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1. Dementia in Stroke Survivors

Author

Tatemichi, T. K., Foulkes, M. A., Mohr, J. P., Hewitt, J. R., Hier, D. B., Price, T. R., Wolf, P. A., Hartmann, Alexander, editor, Kuschinsky, Wolfgang, editor, and Hoyer, Siegfried, editor

Published
1991
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2. Royal academy of medicine in Ireland international conference on homocysteine metabolism from basic science to clinical medicine: Proceedings of meeting held at Dromoland Castle, Co. Clare on July 2nd–6th, 1995

Author

Björkegren, K., Bergmark, C., de Faire, U., Mansoor, M. Azam, Svardal, A., Bostom, A. G., Roubenoff, R., Dellaripa, P., Nadeau, M. R., Sutherland, P., Wilson, P. W. F., Jacques, P. F., Selhub, J., Rosenberg, I. H., Bostom, A. G., Brosnan, J. T., Hall, B., Nadeau, M. R., Selhub, J., Bostom, A. G., Shemin, D., Lapane, K. L., Sutherland, P., Nadeau, M. R., Wilson, P. W. F., Selhub, J., Bostom, A. G., Shemin, D., Nadeau, M. R., Selhub, J., Bostom, A. G., Selhub, J., Jacques, P. F., Nadeau, M. R., Williams, R. R., Ellison, R. C., Cuskelly, G. J., McNulty, H., Strain, J. J., McPartlin, J. M., Scott, J. M., Chadefaux-Vekemans, B., Coudé, M., Aupetit, J., Kamoun, P., Coudé, M., Aral, B., Zabot, M. T., Aupetit, J., Kamoun, P., Chadefaux-Vekemans, B., Calaf, R., Ghiringelli, O., Barlatier, A., Charpiot, P., Rolland, P. H., Garçon, D., Charpiot, P., Augier, T., Chareyre, C., Rolland, P. H., Garçon, D., Chango, A., Hodez, F., Tronel, H., Nuel, G., Michel, F., Frémont, S., Méjean, L., Nicolas, J. P., Candito, M., Chambon, P., Gibelin, P., Amsellem, J., Baudouy, M., Morand, P., Candito, M., Chambon, P., Pringuey, D., Aubin-Brunet, V., Beaulieu, F., Darcourt, G., Bedoucha, P., Alchaar, H., Chatel, M., Candito, M., de Valk, H. W., van der Griend, R., Eeden, M. K. G. van, de Groot, E., Duran, M., Smeitink, J. A. M., de Klerk, J. B. C., Wittebol-Post, D., Rolland, M. -O., Haas, F. J. L. M., Meuwissen, O. J. A. Th., Banga, J. D., Poll-The, B. T., de Vries, J. I. P., Dekker, G. A., van Geijn, H. P., Huigens, P. C., Jakobs, C., von Blomberg, B. M. E., Deulofeu, R., Giralt, M., Aibar, C., Bauchet, C., Ballesta, A. M., Varela, G., Vila, N., Chamorro, A., Casals, F. J., Cremades, J. Diaz, Daly, L., Meleady, R., Graham, I., den Heijer, M., Brouwer, I. A., Gerrits, W. B. J., Bos, G. M. J., Blom, H. J., den Heijer, M., Bos, G. M. J., Koster, T., Vandenbroucke, J. P., Blom, H. J., Briët, E., Rosendaal, F. R., Fischer, G., Behrend, C., Bartholmes, P., Fermo, I., Paroni, R., Vigano, S., D’Angelo, A., Fermo, I., Paroni, R., Vigano, S., D’Angelo, A., Franken, D. G., Boers, G. H. J., Blom, H. J., Hamel, B. C. J., Franken, D. G., Boers, G. H. J., Blom, H. J., Ruijs, J. H. J., Franken, D. G., Blom, H. J., Boers, G. H. J., Tangerman, A., Guttormsen, A. B., Ueland, P. M., Refsum, H., Svarstad, E., Gao, W., Goldman, E., Jakubowski, H., Sebastio, G., Sperandeo, M. P., de