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)

Study of the blood platelet functional activity and intensity of hemolysis in 41 patients with transient disorders of cerebral circulation and comparison of the results with the corresponding indices in healthy individuals, in 40 patients with hypertensive disease free of crisis, and in 25 patients with cerebral atherosclerosis led to the conclusion that the character of cerebral stroke is already determined in the pre-stroke period. It depends on the functional state of the blood platelets in many respects. In patients with hypertensive disease in a period clear of crisis, for instance, there is a tendency towards hypoaggregation possible associated with the presence of latent hemolysis. Platelet hypofunction progresses in the period of hypertensive encephalopathy and still more during its transformation into hemorrhagic stroke. On the contrary, in patients with atherosclerosis but no symptoms of cerebral ischemia the adhesion-aggregation activity of the platelets does not differ essentially from that in healthy individuals. With the development of signs of ischemia of the brain, the platelet activity grows considerably, particularly when transient cerebral circulatory disorders transform into ischemic stroke.
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PMID:[Importance of the thrombocytes and hemolytic syndrome in the pathogenesis of transient cerebral circulatory disorders in hypertension patients]. 63 13

Postmortem surveys on patients treated for chronic hypertension often fail to demonstrate significant vessel changes. Nevertheless, hypertensive alterations in the brain can include infarcts and hemorrhages. Autopsies in a primary care hospital have shown that hypertension can affect arteries, arterioles, and capillaries in various patterns and degrees in the brain. These vascular lesions may be associated with large and small infarcts and hemorrhages in isolated or diffuse patterns. Widespread cerebral edema can occur with rapidly progressive hypertension. Atherosclerosis, arterial and arteriolar fibrinoid necrosis, and micro-aneurysms may be observed. Chronic hypertensive encephalopathy causes vascular dementia and can be associated with subcortical arterial and arteriolar leukoencephalopathy, leukoaraiosis and/or Binswanger's disease. Epidemiologic evaluations based on complete autopsy studies need to be correlated with compliance of therapy, appropriate diagnosis of hypertension, and its long-term effects on the nervous system. Although persistent poorly controlled hypertension is known to damage the brain both acutely and chronically, the effects of intermittent hypertension remain to be defined.
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PMID:Hypertension and vascular dementia. 173 72

Nicardipine is a second generation dihydropyridine-type Ca2+ antagonist with high vascular selectivity and strong cerebral and coronary vasodilatory activity. The compound is used in the treatment of hypertension, primarily in the elderly. In this review the main evidence of the cerebrovascular activity of nicardipine in preclinical studies using in vitro and in vivo models is detailed. A particular physico-chemical property of nicardipine is the almost complete protonation in acid environment. This allows its accumulation in ischemic brain regions and makes it a candidate for the treatment of cerebrovascular disorders characterised by impaired brain perfusion. The main clinical data on the use of nicardipine in cerebral ischemia and related disorders, subarachnoid haemorrhage and stroke, are also reviewed. These studies included 5940 patients affected by chronic cerebrovascular insufficiency (cerebral ischemia, cerebral atherosclerosis mainly associated with hypertension, transient ischemic attacks, sequelae of cerebral infarction, thrombosis or embolia, hypertensive encephalopathy), 1540 patients affected by sequelae of subarachnoid haemorrhage and 206 patients affected by stroke. Both preclinical studies and clinical trials have shown that nicardipine is a safe Ca2+ antagonist with powerful cerebrovascular activity. This suggests its possible use in cerebrovascular disorders in which blockade of Ca2+ channels of the L-type and/or selective cerebral vasodilatation is desirable. Further studies are necessary to establish if modulation of neuronal Ca2+ channels of the L-type by nicardipine may have a neuroprotective effect independent by the cerebrovascular activity of the compound.
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PMID:Nicardipine and treatment of cerebrovascular diseases with particular reference to hypertension-related disorders. 765 45

Hypertensive encephalopathy is a syndrome consisting of headache, seizures, visual changes, and other neurologic disturbances in patients with elevated systemic blood pressure. Diagnosis based on clinical and radiological findings, which are not specific, may be difficult to establish. Furthermore, hypertensive encephalopathy may develop gradually even when blood pressure is lower than that of malignant hypertension. We present clinical, magnetic resonance imaging (MRI) and autopsy findings in a 43-year-old schizophrenic patient with unrecognised hypertensive encephalopathy, which was misinterpreted by MRI as a diffusely growing brain stem tumour. Increased blood pressure was recorded several times, but it was not properly controlled and treated either during his out-door psychiatric examinations or hospitalisation. At autopsy, generalised atherosclerosis, concentric hypertrophy of the left ventricle and arteriolonephrosclerosis were found in addition to microvascular fibrinoid necroses and thromboses in the brain and kidneys, which were almost certainly caused by arterial hypertension evolving from benign into malignant stage. We discuss the differential diagnosis and give a review of the literature.
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PMID:Hypertensive encephalopathy mimicking brainstem tumour in psychiatric patient. 1511 44

Neurological complications whether due to the uremic state or its treatment, contribute largely to the morbidity and mortality in patients with renal failure. Despite continuous therapeutic advances, many neurological complications of uremia, like uremic encephalopathy, atherosclerosis, neuropathy and myopathy fail to fully respond to dialysis. Moreover, dialytic therapy or kidney transplantation may even induce neurological complications. Dialysis can directly or indirectly be associated with dialysis dementia, dysequilibrium syndrome, aggravation of atherosclerosis, cerebrovascular accidents due to ultrafiltration-related arterial hypotension, hypertensive encephalopathy, Wernicke's encephalopathy, hemorrhagic stroke, subdural hematoma, osmotic myelinolysis, opportunistic infections, intracranial hypertension and mononeuropathy. Renal transplantation itself can give rise to acute femoral neuropathy, rejection encephalopathy and neuropathy in graft versus host disease. The use of immunosuppressive drugs after renal transplantation can cause encephalopathy, movement disorders, opportunistic infections, neoplasms, myopathy and progression of atherosclerosis. We address the clinical, pathophysiological and therapeutical aspects of both central and peripheral nervous system complications in uremia.
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PMID:Neurological complications in renal failure: a review. 1556 46