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

Although anticardiolipin antibody (aCL) has been suggested to be a potent risk factor for thrombosis and atherosclerosis in multiple arterial beds, conflicting results still exist between aCL and cerebral ischemia in the general stroke population. To elucidate if this discrepancy relates to the heterogeneity of underlying etiologies, blood beta(2)-glycoprotein I dependent-aCL was evaluated in 432 Taiwanese adults associated with cerebral ischemia who were classified into five subtypes according to their causes of cerebral ischemia. The results were compared with those in 100 healthy controls. A definite increase of aCL-IgG isotype was found in 41 patients (9.35%) and four controls (4.0%). The relative risk was 2.52. The frequency of increased aCL-IgG was 12.2%, 12.8%, 8.8%, 3.9%, and 3.5% in patients with large-artery atherosclerotic disease, stroke of unknown etiology, small-artery occlusive disease, cardioembolism, and stroke of other known etiology, respectively. Only patient with large-artery atherosclerotic disease (p<0.025) and stroke of unknown etiology (p<0.05) had a higher frequency of increased aCL than control. The frequencies of abnormal result of activated partial thromboplastin time, antinuclear factor, Coombs' test, and venereal disease research laboratory were 2.84%, 1.22%, 1.02%, and 1.34% in these 41 patients, respectively. Accordingly, aCL-IgG selectively increases in patients with large-artery atherosclerosis and stroke of unknown etiology, reflecting selective activation of humoral immunity for aCL in the pathogenesis of cerebral ischemia.
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PMID:The increase of blood anticardiolipin antibody depends on the underlying etiology in cerebral ischemia. 1582 27

There is growing evidence that Rho-kinases (ROCKs), the immediate downstream targets of the small guanosine triphosphate-binding protein Rho, may contribute to cardiovascular disease. ROCKs play a central role in diverse cellular functions such as smooth muscle contraction, stress fiber formation and cell migration and proliferation. Overactivity of ROCKs is observed in cerebral ischemia, coronary vasospasm, hypertension, vascular inflammation, arteriosclerosis and atherosclerosis. ROCKs, therefore, may be an important and still relatively unexplored therapeutic target in cardiovascular disease. Recent experimental and clinical studies using ROCK inhibitors such as Y-27632 and fasudil have revealed a critical role of ROCKs in embryonic development, inflammation and oncogenesis. This review will focus on the potential role of ROCKs in cellular functions and discuss the prospects of ROCK inhibitors as emerging therapy for cardiovascular diseases.
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PMID:ROCKs as therapeutic targets in cardiovascular diseases. 1588 72

According to the focal nature of atherosclerosis, ischemic stroke is frequently unilateral. Atherosclerotic plaques are favoured by local hemodynamic factors as low wall shear stress and/or elevated circumferential wall tension. Aim of the present study was to investigate the possible association between hemodynamic forces and cerebrovascular disease. Common carotid mean wall shear stress and circumferential wall tension, Peterson's elastic modulus, and blood flow were measured in 25 patients with a recent unilateral large-artery stroke presenting non-stenotic plaques of the carotid arteries (large-artery group), and in 10 patients affected by a recent unilateral cardioembolic stroke without carotid plaques (cardioembolic group). In the large-artery group, atherosclerosis was slightly more evident in the side of cerebral ischemia. All hemodynamic factors were more unfavourable at the affected side in this group (shear stress: 6.2+/-3.0 versus 8.6+/-4.0 dynes/cm2, p<0.0001; wall tension: (7.3+/-1.3)x10(4) versus (6.6+/-1.3)x10(4) dynes/cm, p<0.00001; Peterson's modulus: (16.8+/-11.9)x10(5) versus (12.4+/-5.7)x10(5) dynes/cm2, p=0.06). No difference was detectable in blood flow and in cardioembolic group. The present data demonstrate an unfavourable hemodynamic profile in the common carotid artery supplying the area of a single large-artery stroke and might help to explain the frequent one-sidedness of this disease.
Atherosclerosis 2006 Mar
PMID:Wall shear stress is lower in the carotid artery responsible for a unilateral ischemic stroke. 1600 10