Franchis, R., Andria, G., Garrow, T. A., Hladovec, J., Sommerova, Z., Písariková, A., Halsted, C. H., Villanueva, J., Chandler, C. J., Stabler, S. P., Allen, R. H., Muskhelishvili, L., James, S. J., Poirer, L., Jacobsen, D. W., Savon, S. R., DiCorleto, P. E., Jourdheuil-Rahmani, D., Rolland, P. H., Garçon, D., Joosten, E., Riezler, R., Allen, R., Joosten, E., Riezler, R., Allen, R., Marquardt, T., Ullrich, K., Harms, E., Koch, H. G., Koch, H. G., Evers, S., Grotemeyer, K. H., Vogelpohl, L., von Eckardstein, A., Ullrich, K., Deufel, T., Kraus, J., Harms, E., Kozich, V., Janosik, M., Sokolová, J., Bukovská, G., Kraus, J. P., Kluitmans, L. A. J., van den Heuvel, L. P., Stevens, E., Trubels, J. M. F., Blom, H. J., Boers, G. H. J., van Oost, B. A., Kraus, J. P., Kittner, S., Macko, R., Hebel, J. R., Rohr, J., Malinow, M. R., Upson, B., Buchholz, D., Earley, C., Johnson, C., Price, T. R., Rosario, J., Sloan, M., Stern, B., Wityk, R., Wozniak, M., Sherwin, R., Stolley, P., Kluijtmans, L., Heuvel, L. van den, Stevens, E., Trijbels, F., Blom, H., Boers, G., van Oost, B., den Heijer, M., Rozen, R., Löhrer, F., Angst, C., Fowler, B., Zaugg, M., Brunner, F., Haefeli, W. E., Nedrebø, B., Ericsson, U. -B., Ueland, P. M., Refsum, H., Lien, E. A., London, J., Paly, E., Paul, V., Paris, D., Kamoun, P., Chassé, J. F., Møller, J., Rasmussen, K., Meleady, R., Graham, I., Daly, L., Verhoef, P., Meleady, R., Graham, I., Daly, L., McMartin, K. E., Phifer, T. J., Alexander, J. S., Middlebrooks, M., Childress, L. E., Nicolas, J. P., Tronel, H., Chango, A., Fremont, S., Felden, F., Guerci, B., Creton, C., Drouin, P., Oakley, G. P., Elias, P. R. P., Hann, A. C., Curtis, C. G., Rose, F. A., Tudball, N., Parrot-Roulaud, F., Cochet, C., Catargi, B., Leprat, F., Latapie, J. -L., Perna, A. F., De Santo, N. G., Ingrosso, D., Galletti, P., Zappia, V., Parrot-Roulaud, F., Sassoust, G., Boissieras, P., Blom, H. J., Majors, A. K., Ehrhart, L. A., Pezacka, E. H., Perry, I. J., Morris, R. W., Ebrahim, S. B., Shaper, A. G., Refsum, H., Ueland, P. M., Pietrzik, K., Dierkes, J., Kroesen, M., Bung, P., Rasmussen, K., Moller, J., Rasmussen, K., Remacha, A., Garcia-Die, F., Cadafalch, J., Barceló, H. J., Parellada, H., Regland, B., Gottfries, C. -G., Andersson, M., Bagby, J., Dyrehag, L. -E., Abrahamsson, L., Ronge, E., Kjellman, B., Frosst, P., Christensen, B., Goyette, P., Rosenblatt, D. S., Genest, J., Rozen, R., Riedel, B., Ueland, P. M., Svardal, A. M., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X. W., Xie, L., Dudman, N., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X. W., Xie, L., Dudman, N., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X., Xie, L., Dudman, N., Smith, B., Kohlman-Trigoboff, D., Simsir, S., Stabler, S. P., Allen, R. H., Strydom, A. J. C., Schlüssel, E., Preibisch, G., Elstner, E. F. E., Pütter, S., Spuijbroek, M. D. E. H., Goddijn-Wessel, T. A. W., Wouters, M. G. A. J., Molen, E. F. v. d., Blom, H. J., Boers, G. H. J., Steegers-Theunissen, R. P. M., Trijbels, J. M. F., Thomas, C. M. G., Eskes, T. K. A. B., Tsai, M. Y., Hanson, N., Key, N., Schwichtenberg, K., Garg, U., Todesco, L., Fowler, B., Pollaert, N., Haefeli, W. E., Thorand, B., Hages, M., Pietrzik, K., Bung, P., Holzgreve, W., Vila, N., Chamorro, A., Deulofeu, R., Aibar, C., Giralt, M., Ballesta, A. M., van