Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are many different etiologies of renal artery disease (atherosclerosis, aneurysm, dissection, arteriovenous fistula, embolism, fibromuscular dysplasia) and also a lot of different therapies (conservative treatment, percutaneous transluminal angioplasty [PTA], endarterectomy, bypass grafting, patch plasty, nephrectomy). Recently conservative treatment and PTA have significantly improved. Patients who are referred to surgery today are of older age with severe and often bilateral disease of the renal arteries. Additional manifestations of general atherosclerosis like coronary artery disease, aortic aneurysm, peripheral occlusive vessel disease and cerebral vascular insufficiency are often present as well. The main goal of all forms of treatment is the preservation of general renal function. With our retrospective study the results after surgical revascularisation of kidneys are evaluated over a short period of time. Only graft revascularisations are included in the study and we were mainly interested in renal function and blood pressure.
 ...
PMID:[Results of surgical revascularization of the kidney]. 822 52

Because there is uncertainty about the role of atherogenic and nonatherogenic risk factors for cerebral ischemia in the young, we carried out a multicenter, hospital-based, case-control study. 333 patients (15-44 years) with focal cerebral ischemia (transient ischemic attack or stroke within 8 weeks of admission) were eligible. 25 patients were excluded, according to the protocol. 308 cases were matched by age and gender to one hospital and one population control. Independent risk was shown by logistic conditional regression for migraine with aura [odds ratio (OR) = 14.8], smoking (OR = 3.7), alcohol (OR = 2.8), serum triglycerides (OR = 1.6), arrhythmias (OR = 9.5), mitral stenosis (OR = 56), coronary heart disease (OR = 4.3) and carotid stenosis or occlusion (OR = 41). Serum HDL-cholesterol had a relative protective effect (OR = 0.8). These data confirm the role of atherosclerosis and cardiac diseases as well as migraine with aura and alcohol consumption in the pathophysiology of cerebral ischemia in the young. More thorough prevention programs may contribute to earlier detection and control of all of these risk factors, but further investigations in patients with as yet unidentified risk factors are warranted because the above-mentioned factors do not account for the total risk of ischemic stroke in the young.
 ...
PMID:Focal cerebral ischemia in young adults: a collaborative case-control study. The National Research Council Study Group. 823 6

Doppler ultrasound examination is an easy and non-invasive examination technique to image the anatomical and functional situation of cervical vessels. An increasing number of ENT-specialists has been using Doppler sonography in the diagnosis of cochlear and vestibular disorders. We analysed the frequency of pathological Doppler examination results of 150 patients with vertigo, hearing loss and tinnitus. Especially patients with vertigo bear a greater risk for stenosis of the extracranial arteries (28%) compared to an asymptomatical population (1%). Patients with hearing loss and tinnitus showed a different degree of artery disorders (23% of the patients with hearing loss; 18% of the patients with tinnitus). Patients bearing no risk for atherosclerosis showed in 13% (vertigo) and 8% (hearing loss and tinnitus) stenosis of the cervical arteries. Thus we found by Doppler ultrasound examination more stenoses in patients with cochlear or vestibular symptoms than in an asymptomatical population. The early attribution of stenosis to a malfunction of the inner ear helps to avoid invasive examinations of cervical vessels. In addition to this, imminent cerebral ischaemia can be revealed at an early stage.
 ...
PMID:[Incidence of Doppler ultrasound detectable stenoses of cervical arteries in patients with cochlear-vestibular symptoms]. 826 28

