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2. Computation of a cardiac severity score with left-censored biomarkers for patients with heart failure

Author

Vasudevan A, Munkres AG, Bottiglieri T, Won JI, Garg P, and McCullough PA

Subjects
cardiac biomarkers, left-censored, limit of detection, therapeutic index, myocardial injury summary score, Pathology, RB1-214
Abstract

Anupama Vasudevan,1,2 Alyssa G Munkres,3 Teodoro Bottiglieri,1,4 Jane I Won,1,2 Puja Garg,1,2 Peter A McCullough 1–3,5,6 1Baylor Research Institute, 2Baylor Heart and Vascular Institute, 3Texas A&M Health Science Center, College of Medicine, 4The Institute of Metabolic Disease, 5Baylor University Medical Center, Dallas, 6The Heart Hospital Baylor, Plano, TX, USA Introduction: Biomarkers reported as being less than the limit of detection (LOD) are challenging to be included in analyses without being dichotomized. Substitutions by the LOD, LOD/2, LOD/√2, or zero have been attempted for left-censored values. We calculated a novel Modified Myocardial Injury Summary Score (MMISS) by incorporating four biomarkers (B-type natriuretic peptide, troponin, galectin-3, and suppression of tumorigenicity 2) to efficiently stratify heart failure (HF) patients. The objective of this study is to evaluate the differences in associations between MMISS, calculated by different methods of substitution, and therapeutic intensity index (TII), a composite pharmacologic score. Methods and results: This is a cross-sectional study including 39 HF patients aged ≥18 years who were treated in the Baylor Health Care System. MMISS was calculated with the left-censored biomarkers substituted by zero, LOD, LOD/2, and LOD/√2. Patients with biomarker values more than LOD (complete cases) were also considered separately. The computed TII was regressed separately on MMISS for each substitution method, while controlling for age and gender. All substitution methods yielded negative associations; however, statistical significance for the association was not achieved using substitution by zero or when considering only the complete cases. The association was quite comparable with the substitution of left-censored values by LOD, LOD/2, and LOD/√2. Conclusion: Substantial loss of information is inevitable if only the data with values above the LOD are considered for analysis or when the left-censored values are substituted with zero. Keywords: cardiac biomarkers, left-censored, limit of detection, therapeutic index, myocardial injury summary score