der Mooren, M. J., Wouters, M. G. A. J., Schellekens, L. A., Eskes, T. K. A. B., Rolland, R., Blom, H. J., Put, N. v. d., Trijbels, F., Heuvel, L. v. d., Blom, H., Eskes, T., Steegers-Theunissen, R., Mariman, E., Heyer, M. d., Rozen, R., Daher, R., Van Lente, F., Vilkovsky, A. B., Maev, I. V., Richter, E. L., Kirnus, M. D., Varela-Moreiras, G., Alonso-Aperte, E., Rubio, M., Gassó, M., Deulofeu, R., Alvarez, L., Caballeria, J., Rodés, J., Mato, J. M., van Aerts, L. A. G. J. M., Peereboom-Stegeman, J. H. J. Copius, Noordhoek, J., Eskes, T. K. A. B., Molen, E. F. v. d., Spuijbroek, M. D. E. H., Eskes, T. K. A. B., Heuvel, L. P. v. d., Monnens, L. A. H., Blom, H. J., van Guidener, C., Janssen, M. J. F. M., Surachno, J., Stehouwer, C. D. A., van den Berg, M., Bierdrager, E., Rauwerda, J. A., Wilcken, B., Hammond, J., Wouters, M. G. A. J., Hamilton, C. J. C. M., Blom, H. J., Boers, G. H. J., Thomas, C. M. G., Borm, G. F., Eskes, T. K. A. B., Wang, H., Tsai, J. -C., Perrella, M. A., Yoshizumi, M., Sibinga, N. E. S., Haber, E., Chang, T. H. -T., Schlegel, R., Lee, M. -E., Woodside, J., McMaster, D., Yarnell, J., Young, I., Mercer, C., Byrne, K., Evans, A., Gey, F., Gao, X. M., Dougan, G., Wordsworth, P., McMichael, A., Young, P. B., Kennedy, D. G., Molloy, A. M., Scott, J. M., Ward, P., Naughten, E., Cahalane, S., Murphy, D., Mayne, P., Chauveau, P., Chadefaux-Vekemans, B., Coudé, M., Aupetit, J., Kamoun, P., Jungers, P., van Asselt, D. Z. B., Blom, H. J., de Wild, G. M., van Staveren, W. A., Hoefnagels, W. H. L., Naruszewicz, M., Staniewicz, A., Dziewanowski, K., Evrovski, J., Cole, D. E. C., Callaghan, Michael, Lindgren, A., Brattström, L., Hultberg, B., Verhoef, P., Hennekens, C. H., Allen, R. H., Stabler, S. P., Willett, W. C., Stampfer, M. J., Frantzen, F., Sundrehagen, E., Verhoef, P., Kok, F. J., Stampfer, M. J., Willett, W. C., Gaziano, J. M., Hennekens, C. H., Allen, R. H., Stabler, S. P., Reynolds, R. D., Hsu, R. -J., Shane, B., Robinson, K., Kottke-Marchant, K., Green, R., Gupta, A., Jacobsen, D., Robinson, K., Mayer, E., Gupta, A., Miller, D., Marchant, K., Green, R., Jacobsen, D., Greene, R., Chong, Y. -Y., Jacobsen, D., Robinson, K., Gupta, M., Sheppard, C. A., Matthews, R. G., Goyette, P., Frosst, P., Rozen, R., Verhoef, P., Kok, F. J., Kruyssen, H. A. C. M., Witteman, J. C. M., Ueland, P. M., Boushey, C., Beresford, S., Omenn, G., Motulsky, A. G., Nygard, O., Vollset, S. E., Kvale, G., Stensvold, I., Ueland, P. M., Refsum, H., Fiskerstrand, T., Ueland, P. M., Refsum, H., Bugge, K. H., Oshaug, A., Bjønnes, C. H., Refsum, H., Wu, J. T., Wu, L. L., and Wilson, L. W.