During the last decade, a multitude of experimental arguments have led to the concept that EDRF is nitric oxide (NO), a messenger not only involved in the control of vasomotor tone but also in vascular homeostasis, neuronal and immunological functions. Regardless of its origin, endogenous NO is produced through the conversion of L-arginine to L-citrulline by NO-synthase (NOS) from which several isoforms have recently been isolated, purified and cloned. NOS-type I (isolated from brain) and type III (isolated from endothelial cells) are termed "constitutive-NOS" and produce picomolar levels of NO from which only a small fraction elicits physiological responses. These isoforms are regulated by Ca(2+)-calmodulin with NADPH, FAD/FMN and tetrahydrobiopterin as co-factors and reveal a high degree of homology with the amino-acid sequence of cytochrome P450 reductase within the C-terminal domain. Functionally, neuronal-NOS type I is important in neurotransmission (modulation of NMDA receptor), the central control of vascular homeostasis and possibly learning and memory. In the peripheral nervous system, NOS appears to be linked to nonadrenergic noncholinergic (NANC) neuronal pathways. Endothelial-NOS type III is essential for the control of vascular tone in response to the release of endogenous mediators, although shear stress is the major trigger of endothelial-NOS activity under physiological conditions. NOS-type III also contributes to the prevention of abnormal platelet aggregation. NOS-types II and IV (isolated from macrophages) are Ca(2+)-calmodulin independent and are termed "inducible-NOS" since their activation is only promoted under pathophysiological situations where macrophages exert cytotoxic effects in response to cytokines. In contrast with NOS-types I and III, activation of NOS-type II in these cells induces the formation of nanomolar levels of NO which act as a defense mechanism of the immune system. Dysfunctions of the L-arginine-NO pathway have been characterized in multiple diseases (atherosclerosis, hypertension, diabetes, sepsis, cerebral ischemia, etc) and the design of more selective activators/inhibitors of NOS isoforms is a new challenge for the understanding of their pathophysiology and treatment.
 ...
PMID:Nitric oxide: an ubiquitous messenger. 829 80

Even during the symptom-free stages, patients with a TIA often experience cerebral blood flow disturbances. In order to evaluate the factors which cause this abnormality, we studied the cerebral blood flow disturbance, anatomy and clinical status in 21 patients after TIAs. The results of 99mTc-hexamethyl-propylene-amine oxime SPECT were compared with CT, cerebral angiogram, cerebrovascular risk factors and clinical findings to determine which factor is most responsible for the hypoperfusion of brain after TIA. The overall sensitivity rates in detecting a lesion were 67% in SPECT and 19% in CT. The hypoperfused area tended to be large in patients who had intracranial, severe stenotic, multiple, or hemodynamically significant arterial lesions on the ipsilateral side. No such relationships were found between other examinations. We conclude that hypoperfusion after TIA essentially reflects a continuous cerebral blood flow disturbance that can be attributed to atherosclerosis of the cerebral arteries, with subsequent embolic and/or hemodynamic cerebral ischemia, although there may be a variety of processes.
 ...
PMID:Factors causing prolonged hypoperfusion after transient ischemic attack. 846 Dec 36

We evaluated the genotypes of the angiotensin-converting enzyme (ACE) gene in 101 subjects with and 109 subjects without a history of ischemic stroke. All were attending a metabolic ward. The two groups were compared for major risk factors for ischemic events. Genotypes were determined by polymerase chain reaction with oligonucleotide primers flanking the polymorphic region in intron 16 of the ACE gene. Deletion polymorphism of the ACE gene (DD genotype) was shown to be more common in subjects with a history of stroke than in those without (relative risk, 1.76; confidence intervals, 1.02 to 3.05). A positive family history for ischemic complications of atherosclerosis was also more common in subjects with documented events (relative risk, 1.99; confidence intervals, 1.10 to 3.59). DD genotype and a positive family history were strong independent discriminators of cerebral ischemia. Plasma levels of tissue-type plasminogen activator (TPA) and plasminogen activator inhibitor-1 help identify subjects with a history of cerebral ischemic episodes. When such fibrinolytic variables were included in the analysis, the DD genotype still strongly and independently discriminated subjects with a stroke history and significantly interacted with TPA levels > 10 ng/mL in such identification. We conclude that in subjects attending a metabolic ward, homozygosity for a deletion polymorphism of the ACE gene consistently discriminates subjects with a stroke history. Interaction with TPA improves such identification.
 ...
PMID:Deletion polymorphism in the angiotensin-converting enzyme gene in patients with a history of ischemic stroke. 862 Mar 47

This article focuses on the key concept that a basal production of nitric oxide (NO) is required as a background for biological modulation, although an excess can be cytotoxic. Studies of ischaemia and neurodegeneration have tended to emphasise detrimental effects of excess NO, but this review contrasts the emerging importance of diminished NO or interference with its action in vasospasm following subarachnoid haemorrhage (SAH) in ageing and in atherosclerosis. Clinical intervention in cerebral ischaemia will require specificity of action, since NO appears to be protective or detrimental depending on the time, source, and distribution of its production. It may be possible to utilise targeted action on the different forms of NO synthase or the specific redox forms of NO in different tissue areas.
 ...
PMID:Nitric oxide and cerebral blood flow: an update. 870 73

