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

Recent research on the effects of behavioral activities on myocardial ischemia in coronary artery disease patients has provided a pathophysiologic model for understanding the mechanisms by which mental stress can trigger clinical cardiovascular events. This article reviews epidemiologic research implicating psychosocial stress as an acute trigger of myocardial infarction in patients with pre-existing coronary artery disease, and evidence for the pathophysiologic effects of acute mental stress in individuals with pre-existing coronary artery disease. Via its actions on the central and autonomic nervous systems, stress can produce a cascade of physiologic responses in vulnerable individuals that may lead to myocardial ischemia, ventricular fibrillation, plaque rupture, or coronary thrombosis. Also reviewed are field and laboratory studies that suggest important causal links between mental stress and myocardial ischemia, and evidence suggesting clinical significance for vulnerability to mental stress-induced ischemia.
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PMID:Mental stress as a trigger of myocardial ischemia and infarction. 872 59

B/A4 is the major component of brain amyloid plaque, one of the hallmarks of Alzheimer's disease (AD). B/A4 is a product of proteolytic processing of its precursor, the Alzheimer amyloid precursor protein (APP). Recently, apolipoprotein E (APO-E) has also been shown to be associated with Alzheimer's disease pathology because it is localized to plaques and tangles, and the gene encoding one of the isoforms of APO-E (E4) is associated with late-onset familial and sporadic AD. In addition, APO-E exhibits high affinity for binding to the B-peptide (B/A4). In this study, we have investigated changes in the steady state levels of APP, APO-E, and the astrocyte-specific marker, glial fibrillary acidic protein (GFAP) mRNA in the gerbil hippocampal CA1 region after a 10-min period of bilateral carotid occlusion-induced forebrain ischemia. Following this insult, we observed a loss of 90% of the CA1 neurons by 72 h post-ischemia. The mRNA levels on day 1 through day 7 post-ischemia were quantitated using an image analyzer. There was an increase in the transcription of APO-E and GFAP mRNAs, with the levels of APO-E mRNA being the highest (3-fold increase on day 7 post-ischemia) (P < 0.005). However, we did not see an increase in APP mRNA. In a parallel study [Hall, E.D. et al., Exp. Neurol., 135(1995) 17-27], we have also seen an increase in levels of APO-E and GFAP protein measured by immunocytochemistry. However, in contrast to the lack of an increase in APP mRNA, immunocytochemical measurement of APP did show an increase, perhaps due to delayed translation of previously formed mRNA. We suggest that neuronal injury or insult results in the induction of certain genes (and, therefore, protein synthesis) in the surrounding reactive astrocytes, and these proteins may contribute to post-injury amyloidogenesis.
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PMID:Induction of apolipoprotein E mRNA in the hippocampus of the gerbil after transient global ischemia. 873 65

Color Doppler US is at present the most reliable noninvasive procedure in the diagnosis of carotid disease and plays a major diagnostic role in the patient at risk for stroke. The anatomofunctional relationships of carotid and vertebrobasilar system suggest a diagnostic combination between Doppler US and transcranial Doppler for complete hemodynamic evaluation of normal and pathologic cerebral vessels. The most relevant disease, as the cause of stroke, is represented by internal carotid atherosclerosis. Mechanisms by which the atheromatous plaque represents a cause of ischemia involve two factors: the embolic factor and the hemodynamic factor. The embolic factor is consequent on unstable plaques and US plays a major role in plaque characterization. Stenotic plaques are the major cause of the hemodynamic factor. Color Doppler US inables quantification of stenosis and selects surgical patients with greater than 70% stenosis. In internal carotid dissection as the acute cause of cerebrovascular insufficiency color Doppler US findings are significant for early diagnosis and follow-up.
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PMID:[The role of Doppler US in the study of carotid system]. 885 21

This study was designed to clarify the functional results, morbidity and the patient-partner satisfaction observed with, the American Medical System 700 CX three-piece inflatable prosthesis in the treatment of impotence associated with Peyronie's disease. Thirty-three patients were treated and additional plaque surgery was performed in 13 cases (40%). Within 10 days of surgery, four patients (12%) developed a wound infection which was treated conservatively and one patient (3%) experienced glandular ischemia. At the 6-week follow-up, complete penile straightening was achieved in 23 patients (70%), while penile rigidity was considered optimal by all patients. On the contrary, the penis was considered short by 10 patients (30%). Five diabetic patients (15%) complained of severe scrotal and penile pain during full activation of the implant and in one of these patients (3%) the implant had to be removed. Due to spontaneous erections occurring after implant activation one patient (3%) required replacement of the reservoir from the Retzius space into the peritoneum. At the long-term follow-up (mean +/- SE: 17 +/- 2.2 months), 23 patients were evaluated and all found to be engaging in intercourse with the prosthesis. However, five patients (21%) and three of the 13 partners (25%) assessed were not yet completely satisfied. The American Medical System CX700 inflatable penile prosthesis obtains complete penile straightening in 70% and rigidity in 100% of impotent patients with Peyronie's disease. Patients should be fully informed about possible surgical morbidity and actual post-operative penile length.
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PMID:AMS 700 CX inflatable penile implants for Peyronie's disease: functional results, morbidity and patient-partner satisfaction. 885 96

