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Hyperlipoproteinemia and Cerebral Strokes

Published online by Cambridge University Press:  03 July 2018

Anatole S. Dekaban*
Affiliation:
Developmental and Metabolic Neurology Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland; Department of Neurology, George Washington University Medical School, Washington, D.C.
Jan K. Steusing
Affiliation:
Developmental and Metabolic Neurology Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland; Department of Neurology, George Washington University Medical School, Washington, D.C.
Harold Stevens*
Affiliation:
Developmental and Metabolic Neurology Branch, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland; Department of Neurology, George Washington University Medical School, Washington, D.C.
*
Dept. of Health, Education and Welfare, Public Health Services National Institutes of Health; Bldg. 10, Room 4N-248; Bethesda Maryland 20014. U.S.A.
Dept. of Health, Education and Welfare, Public Health Services National Institutes of Health; Bldg. 10, Room 4N-248; Bethesda Maryland 20014. U.S.A.
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Abstract

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Determination of lipoprotein patterns and of major plasma lipids was carried out in 171 patients with strokes. Of these, 22 had hyperlipoproteinemia (HLIPR) by paper electrophoresis and by elevation of principal plasma lipids (either cholesterol over 300 mg/100 ml or triglycerides over 200 mg/100 ml or both these components). More than two-thirds of the patients had at least one close relative with elevated blood lipids. Using criteria of the World Health Organization, these patients were classified as follows: 5 had HLIPR type IIa, 8 had HLIPR type IIb, 3 had HLIPR type III and 6 had HLIPR type IV. Phospholipids showed relatively little change from the values of normal controls. The numerical distribution of patients with stroke and HLIPR into the four different types corresponds quite well with the approximate frequency of these types of HLIPR in the general population. Thus, this study does not indicate that the patients with a particular type of HLIPR are at a greater risk to have a stroke than those belonging to other types.

Résumé

Résumé

La détermination des types lipoprotéiniques et des lipides plasmatiques principaux est rapportée chez 171 patients avec accident cérébrovasculaire (ACV). Des deux-ci, 22 souffraient d’hyperlipoprotéinémie (HLIPR) tel que jugé par électrophorèse et par élévation des principaux lipides plasmatiques (soit le cholestérol audessus de 300 mg/100 ml ou les triglycérides au-dessus de 200 mg/ml, ou les deux). Plus des deux tiers des patients avaient au moins un proche parent avec une élévation des lipides sanguins. Utilisant les critères de l’Organisation Mondiale de la Santé, ces patients étaient classés comme suit: 5 avaient HLIPR de type IIa, 8 avaient HLIPR de type IIb, 3 avaient HLIPR de type III et 6 avaient HLIPR de type IV. Les phospholipides montraient relativement peu de changements par rapport aux valeurs chez des contrôles normaux. La distribution numérique de patients avec ACV et HLIPR dans les quatre différents groupes correspond très bien avec la fréquence approximative de ces types de HLIPR dans la population en général. Donc, cette étude n’indique pas que les patients avec un type particulier de HLIPR sont plus susceptibles d’avoir un ACV que ceux appartenant aux autres types.

Type
Research Article
Copyright
Copyright © Canadian Neurological Sciences Federation 1977