The pathogenic role of aortic arch atherosclerosis (AAA) in embolic stroke is not well understood. We investigated, prospectively, the prevalence and severity of AAA in patients with embolic stroke to ascertain its role as a risk factor for cerebral ischemia. We examined 100 consecutive patients who had experienced acute symptoms due to cerebral ischemia. Clinical examination, electrocardiogram, x-ray, ultrasound examination of craniocervical arteries, transesophageal echocardiography (TEE), cranial computerized tomography, and magnetic resonance imaging were undertaken. Seventy-five patients showed evidence of AAA; 34 patients had moderate to severe (> 5 mm thickening) AAA. Age was positively related to the severity of AAA, as were smoking, coronary heart disease, diabetes mellitus, internal carotid artery (ICA) occlusive disease, and embologenic heart disease. Hypertension, which was evident in 52 patients, did not distinguish those cases showing AAA. Twelve patients showed evidence of high-degree ICA stenosis on the symptomatic side, although the extent of ICA stenosis and AAA were unrelated. A cardiac source of emboli was found in 28 patients. AAA was found to be the probable source for embolic stroke in 14 patients. These data indicate that aortic arch atherosclerosis is an important source of cerebral emboli which may increase the risk for ischemic stroke. Furthermore, we suggest that TEE examination of the aortic arch may be important for the diagnosis of AAA and ultimately for the prophylactic treatment of severe cerebral ischemia.
 ...
PMID:Embolism from the aortic arch in patients with cerebral ischemia. 891 14

The aorta is the most frequent site for atherosclerosis, and is more frequent than the internal carotids or cerebral arteries. Transesophageal echocardiography has made it possible to identify atheromatous lesions of the aortic arch which are situated before the branches to the neck vessels and are capable of causing embolic cerebral events. These atheromatous plaques can be irregular, may protrude into the aortic lumen and sometimes have loose thrombus attached to them. The risk of strokes and transient ischemic attacks appears to be higher when plaques are more than 4 mm in thickness and when mobile components are present. Atheroma in the ascending aorta and aortic arch is a significant risk factor for cerebral ischemia, independent of high-grade carotid stenosis. Aortic atherosclerotic lesions should particularly be looked for in patients with a history of repeated peripheral and cerebral embolism, in whom no obvious embolic cause is found. A standard protocol for treatment of these potentially embolic aortic lesions has not yet been agreed upon, but the use of antiplatelet drugs or vitamin-K antagonists treatment should be considered.
 ...
PMID:[Cerebrovascular complication caused by aortic atheroma]. 903 39

To clarify the neuropathologic criteria for the diagnosis of vascular dementia principally caused by large-vessel cerebral infarction, we solicited autopsy cases of vascular dementia from 10 university neuropathology laboratories. We included only those cases with progressive dementia clinically diagnosed as Alzheimer's disease (AD) or multi-infarct dementia, in whom autopsy revealed only cerebral infarction, without significant neuropathologic features of AD or other neurodegenerative disorders. Only six cases, all men, met these criteria. Each of them had, for a year or longer, gradually increasing cognitive impairment sufficient to interfere with daily activities, without clear evidence of "stepwise" progression. The age of onset of dementia was 66 years or less in five of the six patients. The duration of dementia ranged from 2 to 14 years. Five of the six cases had a history of either cerebral ischemia or acute stroke with residual focal neurologic deficits. Only two were known to have hypertension. At autopsy severe atherosclerosis of the cerebral arteries was present in three cases; two of these had a thrombotic occlusion of one internal carotid artery and one had partial obstruction of other cerebral arteries. In five of six brains, gross infarctions were present involving the thalamus, caudate, putamen, or large portions of the frontal, parietal, and temporal lobes of one or both hemispheres. Vascular amyloid was absent in all but one of these five brains. In four cases, the dementia was clinically indistinguishable from AD except for a history of focal neurologic deficits. The difficulty encountered in finding large numbers of cases of VaD without coexisting neuropathologic evidence of AD suggests that "pure" vascular dementia is very uncommon.
 ...
PMID:Clinical-neuropathologic findings in multi-infarct dementia: a report of six autopsied cases. 940 94


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>