Published
1995
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6. Estimating the causal influence of body mass index on risk of Parkinson disease: A Mendelian randomisation study

Author

Noyce, A J, Kia, D A, Hemani, G, Nicolas, A, Price, T R, De Pablo-Fernandez, E, Haycock, P C, Lewis, P A, Foltynie, T, Smith, G D, Schrag, A, Lees, A J, Hardy, J, Singleton, A, Nalls, M A, Pearce, N, Lawlor, D A, and Wood, N W

Abstract

Both positive and negative associations between higher body mass index (BMI) and Parkinson disease (PD) have been reported in observational studies, but it has been difficult to establish causality because of the possibility of residual confounding or reverse causation. To our knowledge, Mendelian randomisation (MR)—the use of genetic instrumental variables (IVs) to explore causal effects—has not previously been used to test the effect of BMI on PD.

Published
2017

7. Establishing the role of rare coding variants in known Parkinson's disease risk loci

Author

Jansen, IE, Gibbs, JR, Nalls, MA, Price, T R, Lubbe, S, van Rooij, J, Uitterlinden, André, Kraaij, Robert, Williams, NM, Brice, A, Hardy, J, Wood, NW, Morris, HR, Gasser, T, Singleton, AB, Heutink, P, Sharma, M, Int Parkinsons Genomics, C, Internal Medicine, Erasmus MC other, Neurology, and Amsterdam Neuroscience - Neurodegeneration

Subjects
0301 basic medicine, Risk, Aging, Datasets as Topic, Muscle Proteins, Genomics, Genome-wide association study, Disease, genetics [Genetic Loci], Biology, genetics [Muscle Proteins], Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Article, Mitochondrial Proteins, 03 medical and health sciences, genetics [Parkinson Disease], Humans, Genetic Predisposition to Disease, ddc:610, genetics [Seminal Plasma Proteins], LRRK2 protein, human, genetics [Genetic Predisposition to Disease], Gene, Exome sequencing, Genetic association, Genetics, SPATA19 protein, human, General Neuroscience, Seminal Plasma Proteins, Genetic Variation, Membrane Proteins, Parkinson Disease, LRRK2, genetics [Genetic Variation], genetics [Membrane Proteins], 030104 developmental biology, Genetic Loci, genetics [Leucine-Rich Repeat Serine-Threonine Protein Kinase-2], genetics [Mitochondrial Proteins], GENX-3414 protein, human, Neurology (clinical), Geriatrics and Gerontology, Developmental Biology, Common disease-common variant, Genome-Wide Association Study
Abstract

Many common genetic factors have been identified to contribute to Parkinson's disease (PD) susceptibility, improving our understanding of the related underlying biological mechanisms. The involvement of rarer variants in these loci has been poorly studied. Using International Parkinson's Disease Genomics Consortium data sets, we performed a comprehensive study to determine the impact of rare variants in 23 previously published genome-wide association studies (GWAS) loci in PD. We applied Prix fixe to select the putative causal genes underneath the GWAS peaks, which was based on underlying functional similarities. The Sequence Kernel Association Test was used to analyze the joint effect of rare, common, or both types of variants on PD susceptibility. All genes were tested simultaneously as a gene set and each gene individually. We observed a moderate association of common variants, confirming the involvement of the known PD risk loci within our genetic data sets. Focusing on rare variants, we identified additional association signals for LRRK2, STBD1, and SPATA19. Our study suggests an involvement of rare variants within several putatively causal genes underneath previously identified PD GWAS peaks.

Published
2017

11. The spectrum of highly ionized praseodymium and dysprosium from the Texas tokamak plasma in the 50–250-Å range.

Author

Finkenthal, M., Lippmann, A. S., Huang, L. K., Yu, T. L., Stratton, B. C., Moos, H. W., Klapisch, M., Mandelbaum, P., Bar Shalom, A., Hodge, W. L., Phillips, P. E., Price, T. R., Porter, J. C., Richards, B., and Rowan, W. L.

Subjects
SPECTRUM analysis, PRASEODYMIUM, DYSPROSIUM, TOKAMAKS
Abstract

Presents an analysis of the spectra of highly ionized praseodymium and dysprosium recorded for the Texas tokamac plasma. Description of the spectra; Identification of the lines of highly ionized praseodymium and dysprosium; Composition of the bands.

Published
1986
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15. NeuroChip, an updated version of the NeuroX genotyping platform to rapidly screen for variants associated with neurological diseases

