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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extracranial carotid artery disease is a frequent cause of transient ischemic attack (about 50%), but a much less common cause of cerebral infarction (about 15%). Transient ischemic attack almost invariably precedes strokes caused by extracranial carotid stenosis, but rarely heralds strokes that result from cardiogenic embolism or intracranial vascular disease. When extracranial carotid stenosis produces a transient ischemic attack or stroke, artery-to-artery embolism is the predominant mechanism. Asymptomatic significant (>50%) carotid stenosis poses special clinical questions in patients scheduled to undergo general surgical or major cardiovascular operations. With general surgical procedures, there is no increased risk of stroke. With cardiovascular operations, however, there may be an increased risk of stroke in patients with critical (>90%) carotid stenosis or occlusion. When perioperative stroke occurs, the most common cause is embolism rather than focal hemodynamic change. For symptomatic high-grade (>70%) extracranial carotid stenosis, carotid endarterectomy is the treatment of choice in patients who are not high-risk surgical candidates. Alternatively, for high-risk patients, new drugs such as ticlopidine appear quite promising, and percutaneous angioplasty may also prove effective. Prevention of stroke must continue to be a major goal of national medical policy. Because cigarette smoking is the most important risk factor for extracranial carotid disease, more strenuous efforts must be directed toward eliminating this health risk.
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PMID:Extracranial carotid artery. Current concepts of diagnosis and management. 1522 89

Considerable evidence now indicates that Alzheimer's disease (AD) is a vascular disorder with neurodegenerative consequences. As a result, AD and vascular dementia (VaD) can each be described as a 'vasocognopathy'. The term better describes the origin of the disease (vaso: vessel/blood flow), its primary effect on a system (-cogno: relating to cognition) and its clinical course (-pathy: disorder). Evidence that AD is a vasocognopathy is partly supported by the following multidisciplinary findings: (1) epidemiologic studies linking AD and vascular risk factors to cerebral hypoperfusion; (2) evidence that AD and vascular dementia (VaD) share practically all reported risk factors; (3) evidence that pharmacotherapy which increases or improves cerebral perfusion lowers AD symptoms; (4) evidence of preclinical detection of AD candidates using regional cerebral perfusion and glucose uptake studies; (5) evidence of overlapping clinical symptoms in AD and VaD; (6) evidence of parallel cerebrovascular and neurodegenerative pathologic markers (including plaques and tangles) in AD and VaD; (7) evidence that cerebral infarction increases AD incidence by 50%; (8) evidence that chronic brain hypoperfusion can trigger hypometabolic, cognitive and neurodegenerative changes typical of AD; (9) evidence that most autopsied AD brains contain cerebrovascular pathology; (10) evidence that mild cognitive impairment (a transition stage for AD) converts to AD or VaD in 48% and 56% of cases, respectively, within several years. The collective evidence presented here poses a powerful argument for the re-classification of AD as a vascular disorder. Re-classification would allow a new strategy that could result in the tactical development and application of genuinely effective treatments, provide earlier diagnosis and reduce AD prevalence by focusing on the root of the problem.
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PMID:Alzheimer's disease is a vasocognopathy: a new term to describe its nature. 1526 69

To define the clinical significance of plasma thrombomodulin (TM) values in elderly, we examined plasma TM in healthy young subjects, healthy elderly subjects and patients with cerebral infarction sequelae. We also studied the relationship with effective renal plasma flow (ERPF) and with the liver's protein-production ability. The TM values of healthy elderly subjects were higher than those of healthy young subjects. There existed an inverse correlation between TM values and ERPF. Accordingly, high TM values might significantly influence renal arteriosclerosis. From the inverse correlation identified between TM and serum cholinesterase, it was estimated that high TM might appear in conjunction with the liver's protein production ability. Patients with cerebral infarction showed higher plasma TM values. It is thought that angiopathy has been maintained in patients as the anamnesis of cerebral infarction even though it occurred in the past. The TM values of patients with diabetes mellitus (DM) were higher than those without it. Moreover, the TM values of patients with DM complicated by retinopathy were higher than those uncomplicated by retinopathy. It is therefore estimated that increased TM might occur with angiopathy resulting from DM. A possibility thus exists that plasma TM could be utilized as one of the markers for endothelial injury.
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PMID:Plasma thrombomodulin values and hepatorenal function in the elderly. 1537 35