Carotid artery stenosis is generally thought to induce stroke by either compromising cerebral perfusion or inciting embolic phenomena. Carotid baroreceptors and chemoreceptors are vital adaptations for cerebrovascular autoregulation that can behave mal-adaptively in the setting of modern diseases such as atherosclerosis. We hypothesize that acute cerebrovascular events may be partially attributable to autonomic dysfunction and cerebrovascular autoregulatory failure secondary to carotid sensor maladaptations. Specifically, we propose that atherosclerotic disease at the carotid bifurcation can interfere with baroreceptor and chemoreceptor function by buffering against accurate detection of physical and chemical parameters. Misperceptions of hypoxia and hypotension can trigger sympathetic bias and autonomic dysfunction which perturb cerebrovascular autoregulation and vasomotor tone, thereby compromising cerebral perfusion. The preferential association of strokes with morning arousal, stress, acute physical activity, winter months, illness, and older age may relate to this phenomenon. Sympathetic bias promotes inflammation and coagulation, a link likely forged during prehistoric evolution when trauma represented a more significant factor in natural selection. In the setting of carotid sensor dysfunction, the resulting inflammation and coagulation can promote acute cardiovascular events. The ensuing cerebral ischemia can induce further derangement of cerebrovascular autoregulation and upregulate adrenergia, inflammation, and coagulation in a feed-forward manner. Inflammation and coagulation can also exacerbate carotid sensor dysfunction by iteratively worsening atherosclerosis. Angioplasty, stenting, and endarterectomy may inadvertently cause acute and chronic carotid sensor dysfunction through manipulation, material interposition, and balloon-induced baroreceptor injury. Acute strokes during these procedures may result from carotid sensor dysfunction rather than embolization. Carotid body and sinus electro-modulation and non-balloon atherectomy represent new methods to prevent or treat cerebrovascular events. Pharmacologic modulation of autonomic balance, such as adrenergic blockade, long presumed contraindicated due to risk of cerebral hypoperfusion, may counter-intuitively offer benefit during acute strokes. Novel diagnostic paradigms may include functional analysis of carotid sensors as well as measurement of the anatomic thickness of calcified and non-calcified plaque near the carotid body. Carotid sensor dysfunction may be a source of systemic sympathetic bias and autonomic dysfunction observed during aging and, by association, many of the ailments associated with senescence. Modulation of carotid sensors may yield pervasive health benefits beyond those found by treating cerebrovascular disease.
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PMID:The link between carotid artery disease and ischemic stroke may be partially attributable to autonomic dysfunction and failure of cerebrovascular autoregulation triggered by Darwinian maladaptation of the carotid baroreceptors and chemoreceptors. 1627 32

Although anticardiolipin antibody (aCL) has been suggested to be a potent risk factor for thrombosis and atherosclerosis in multiple arterial beds, conflicting results exist between aCL and cerebral ischemia in the general stroke population. To elucidate if this discrepancy relates to the heterogeneity of underlying etiologies, the blood beta(2)-glycoprotein I dependent-aCL in 432 Taiwanese adults was examined. The associated cerebral ischemia in these patients was classified into five subtypes according to the cause of cerebral ischemia. The results were compared with those in 100 healthy controls. A definite increase of aCL-IgG isotype was found in 41 patients (9.35%) and four controls (4.0%). The relative risk was 2.52. The frequency of increased aCL-IgG was 12.2%, 12.8%, 8.8%, 3.9%, and 3.5% in patients with large-artery atherosclerotic disease, stroke of unknown etiology, small-artery occlusive disease, cardioembolism, and stroke of other known etiology, respectively. Only patients with large-artery atherosclerotic disease (p<0.025) and stroke of unknown etiology (p<0.05) had higher frequencies of increased aCL than those in control subjects. The frequencies of abnormal results of activated partial thromboplastin time, antinuclear factor, Coombs' test, and venereal disease research laboratory were 2.84%, 1.22%, 1.02%, and 1.34% in these 41 patients, respectively. Accordingly, aCL-IgG selectively increases in patients with large-artery atherosclerosis and stroke of unknown etiology, reflecting selective activation of humoral immunity for aCL in the pathogenesis of cerebral ischemia.
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PMID:The increase of blood anticardiolipin antibody depends on the underlying etiology in cerebral ischemia. 1644 37

Diabetes mellitus is accompanied by several cardiovascular complications including atherosclerosis, cerebral ischaemia and stroke. We examined the neuroprotective effect of a 1,4-dihydropyridine derivative cerebrocrast (C, a new antidiabetic agent, synthesized in the Latvian Institute of Organic Synthesis) on the level of ATP in the brain, and on changes of the EEG and ECG, as well as blood pressure parameters in anaesthetized Wistar male rats before and during 10-min occlusion of both common carotid arteries. Cerebrocrast was administered i.v. at doses of 1.0 and 10 microg/kg in the v. femoralis 20 min prior to ischaemia. After 10-min ischaemia animals were decapitated and the brain was immediately frozen in liquid nitrogen and subsequently used for analysis of changes of ATP contention. Cerebrocrast, administered at doses of 1.0 and 10 microg/kg 20 min prior to occlusion of both common carotid arteries, completely prevented a fall in the ATP content of brain compared with the control rats. In control rats the content of ATP in brain during ischaemia decreased from 2.77 +/- 0.22 (basal level) to 1.74 +/- 0.20 micromol/g as a result of ischaemia. By administration of cerebrocrast 20 min before occlusion of the arteries, the content of ATP in the brain remained at the level of preischaemia (1.0 microg/kg C + ischaemia 2.82 +/- 0.36; 10 microg/kg C + ischaemia 2.42 +/- 0.22 micromol/g). Analysis of EEG parameters both before and during 10 min of occlusion showed that at a C dose of 1.0 microg/kg before occlusion produced a regular alpha rhythm during ischaemia and prevented cerebral bioelectric activity from significant changes. The depression of basal rhythm was observed at a C dose of 10 microg/kg during ischaemia in two rats out of six as well as an increase in the ECG ST segment above the isoelectric line. Blood pressure was decreased by about 10-20 mm Hg. We propose that pretreatment of rats with cerebrocrast at doses of 1.0 or 10 microg/kg 20 min prior to ischaemia can prevent ischaemic damage of rat brain, maintain necessary energy consumption, promote ATP production in brain cells, and prevent significant changes in EEG and ECG parameters. These properties are important in diabetes mellitus and its evoked cardiovascular complications as stroke, ischaemia, etc.
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PMID:Protective effect of cerebrocrast on rat brain ischaemia induced by occlusion of both common carotid arteries. 1644 67