Author

Blauwendraat, C., Faghri, F., Pihlstrom, L., Geiger, J. T., Elbaz, A., Lesage, S., Corvol, J. -C., May, P., Nicolas, A., Abramzon, Y., Murphy, N. A., Gibbs, J. R., Ryten, M., Ferrari, R., Bras, J., Guerreiro, R., Williams, J., Sims, R., Lubbe, S., Hernandez, D. G., Mok, K. Y., Robak, L., Campbell, R. H., Rogaeva, E., Traynor, B. J., Chia, R., Chung, S. J., Hardy, J. A., Brice, A., Wood, N. W., Houlden, H., Shulman, J. M., Morris, H. R., Gasser, T., Kruger, R., Heutink, P., Sharma, M., Simon-Sanchez, J., Nalls, M. A., Singleton, A. B., Scholz, S. W., Noyce, A. J., Giri, A., Oehmig, A., Tucci, A., Schulte, C., Cookson, M. R., Kia, D., Danjou, F., Charlesworth, G., Plun-Favreau, H., Holmans, P., Jansen, I., Hardy, J., Bras, J. M., Quinn, J., Botia, J. A., Billingsley, K., R'Bibo, L., Lungu, C., Martinez, M., Escott-Price, V., Mencacci, N. E., Topley, Lewis, Denny, P., Rizzu, P., Taba, P., Lovering, R., Ogalla, R. D., Foulger, R., Finkbeiner, S., Sveinbjornsdottir, S., Scholz, S., Koks, S., Foltynie, T., Price, T. R., Sheerin, U. -M., Williams, N., Reed, X., Wang, L., Brockmann, K., Oertel, W., Klein, C., Mohamed, F., Malard, L., Corti, O., Drouet, V., Goldwurm, S., Tesei, S., Canesi, M., Valente, E. M., Petrucci, S., Ginevrino, M., Toft, M., Aasly, J., Henriksen, S. P., Saetehaug, C., Orr-Urtreger, A., Giladi, N., Ferreira, J., Guedes, L. C., Bouca-Machado, R., Coelho, M., Rosa, M. M., Tolosa, E., Fernandez-Santiago, R., Ezquerra, M., Marti, M. J., Glaab, E., Balling, R., and Chung, S. -J.

Subjects
0301 basic medicine, Aging, methods [Genome-Wide Association Study], 0302 clinical medicine, Corticobasal degeneration, neurodegenerative diseases, humans, risk, high-throughput screening assays, education.field_of_study, General Neuroscience, neurodegeneration, genetics [Genetic Variation], 3. Good health, Neurochip, alleles, methods [Genotyping Techniques], Frontotemporal dementia, Risk, Population, methods [High-Throughput Screening Assays], Computational biology, Genetic screening, genotyping, NeuroChip, NeuroX, apolipoproteins E, genetic variation, genome-wide association study, genotyping techniques, Article, Progressive supranuclear palsy, 03 medical and health sciences, Apolipoproteins E, medicine, Humans, Dementia, ddc:610, education, Genotyping, Alleles, business.industry, medicine.disease, 030104 developmental biology, genetics [Neurodegenerative Diseases], genetics [Apolipoproteins E], Neurology (clinical), Geriatrics and Gerontology, business, Neuroscience, 030217 neurology & neurosurgery, Imputation (genetics), Developmental Biology
Abstract

Genetics has proven to be a powerful approach in neurodegenerative diseases research, resulting in the identification of numerous causal and risk variants. Previously, we introduced the NeuroX Illumina genotyping array, a fast and efficient genotyping platform designed for the investigation of genetic variation in neurodegenerative diseases. Here, we present its updated version, named NeuroChip. The NeuroChip is a low-cost, custom-designed array containing a tagging variant backbone of about 306,670 variants complemented with a manually curated custom content comprised of 179,467 variants implicated in diverse neurological diseases, including Alzheimer's disease, Parkinson's disease, Lewy body dementia, amyotrophic lateral sclerosis, frontotemporal dementia, progressive supranuclear palsy, corticobasal degeneration, and multiple system atrophy. The tagging backbone was chosen because of the low cost and good genome-wide resolution; the custom content can be combined with other backbones, like population or drug development arrays. Using the NeuroChip, we can accurately identify rare variants and impute over 5.3 million common SNPs from the latest release of the Haplotype Reference Consortium. In summary, we describe the design and usage of the NeuroChip array and show its capability for detecting rare pathogenic variants in numerous neurodegenerative diseases. The NeuroChip has a more comprehensive and improved content, which makes it a reliable, high-throughput, cost-effective screening tool for genetic research and molecular diagnostics in neurodegenerative diseases.

