The isoprenoid pathway in lone atrial fibrillation with embolic stroke.

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dc.contributor.authorRavikumar, Aen_US
dc.contributor.authorKurup, P Aen_US
dc.date.accessioned2001-03-29en_US
dc.date.accessioned2009-05-27T04:17:23Z
dc.date.available2001-03-29en_US
dc.date.available2009-05-27T04:17:23Z
dc.date.issued2001-03-29en_US
dc.description.abstractBACKGROUND: The isoprenoid pathway was assessed and compared in patients of lone atrial fibrillation with embolic stroke as well as in patients with right hemispheric, left hemispheric and bihemispheric dominance to determine the role of hemispheric dominance in its pathogenesis. METHODS AND RESULTS: The activities of hydroxyl methyl glutaryl-CoA reductase and RBC sodium-potasium ATPase as well as serum levels of plasma magnesium, digoxin, dolichol and ubiquinone were measured. The tyrosine/tryptophan catabolic patterns, glycoconjugate metabolism, free radical metabolism and RBC membrane composition were also assessed. In patients with lone atrial fibrillation with embolic stroke, there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels, and low ubiquinone and elevated free radical levels. There was also an increase in tryptophan catabolites and a reduction in tyrosine catabolites: and an increase in the cholesterol: phospholipid ratio with a reduction in the glycoconjugate levels of the RBC membrane. The same biochemical patterns were obtained in individuals with right hemispheric dominance whereas the patterns were reversed in patients with left hemispheric dominance. CONCLUSIONS: Lone atrial fibrillation with embolic stroke is associated with an upregulated isoprenoid pathway and elevated digoxin secretion from the hypothalamus. This occurs in right hemisphere-dominant individuals.en_US
dc.description.affiliationDepartment of Medicine, Medical College Hospital, University of Kerala, Trivandrum.en_US
dc.identifier.citationRavikumar A, Kurup PA. The isoprenoid pathway in lone atrial fibrillation with embolic stroke. Indian Heart Journal. 2001 Mar-Apr; 53(2): 184-8en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/2816
dc.language.isoengen_US
dc.source.urihttps://indianheartjournal.comen_US
dc.subject.meshAgeden_US
dc.subject.meshAtrial Fibrillation --complicationsen_US
dc.subject.meshDigoxin --metabolismen_US
dc.subject.meshDolichol --metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshFunctional Lateralityen_US
dc.subject.meshHumansen_US
dc.subject.meshIntracranial Embolism --complicationsen_US
dc.subject.meshMagnesium --metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPolyisoprenyl Phosphate Monosaccharides --metabolismen_US
dc.subject.meshPrognosisen_US
dc.subject.meshSensitivity and Specificityen_US
dc.subject.meshSodium-Potassium-Exchanging ATPase --metabolismen_US
dc.subject.meshUbiquinone --metabolismen_US
dc.titleThe isoprenoid pathway in lone atrial fibrillation with embolic stroke.en_US
dc.typeClinical Trialen_US
dc.typeComparative Studyen_US
dc.typeControlled Clinical Trialen_US
dc.typeJournal Articleen_US
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