Acute coronary syndromes are responsible for more than half a million hospital admissions each year in the United States alone. Plaque rupture is the precipitating pathophysiologic event. The degree of narrowing of plaques that rupture is not necessarily severe, in the range of 30% to 70% diameter stenosis. Plaques containing large lipid pools with only thin fibrous caps are most at risk. The site of rupture is most often at the shoulder of the plaque, where stress is highest. Clusters of macrophages are often seen at these points. Most plaque ruptures heal without causing symptoms, perhaps leaving a narrowing somewhat more severe than before. Plaque ruptures that expose larger areas of thrombogenic intramural debris to flowing blood in areas of high turbulence are most likely to provoke more extensive thrombosis. Risk factors, particularly smoking and hypercholesterolemia, cause increased thrombin deposition at the site of deep arterial injury. Thrombin deposition causes local coronary vasoconstriction that may contribute to the development of ischemia. Whether plaque rupture with thrombosis causes infarction, unstable angina, or no symptoms at all depends on the site of the lesion, its severity, and whether the jeopardized myocardium is served by collaterals. Aspirin, heparin, and, potentially, the newer agents provide benefit in each of the acute coronary syndromes.
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PMID:Pathophysiology and initial management of the acute coronary syndromes. 887 45

The blue toe syndrome is characterized by tissue ischemia secondary to cholesterol crystal or atherothrombotic embolization leading to occlusion of small vessels. Embolization occurs typically from an ulcerated atherosclerotic plaque located in the aorto-iliac-femoral arterial system. Clinical presentation can range from a cyanotic toe to a diffuse multiorgan systemic disease that can mimic other systemic illness. Mortality can be higher than 70% depending on the scope of the illness. Embolization can occur spontaneously or from a variety of insults such as invasive vascular procedures, anticoagulation, or thrombolytic therapy. Angiography, duplex ultrasonography, computerized tomographic scanning, and magnetic resonance imaging have been used to image the offending lesions, with angiography considered the "gold standard" despite its inherent risks. Recently, transesophageal echocardiography has been shown to be a helpful tool in imaging the thoracic aorta and delineating in great detail the anatomy of the aortic atheroma. At present, surgery remains the most viable treatment option. However, we look to the future for large randomized trials to help predict embolization and thus the proper medical therapy.
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PMID:Evaluation and management of cholesterol embolization and the blue toe syndrome. 888 81

Carotid artery atherosclerotic plaques (APs) can lead to brain ischemia, an event shown to correlate with both the degree of stenosis and the composition of the AP. Currently, accurate estimates of stenosis can be obtained by either x-ray angiography or three-dimensional time-of-flight (TOF) magnetic resonance angiography (MRA). Our purpose was to determine whether three-dimensional TOF MRA images could also provide information on plaque location, morphology, and composition. Seven pre-endarterectomy patients underwent three-dimensional TOF MRA. After endarterectomy, plaque histology was evaluated. Three-dimensional TOF MRA images contained sufficient soft tissue contrast to differentiate the plaques from the surrounding tissues in all cases. Estimation of plaque morphology had 80% correlation with histology. Finally, intraplaque hemorrhage and calcification were deplicted as regions of moderately high and very low intensity, respectively. These preliminary results suggest that three-dimensional TOF MRA may be useful in studying the development and progression of carotid atherosclerosis.
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PMID:Atherosclerosis of the carotid artery: evaluation by magnetic resonance angiography. 889 10

The accuracy of three-dimensional CT angiography (3D-CTA) for delineating atherosclerotic carotid stenosis was examined in comparison with digital subtraction angiography (DSA) in symptomatic patients. In cases undergoing carotid endarterectomy (CEA), the clinical usefulness of 3D-CTA for surgical planning was also evaluated in the light of intraoperative findings. From July 1992 to June 1995, 52 patients suffering from internal carotid ischemia and/or presenting carotid bruit were evaluated to detect carotid bifurcation stenosis by 3D-CTA. Shaded surface reconstruction (SSR) for three-dimensional display and maximum intensity projection (MIP) were employed in multiple projection to evaluate sites of stenosis. DSA was performed in 18 out of 31 patients having atherosclerotic carotid stenosis shown by 3D-CTA. MIP reconstructions accurately delineated sites of stenosis close to DSA and allowed precise depiction of ulcerated plaque and intramural calcification. The percentage of carotid stenosis was determined by comparing the narrowest point to the internal carotid artery (ICA) beyond the bulb on both 3D-CTA and DSA. Assessment of carotid stenosis was highly correlated between 3D-CTA and DSA (r = 0.987, p < 0.0001). In this series, 9 carotid arteries in 8 patients underwent CEA for severe stenosis. 3 patients with ICA occlusion and 1 patient with elongated severe stenosis underwent STA-MCA anastomosis. Using MIP reconstructions and two-dimensional original images it was found that ICA occlusion was apparently distinguished from high grade ICA stenosis. SSR provided valuable informations during CEA for atherosclerotic plaque regarding anatomical relationship with the internal jugular vein and bony structures. This advanced means of 3D-CTA can be adequate as a screening method to detect carotid stenosis in symptomatic patients and useful for surgical planning of CEA and post-operative follow-up examination.
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PMID:[Evaluation of carotid artery stenosis with three-dimensional CT angiography and surgical revascularization]. 893 67