Published
2017

18. Preparation and Corrosion of Biodegradable Iron Based Porous Materials

Author

Sedlarikova, Marie, Vondrak, Jiri, Kosicek, Adam, Havova, Mariana, Smith, A B, Hill, H B, Meadow, R D, Doe, J B, and, Xu, and Price, T R

Abstract

The research focused on samples of porous iron based materials. They were prepared by filing polyurethane foam with a mixture of iron and other metal powders (Ag, Mg and Si) and by annealing the samples in nitrogen atmosphere. Their fundamental behavior in physiologic solutions, their modifications and in blood plasma was tested. Usually, increasing the proportion of metal additives resulted in increased corrosion rate and in partial passivation. Addition of hydrogen peroxide increased corrosion rate.

Published
2016

41. Intracerebral hemorrhage, cerebral infarction, and subdural hematoma after acute myocardial infarction and thrombolytic therapy in the Thrombolysis in Myocardial Infarction Study. Thrombolysis in Myocardial Infarction, Phase II, pilot and clinical trial.

Author

Gore, J M, primary, Sloan, M, additional, Price, T R, additional, Randall, A M, additional, Bovill, E, additional, Collen, D, additional, Forman, S, additional, Knatterud, G L, additional, Sopko, G, additional, and Terrin, M L, additional

Published
1991
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47. Effect of treating isolated systolic hypertension on the risk of developing various types and subtypes of stroke: the Systolic Hypertension in the Elderly Program (SHEP).

Author

Perry HM Jr., Davis BR, Price TR, Applegate WB, Fields WS, Gurlnik JM, Kuller L, Pressel S, Stamler J, Probstfield JL, Systolic Hypertension in the Elderly Program (SHEP) Cooperative Research Group, Perry, H M Jr, Davis, B R, Price, T R, Applegate, W B, Fields, W S, Guralnik, J M, Kuller, L, Pressel, S, and Stamler, J

Abstract

Context: The Systolic Hypertension in the Elderly Program (SHEP) demonstrated that treating isolated systolic hypertension in older patients decreased incidence of total stroke, but whether all types of stroke were reduced was not evaluated.Objective: To investigate antihypertensive drug treatment effects on incidence of stroke by type and subtype, timing of strokes, case-fatality rates, stroke residual effects, and relationship of attained systolic blood pressure to stroke incidence.Design: The SHEP study, a randomized, double-blind, placebo-controlled trial began March 1, 1985, and had an average follow-up of 4.5 years.Setting and Participants: A total of 4736 men and women aged 60 years or older with isolated systolic hypertension at 16 clinical centers in the United States.Interventions: Patients were randomly assigned to receive treatment with 12.5 mg/d of chlorthalidone (step 1); either 25 mg/d of atenolol or 0.05 mg/d of reserpine (step 2) could be added (n = 2365); or placebo (n = 2371).Main Outcome Measures: Occurrence, type and subtype, and timing of first strokes and stroke fatalities; and change in stroke incidence for participants (whether in active treatment or placebo groups) reaching study-specific systolic blood pressure goal (decrease of at least 20 mm Hg from baseline to below 160 mm Hg) compared with participants not reaching goal.Results: A total of 85 and 132 participants in the active treatment and placebo groups, respectively, had ischemic strokes (adjusted relative risk [RR], 0.63; 95% confidence interval [CI], 0.48-0.82); 9 and 19 had hemorrhagic strokes (adjusted RR, 0.46; 95% CI, 0.21-1.02); and 9 and 8 had strokes of unknown type (adjusted RR, 1.05; 95% CI, 0.40-2. 73), respectively. Four subtypes of ischemic stroke were observed in active treatment and placebo group participants, respectively, as follows: for lacunar, n = 23 and n = 43 (adjusted RR, 0.53; 95% CI, 0.32-0.88); for embolic, n = 9 and n = 16 (adjusted RR, 0.56; 95% CI, 0.25-1.27); for atherosclerotic, n = 13 and n = 13 (adjusted RR, 0. 99; 95% CI, 0.46-2.15); and for unknown subtype, n = 40 and n = 60 (adjusted RR, 0.64; 95% CI, 0.43-0.96). Treatment effect was observed within 1 year for hemorrhagic strokes but was not seen until the second year for ischemic strokes. Stroke incidence significantly decreased in participants attaining study-specific systolic blood pressure goals.Conclusions: In this study, antihypertensive drug treatment reduced the incidence of both hemorrhagic and ischemic (including lacunar) strokes. Reduction in stroke incidence occurred when specific systolic blood pressure goals were attained. JAMA. 2000;284:465-471 [ABSTRACT FROM AUTHOR]

Published
2000
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