Thrombin-activatable fibrinolysis inhibitor (TAFI) was reported as an anaphylatoxin-inactivating enzyme generated by proteolytic cleavage of its zymogen, and is the same enzyme as that first designated by our group as procarboxypeptidase R (proCPR). Its level in plasma appears to influence vascular disease. In addition, TAFI activity is strongly influenced by genetic polymorphism, especially at amino acids 147 and 325. We investigated whether these TAFI polymorphisms would act as a risk factor for cerebral infarction (CI) by examining 253 samples in which the diagnosis was cliniconeuropathologically confirmed. We found little that was statistically significant in terms of these polymorphisms among patients with no vascular problems or in a population-based control group. In the present study of an elderly Japanese group, our samples revealed a lower percentage of the Ile allele at Thr/Ile-325 compared with western counterparts. Although patients with severe infarcts had a lower percentage of the Ile allele (10%) at amino acid position 325 compared with the slightly and moderately affected patients and the population-based control group (15-18%), no statistical significance was found. None of our results showed any statistical correlation between TAFI polymorphisms and CI.
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PMID:TAFI polymorphisms at amino acids 147 and 325 are not risk factors for cerebral infarction. 1552 22

Homocystinuria is a congenital metabolic disorder, and has been known as life-threatening risk factor of vascular disease including ischemic stroke. We report a case of cerebral infarction due to homocystinuria. The patient was a 21-year-old woman exhibiting left hemiparesis and a previous history of ectopia lentis. Magnetic resonance imaging showed multiple fresh infarctions in the right frontal and temporal lobes, basal ganglia, corona radiata, and internal capsule. The right common carotid angiogram demonstrated complete occlusion at the origin of the right internal carotid artery. Further investigation clarified increased level of serum methionine and homocysteine and urinary homocystin due to cystathionine beta-synthase deficiency. Homocystinuria was diagnosed as the cause of cerebral infarction. The patient was treated by low methionine diet and administration of folic acid, cobalamin, and aspirin. It should be recognized that some patients with homocystinuria are missed in the neonatal screening for congenital metabolic disorders. Recent studies indicated that the homocysteinemia is one of risk factors of ischemic stroke in the general population as well as in the patients of homocystinuria. We recommend metabolic screening for homocystinuria, when treating a juvenile patient with ischemic stroke of unknown etiology.
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PMID:[A case of young adult presenting with cerebral infarction caused by homocystinuria]. 1555 67

Cerebral small vessels disease are characterized by lesions of the wall of the small cerebral arteries. They are responsible for 25 to 30% of strokes due to cerebral infarction or hemorrhage and/or cognitive impairment, dementia. Lipohyalinosis and cerebral amyloid angiopathy are the most common etiologies. They are associated with age, arterial hypertension, and diabetes. The localization of the lesions by MRI could help to differentiate both etiologies: deep localisation for lipohyalinosis and lobar (cortical) for cerebral amyloid angiopathy. Physiopathology of these diseases is not presently understood, and no specific treatment is available. Therefore, treatment of vascular risk factors (diabetes, arterial hypertension) is the only therapeutic measure available.
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PMID:[Cerebral microangiopathies]. 1592 21

Diverse pathologic conditions affect the central nervous system (CNS) and pituitary gland during pregnancy and the puerperium. Some are specific to the physiologic process of reproduction (eg, eclampsia, postpartum cerebral angiopathy, Sheehan syndrome, lymphocytic adenohypophysitis). Others are nonspecific but occur more often in pregnant women (eg, cerebral infarction, dural venous thrombosis, pituitary apoplexy). Recognition of the characteristic imaging findings in eclampsia, for example, may allow exclusion of other disorders. Even when imaging changes are nonspecific, knowledge of those entities associated with pregnancy and awareness of the increased likelihood of certain diseases in pregnancy will allow a more informed differential diagnosis. Differentiation of primary nonaneurysmal subarachnoid hemorrhage (SAH) from aneurysmal SAH is an example. Moreover, earlier use of imaging will result in fewer delayed diagnoses. For example, magnetic resonance venography allows early diagnosis of cerebral venous thrombosis. Even when the imaging changes are less specific, knowledge of likely possibilities will lead to more appropriate earlier use of imaging. For example, the stimulatory effects of pregnancy on prolactinoma, meningioma, hemangioblastoma, vestibular schwannoma, and metastatic tumors such as breast cancer and choriocarcinoma suggest the early use of CNS imaging to avoid the consequences of a delayed diagnosis.
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PMID:Imaging of neurologic disorders associated with pregnancy and the postpartum period. 1723 1

