emboli. An extracorporeal circuit filled with a saline/Tween solution and driven by a peristaltic pump was used. The tubing was placed in a skull in the position of the middle cerebral artery. Using transcranial Doppler ultrasound, flow was insonated via the transtemporal window. The following embolic materials of measured sizes (range of maximum dimension, 0.5-5.0 mm) were introduced into the circuit: thrombus (n = 20), platelet-rich aggregates (n = 15), atheromatous material (n = 20), and fat (n = 20). The Doppler signal was recorded during the passage of each embolus. Off-line analysis was performed to measure the maximum amplitude and duration of the signal. For all embolic materials there was a highly significant relation between embolus size and maximum amplitude of the Doppler signal. The closest correlation was obtained when the logarithm of maximum amplitude was used (for thrombi, r = 0.74; for platelet, r = 0.87; for atheroma, r = 0.46; and for fat, r = 0.68). The slope of the regression line differed for the different embolic materials and was significantly steeper for platelets than for atheroma (p 2 mm) there was little further increase in maximum amplitude with increases in embolus size. For all embolic materials there was a highly significant linear relation between embolus size and duration of the high-amplitude (> 150 dB) signal (for thrombi, r = 0.75; for platelet, r = 0.90; for atheroma, r = 0.77; and for fat, r = 0.86). Platelet emboli result in lower-amplitude signals, and therefore analysis of maximum amplitude may provide information on the type of embolic material. However, it may be difficult to determine whether a given signal is associated with a large platelet embolus or a small atheroma embolus. Duration of the high-amplitude signal will allow accurate estimation of the size of emboli, particularly where the emboli are all of the same material.