The results of surgical bypass and endarterectomy in Takayasu's arteritis (TA) were reported to be poor compared to usual atherosclerosis patients. However, if ischemic symptoms due to occlusive disease were severe, surgical procedures were inevitable. We report surgical experience of 5 patients with TA. Five women (ranged from 26 to 58 yr) were operated between June 1998 and May 2004. Three patients showed occlusion of main branches of aortic arch and had symptoms of cerebral ischemia. One patient showed near total occlusion in the midabdominal aorta and had symptoms of orthopnea and uncontrolled hypertension. One patient showed total occlusion of abdominal aorta at the level of aortic bifurcation and had a symptom of severe claudication on both legs. Bypasses from the ascending aorta to the carotid artery were performed in 3 cases. Bypass from the thoracic aorta to the left common iliac artery was performed in one case and endarterectomy of abdominal aorta in one case. The ischemic symptoms related with arterial occlusion were resolved after surgery. And the symptoms of cardiac failure disappeared. The symptomatic TA frequently required arterial reconstruction. The symptomatic improvement and excellent mid-term patency could be expected after arterial reconstruction and endarterectomy.
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PMID:Surgical management of Takayasu's arteritis. 1647 59

The nomenclature of the American College of Rheumatology leads to misunderstandings in multidisciplinary discussions on patients with systemic lupus erythematosus (SLE) who also have neurological or psychiatric symptoms. These proposed neuropsychiatric syndromes are rarely syndromes and the symptoms are rarely neuropsychiatric. It is better first of all to determine whether the SLE patients have neurological or psychiatric symptoms, and if these symptoms are present, the first question is what is the cause. Vasculitis of the cerebral blood vessels should be considered as a possible explanation only if ischaemic lesions in the brain have been demonstrated, other causes of cerebral ischaemia in SLE are unlikely, and the clinical signs are consistent with cerebral vasculitis. These other causes of cerebral ischaemia include: antiphospholipid antibodies, atherosclerosis, heart valve disorders and thrombotic thrombocytopenic purpura.
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PMID:[Neurological or psychiatric symptoms in patients with systemic lupus erythematosus (SLE): terminological problems, pathogenesis, diagnosis and therapy]. 1652 4

Resveratrol is a natural phytoestrogen and possesses many biological functions such as anti-inflammatory activity and protection against atherosclerosis and myocardial infraction. The present study was carried out to elucidate the neuroprotective effect and possible mechanism of resveratrol on cerebral ischemia-induced hippocampus neuron loss. Sixty adult male rats underwent general anesthesia (urethane, 1.4 g/kg, i.p.) and were divided into three groups: sham operation, ischemia treatment, and ischemia combined with resveratrol administration (20 mg/kg, i.v.). The carotid artery was bilaterally ligated to induce cerebral ischemia. Microdialysis and high-performance liquid chromatography were used to analyze dihydroxybenzoic acid (DHBA) that reflected the hippocampal hydroxyl radical level. Hippocampal nitric oxide was assayed among different groups. During cerebral ischemia, the hydroxyl radical levels were elevated in rats and animals displayed severe neuronal loss. A single dose of resveratrol significantly increased the nitric oxide level and decreased the hydroxyl radical level. The reduction of cerebral blood flow and neuronal loss were also attenuated by resveratrol treatment. The results demonstrated that a single infusion of resveratrol could elicit neuroprotective effects on cerebral ischemia-induced neuron damage through free radical scavenging and cerebral blood elevation due to NO release.
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PMID:Neuroprotective effects of resveratrol on cerebral ischemia-induced neuron loss mediated by free radical scavenging and cerebral blood flow elevation. 1660 41

Estrogens have proven vasoprotective properties against atherosclerosis that depend on the direct effect on vascular smooth muscle and endothelium and on systemic actions that imply serum lipids, coagulation and fibrinolytic cascades, vasoactive proteins and antioxidant systems. They also have neuroprotective effects against cerebral ischemia that include antioxidant and anti-inflammatory effects, modulation of protein synthesis, inhibition of apoptosis and trophic effects and preservation of microvascular blood flow in the ischemic area. Estrogenic actions depend on activation of specific estrogen receptors that modulate gene expression and produce long-term effects on vascular endothelial and smooth muscle cells, neurons and glia, on interaction with plasma membrane sites that produce rapid non-genomic actions and also on receptor-independent mechanisms. This paper reviews what it is known about the mechanisms underlying the vaso- and neuroprotective effects of estrogens. Experimental and clinical evidences of such protective effects are also discussed. Therapeutical implications for stroke prevention and treatment derived from the available evidence are considered.
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PMID:Estrogens as neuroprotectants against ischemic stroke. 1665 14


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