Nourishment of arteries is accomplished by diffusion from the lumen of the vessel and from vasa vasorum. Most normal arteries have an extensive network of vasa in the adventitia that arise from branch points of parent arteries. When the thickness of arteries exceeds the ability of simple diffusion of nutrients from the lumen (larger muscular of atherosclerotic arteries), vasa extend into the media and intima. Vasa in the intima-media arise predominantly from adventitial vasa, but can arise from the lumen in vascular grafts and recanalized arteries after thrombosis. Vasa respond to vasoactive stimuli, and can regress after they vascularize arterial grafts and in response to regression of the atherosclerotic lesions. Therefore, vasa can increase blood flow to the artery wall by dilation of existing arteries or by formation of new vessels (neovascularization). Conversely, vasa can reduce blood flow to the artery wall by active constriction or by regression (involution) of existing vasa. The pathophysiological significance of vasa vasorum in normal and diseased arteries is related to their structure. Vasa in the intima-media are thin-walled endothelial cell tubes with thin or absent medial smooth muscle cells. Therefore, they are prone to collapse and rupture in response to arterial pressure, mechanical forces in the artery, necrotic substances found in diseased arteries, and vasospasm. Vasa also provide the artery with a vast absorptive endothelial surface that may have important implications for arterial lipid kinetics, and delivery and removal of neurohumoral agents from the artery wall. These properties have lead to speculation about their role in the pathogenesis of atherosclerosis, plaque rupture and thrombosis, medial ischemia leading to arterial dissection and aneurysm, restenosis after angioplasty, and post-stenotic dilatation. Finally, larger veins also have an extensive network of vasa that have been implicated in the pathogenesis of venous thrombosis and varicose veins.
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PMID:[The vasa vasorum of the arteries]. 898 46

These preclinical studies investigate a new concept in coronary angioplasty and balloon catheter technology (the P100 catheter). The study sought to evaluate the morphology of experimental coronary arterial plaques dilated with the P100 in comparison to standard balloons, to determine the in vitro flow rates occurring during the inflation of the P100 in comparison to available perfusion catheters, and to assess the in vivo coronary flow velocity and the presence of ischemia during prolonged inflations with the P100. The development of myocardial ischemia is a major limitation of standard balloon angioplasty. To limit ischemia, autoperfusion catheters have been developed, in which blood flows through the balloon in the central catheter shaft. However, as the flow lumen profile is reduced to enhance the performance of these devices, so is the accompanying flow. An angioplasty catheter was designed to evaluate the feasibility of continuous autoperfusion around the dilatation balloon. The balloon surface was engineered to develop a helical trough for blood flow to occur during inflation. Arterial plaque morphology following angioplasty with the P100 (n = 8) and with standard balloons (n = 8) was evaluated in a swine model. In vitro flow rates during inflation of the P100 and available perfusion catheters were determined using 33% glycerol solution. In vivo coronary flow velocity was determined with a Doppler-tipped wire during 60-min continuous inflations with the P100, and 15-sec inflations with a standard balloon in 12 vessel segments in 7 dogs; using 3.0-3.5-mm-diameter balloons. All lesions were successfully dilated (< 50% luminal diameter stenosis) with the P100 and standard balloons. There were no morphologic differences in plaques dilated with P100 compared to standard balloons. In vitro flow rates with conventional 3.0-mm balloon perfusion catheters ranged from 27.1 +/- 2.1 ml/min (RX Flowtrack) to 38.7 +/- 0.9 ml/min (Stack Perfusion), P < .05. Flow with the P100 ranged from 54.8 +/- 4.3 ml/min (2.5-mm balloon) to 103.2 +/- 4.5 ml/min (3.5-mm balloon), P < .05. Distal average peak coronary flow velocity during prolonged P100 inflations varied from 69 +/- 7% of baseline at 5 min to 83 +/- 8% of baseline at 40 min, with an upward trend in velocity the longer the balloon was inflated. Hemodynamics remained stable. Experimental plaques are successfully dilated with a helical balloon by a mechanism that appears similar to the dilatation mechanism of standard balloons. These preclinical studies show that angioplasty and autoperfusion can be accomplished by a balloon that does not have complete surface area contact with the vessel wall. A gap created by the helix can thus provide a conduit for blood flow. Clinical studies will determine whether this innovation, which alters the tubular geometry of current angioplasty balloons, will provide autoperfusion and equivalent dilatation effects in human.
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PMID:New concept in coronary angioplasty: dilatation with a helical balloon that allows simultaneous autoperfusion. 899 27


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