References

Ballantyne, D., Grossart, K. W. G., Ballantyne, J. P., Young, A. and Lawrie, T.D.: (1974) Relationship of plasma lipids and lipoprotein concentration to cerebral atherosclerosis and electroencephalographic findings. J. Neurol. Sci. 23: 323329.Google Scholar
Bansal, B. C. Gupta, R. R. and Bansal, M. R.: (1975) Serum lipids and uric acid relationship in ischemie thrombotic cerebrovascular disease. Stroke 6: 304397 Google Scholar
Brown, D. F.: (1969) Blood lipids and lipoproteins in atherogenesis. Am. J. Med. 46: 691704.Google Scholar
Brown, M. S. and Goldstein, J. L.: (1975) Familial hypercholesterolemia: genetic, biochemical and pathophysiological considerations. Adv Int. Med. 20: 273296.Google Scholar
Cornfield, J.: (1962) Joint dependence of risk of coronary heart disease on serum cholesterol and systolic blood pressure: A discriminant function and analysis. Fed. Proc. 21, Part II: 5861.Google Scholar
de Gennes, J. L., Rouffy, J. and Chain, F.: (1968) Complications vasculaires cerébrales des xanthomatoses tendineuses hypercholestérolémiques familiales. Bull. Soc. Med. Hop. Paris 119: 569586.Google Scholar
Dryer, R. L., Tammes, A. R. and Routh, J. I.: (1957) The determination of phosphorous and phosphatase with N-phenyl-p-phenylenediamine. J. Biolog. Chem. 225: 177183.Google Scholar
Fredrickson, D. S. and Levy, R. I.: (1972) Familial hyperlipoproteinemia. In: The Metabolic Basis of Inherited Disease. (ed.) Stanbury, J. B., McGraw-Hill, New York p 545614.Google Scholar
Garland, P. E. and Randle, P. J.: (1962) A rapid enzymatic assay for glycerol. Nature 196: 987988.CrossRefGoogle ScholarPubMed
Gertler, M. M., Leetma, H. E., Koutrouby, J. and Johnson, E. D.: (1975) The assessment of insulin, glucose and lipids in ischemie thrombotic cerebrovascular disease. Stroke 6: 7784.CrossRefGoogle Scholar
Gordon, T., Sorlie, P. and Kannel, W. B.: (1971) The Framingham Study. An epidemiological investigation of cardiovascular disease. Section 27 Coronary heart disease atherothrombotic brain infarction, intermittent claudication. A multi variant analysis of some factors related to their incidence. Framingham Study, 16-year follow-up. U.S. Dept. of Health, Education and Welfare.Google Scholar
Gordon, T. and Kannel, W. B.: (1972) Predispostion to atherosclerosis in the head, heart and legs. The Framingham Study J.A.M.A. 221: 661666.Google Scholar
Lees, R. S. and Hatch, F. T.: (1963) Sharper separation of lipoprotein species by paper electrophoresis in albumin containing buffer J. Lab. and Clin. Med. 61: 518528.Google Scholar
Mathews, N. T., Davis, D., Meyer, J. S. and Chandar, K. (1975). Hyperlipoproteinemia in occlusive cerebrovascular disease. J.A.M.A. 232: 262266.Google Scholar
Pinter, J. K., Hayaski, J. A. and Watson, J. A.: (1967) Enzymatic assay of glycerol, dihydroxyacetone and glyceraldehyde. Arch. Biochem. Biophys. 121: 404414.Google Scholar
Roberts, W. C. Ferrans, V. J., Levy, R. I. and Fredrickson, D. S.: (1973). Cardiovascular pathology in hyperlipoproteinemia. Anatomic observations in 42 necropsy patients with normal or abnormal serum lipoprotein patterns. Am. J. Cardiol. 31: 557570.Google Scholar
Rosenthal, H. L., Pfluke, M. L. and Buscaglia, S.: (1957) A stable iron reagent for determination of cholesterol. J. Lab. and Clin. Med. 50: 318322.Google Scholar
Skipski, V. P., Peterson, R. F. and Barkley, M.: (1964) Quantitative analysis of phospholipids by thin layer of chromatography Boichem. J. 90: 374378.Google Scholar
Walsh, P. N., Pareti, F. I. and Corbett, J. J.: Platelet coagulant activities and serum lipids in transient cerebral ischemia. New Engl. J. Med. 295: 854858, October 1976.Google Scholar
World Health Organization Memorandum: (1972) Classification of hyperlipidemias and hyperlipoproteinemias. Circulation 45: 501508.Google Scholar
Zak, B., Dickeman, R. C. White, E. G., Burnett, H. and Charney, P. J.: (1954) Rapid determination of free and total cholesterol. Am. J. Clin. Path. 24: 13071315.Google Scholar