Incidence of cerebral vascular disease (CVD) is higher in patients with diabetes mellitus (DM) than that in individuals without DM, and neuronal apoptosis determines the severity of cerebral infarction. However, there is no effective therapy for CVD. Granulocyte-colony stimulating factor (G-CSF), a potent hematopoietic factor, could inhibit apoptosis of hematopoietic progenitor cells. However, its effect on neuronal cells is still unclear. In this study, we investigated the anti-apoptosis properties of G-CSF in neurons following focal cerebral ischemia in diabetic rats. The diabetic condition was generated in rats by intravenous injection of streptozotocin. After 6 weeks, diabetic rats underwent middle cerebral artery occlusion (MCAO) and received subcutaneous administration of G-CSF (50 microg/kg) daily for 7, 14 or 21 days. We analyzed the changes in neurological severity scores, infarct volume, number of apoptotic neurons, and the expression of G-CSF receptor, phosphorylated signal transducer and activator of transcription 3 (pSTAT3), cellular inhibitor of apoptosis protein 2 (cIAP2), Bcl-2, and Bax in the brain tissue. Bax is a pro-apoptotic member of the Bcl-2 protein family. The DM rats treated with G-CSF not only showed the reduced infarct volume and decreased apoptosis cell number, but also presented improved neurological scores. The G-CSF also increased the expression of pSTAT3, Bcl-2, and cIAP2 proteins as well as Bcl-2 mRNA, but inhibited Bax protein expression in the brain. These results indicate that G-CSF partially increases neuronal survival by affecting apoptosis pathways. G-CSF provides a potential treatment for stroke and other neurological dysfunction accompanied by neuronal apoptosis.
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PMID:Granulocyte-colony stimulating factor inhibits neuronal apoptosis in a rat model of diabetic cerebral ischemia. 1883 93

Fibromuscular dysplasia (FMD) is a noninflammatory, nonatheromatous segmental angiopathy. The renal arteries are affected most commonly, followed by the internal carotid and vertebral arteries. FMD of the internal carotid and vertebral arteries usually occurs in the extracranial portions and is mostly observed at the level of the second cervical vertebra. FMD of the intracranial arteries is rare, but tends to occur in children and young adults. FMD is more common in females than in males, and it is often observed in middle-aged women. Although the etiology of FMD is not well understood, several mechanisms have been proposed, such as genetic predisposition, hormonal factors, and arterial wall ischemia. The pathology of FMD is characterized by smooth muscle hyperplasia or thinning, elastic fiber destruction, fibrous tissue proliferation, and arterial wall disorganization. Cerebrovascular fibromuscular dysplasia (cFMD) is relatively rare in Japan but is regarded as one of the cardinal causes of stroke in the younger population. cFMD without complications causes nonspecific symptoms such as headache or vertigo, but when it results in an arterial dissection or aneurysm, it leads to cerebral infarction or subarachnoid hemorrhage. Conventional angiographic findings mostly reveal a pattern called the "string of beads", which is pathologically correlated to medial fibromuscular dysplasia. Doppler echography, computed tomography and magnetic resonance angiography (MRA) may be useful for detecting cFMD lesions in some cases. MRA should be performed to rule out the presence of intracranial aneurysms. Antiplatelet and anticoagulation agents are prophylactics against cFMD complications. Surgical treatments such as graduated intraluminal dilatation had previously been the mainstays for treating cFMD. Percutaneous transluminal angioplasty with or without stenting has now become the preferred invasive treatment for symptomatic cFMD.
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PMID:[Cerebral infarction attributable to cerebrovascular fibromuscular dysplasia]. 1897

Thrombolytic serine proteases not only initiate fibrinolysis, but also are up-regulated in vascular disease and acute inflammatory responses. Although the serine protease inhibitor (serpin) plasminogen activator inhibitor-1 (PAI-1) is considered a main regulator of thrombolysis, PAI-1 is also associated with vascular inflammation. The role of other serpins that target thrombolytic proteases, PAI-2, PAI-3, and neuroserpin (NSP), in vascular inflammation is, however, less well defined. NSP is a mammalian serpin that, similar to PAI-1, inhibits urokinase- and tissue-type plasminogen activators (uPA and tPA, respectively) and has been most closely associated with the nervous system, with a demonstrated protective role after cerebral infarction in mouse models. However, the role of NSP in systemic arterial inflammation and plaque growth is not known. Serp-1 is a myxoma viral serpin that also inhibits tPA and uPA, as well as additionally inhibiting plasmin and factor Xa (fXa). Serp-1 has proven highly potent anti-inflammatory and anti-atherogenic activity. Here we assess the effects of NSP treatment on plaque growth and T-helper (Th) lymphocyte activity in a mouse aortic allograft transplant model, with comparison to Serp-1. NSP and Serp-1 both significantly reduced plaque growth and T-cell invasion. T-bet (a Th1 differentiation marker) was significantly reduced in transplanted aorta with associated reductions in Th1 and Th17, but not Th2, in splenocytes. NSP had additional Th modifying activity in non-transplanted mice. In summary, this is the first report that NSP possesses anti-inflammatory activity in systemic arteries, modifying Th cell responses and significantly reducing plaque growth in mouse aortic allografts.
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PMID:Neuroserpin, a thrombolytic serine protease inhibitor (serpin), blocks transplant vasculopathy with associated modification of T-helper cell subsets. 2013 65


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