Published
2017

12. Abstracts from the sixth meeting of the international association of pancreatology, November 2–4, 1994, Chicago, IL

Author

Burdick, Michael, Hollingsworth, Tony, Gansauge, S., Gansauge, F., Link, K. H., Schoenberg, M. H., Poch, B., Beger, H. G., Wagner, A. C. C., Steffen, H., Göke, B., Gaisano, H. Y., Sheu, L., Foskett, J. K., Trimble, W. S., Lee, Y. L., Kwon, H. Y., Park, H. S., Lee, S. M., Park, H. J., aguchi, S., Green, G. M., Mitamura, K., Komatsu, Y., Arai, I., Yamaura, H., Wang, OJ, Adrian, TE, Teyssen, S., Niebel, W., Niebergall, E., Singer, M. V., Umehara, K, Ohara, T, Kataoka, K, Okamura, H, Kato, M, Sakagami, J, Ohta, A, Murase, M, Hosoda, M, Yamane, Y, Kashima, K, Ibata, Y, Balthazar, Emil J., Banks, P. A., Garzof, S. G., Langevin, R. E., Silverman, S. G., Sica, G. T., Bassi, C., Benini, A., Muner, A., Falconi, M., Abbas, H., Pederzoli, P., Salvia, R., Minelli, E. Bertazzoni, Shaskar, S. Shanmuga, Shearer, M. G., Imrie, C. W., Brodmerkel, G. J., Reed, P. A., Carr-Locke, DL, Musa, A, Lichtenstein, DR, Dam, J Van, Banks, PA, Eisele, S., Schoenberg, M. H., Böchjer, M., Beger, H. G., Foitzik, Th., Fern’andez-del Castillo, C., Rattner, D. W., Ferraro, M. J., Warshaw, A. L., Foitzik, Th., Schmidt, J., Hotz, H., Warshaw, A. L., Buhr, H. J., Klar, E., Heinisch, A., Kadow, R., Bioss, U., Schölmerich, J., Zimgibl, H., Leser, H. -G., Manes, G., Rabitti, P. G., Laccetti, M., Cavallera, A., Paceili, L., Gagiione, G., Uomo, G., Marinqhini, A., Zinsmeister, A. R., Melton, L. J., DiMagno, E. P., Marotta, F., Chui, D. H., Barbi, G., Zhong, G. G., Marotta, F., Chui, D. H., Tajiri, H., Bellini, O., Zhong, G. G., Barbi, G., McKay, C, Baxter, J. N., Imrie, C. W., Mithöfer, K., Fern’andez-delCastillo, C., Frick, T. W., Lewandrowski, K., Rattner, D. W., Warshaw, A. L., Pezzilli, R., Billi, P., Miniero, R., Gullo, L., Barakat, B., Migliuli, M., Rau, B., Schad, M., Schoenberg, M., Beger, H. G., Richter, F., Matthias, R., Sakagami, J, Kataoka, K, Ohta, A, Umehara, K, Imoto, M, Murase, M, Hosoda, M, Yamane, Y, Kato, M, Kashima, K, Ashihara, T, Schofield, D, Sharer, NM, Heywood, KM, Waters, HM, Braganza, JM, Scott, P, Sharer, NM, Bilton, D, Deardon, D, Lee, S, Taylor, PM, McCloy, RF, Braganza, JM, Shen, J., Shao, H., Wu, Z. P., Jin, J. J., Shiel, N, Cassidy, O, Sharma, H, Braganza, J. M., Soöckmann, F., Ahrens, J., Leonhardt, U., Otto, J., Ritzel, U., Ramadori, G., Tian, Fuzhou, Hu, JZ, Huang, DR, Wang, XH, Lian, HW, Zhang, BY, Miao, JG, Li, Xu, Zhou, HT, Uomo, G., Rabitti, P. G., Laccetti, M., Manes, G., Esposico, P., Perrocti, F., Visconci, M., Vaccaro, M. I., Dagrosa, M. A., Mora, M. I., Sordelli, D. O., Vogt, W., MeOmann, H., Heinisch, A., Linseis, A., Holstege, A., Schölmerich, J., Leser, H. -G., Weiser, M. R., Gibbs, S. A. L., Hechcman, H. B., Moore, F. D., Worthington, H. V., Runt, L. P., HcCloy, R. F., KacLennan, I. A., Braqanza, J. M., Heath, D, Alexander, D, Wilson, C, Larvin, M, Imrie, CW, McMahon, MJ, Larvin, M, Ward, J, Robinson, PJ, Chalmers, AG, McMahon, MJ, Apte, M, Wilson, J, McCaughan, G, Korsten, M, Norton, I, Piroia, R, Bimmler, D., Frick, T. W., Scheele, G. A., Bockman, Dale E., Büchler, Markus, Beger, Hans G., Cavallini, G., Brunori, M. P., Rigo, L., Bovo, P., Filippini, M., Vaona, B., Di Francesco, V., Frulloni, L., Marcori, M., Farri, P. C., Laardini, M. T., Pederzoli, P., Chowdhury, Riaz, Ochi, Koji, Mizushima, Takaaki, Tsurumi, Tetsuya, Harada, Hideo, Laver, P., Hoist, J. J., Ohe, M. v. d., Goebell, H., Mi Zumoto, A., Sarr, M. G., DiMagno, E. P., Moore, R., Frey, C. F., Debas, H. T., Mulvihill, S. J., Onizuka, S., Kuroda, H., Kuroda, Y., Hongo, H., Matsuzaki, S., Ito, M., Sekine, L., Tsunoda, T., Pap, ’A., Hrisztov, V., Pap, ’A., Marosi, E., Simon, K., Tak’acs, T., Pederzoli, P., Falconi, M., Bassi, C., Bonora, A., Talamini, G., Saivia, R., Benini, L., Caldiron, E., Vesentini, S., Cavallini, G., Raijman, Isaac, Kortan, Paul, Haber, Gregory B., Ramesh, H, Varghese, CJ, Schofield, D, Kay, PM, Bottiglieri, T, Uden, S, Bilton, D, Braganza, JM, Gut, A, Segal, I, Snehalatha, C, Mohan, V, Braganza, JM, Silva, E., Ceneviva, R., Velludo, M. A. L., Silvan, E., Ruebner, B., Ceneviva, R., Velludo, M. A. L., Roselino, J. E. S., Foss, M. C., Talaraini, G., Falcaoi, M., Frmlltai, L, K Fraacesca, V., Maxwi, M., Vaosa, B., Baro, P., Baxu, C., Pedercoli, P., Cavalliai, G., Taiamini, G., Iacano, C., Faicsai, M., Frulloni, L., Rige, L., Castagnisi, A., Marcori, M., Angelini, G., Bassi, C., Bom, P., Vaoss, B., Vantini, I., Sen, G., Pederzali, P., Cavallini, G., Štimee, B, Bulajič, M, Milosavljevi’c, T, Krsti’c, R, Markovi’c, M, Korneti, V, Ugljcš’c, M, Abruzzesse, IL, Evans, DB, Larry, L, King, T, Raijman, I, Roubein, L, Frazier, M, lacono, C., Faca, E., Falezza, G., Bonora, E., Aurola PP, Serio, G., lacono, C., Nicoli, N., Mansueto, G. C., Zicari, M., Marchiori, L., Mangiante, G., Seno, G., Imarnura, M., Yamauchi, H., Inoue, M., Onda, M., UchlDa, E., Almqtq, T., Yamanaka, Y., Kqbayashi, T., Yokqyama, T., Aida, K., Sasajima, K., Tajiri, T., Egami, K., Yamashita, K., Naitq, Z., Asano, G., Lewandrowski, K. B., Kirby, R. E., Southern, J. F., Compton, C. C., Warshaw, A. L., Lip, J, Strömmer, L, Permert, J, Larsson, J, Adrian, TE, Loftus, E. V., Adkins, M. C., Olivares-Pakzad, B., Batts, K. P., Stephens, D. H., Farnell, M. B., Sarr, H. G., Thompson, G. B., van Heerden, J. A., Kelly, D. G., Miller, L. J., Pearson, R. K., Clain, J. E., Petersen, B. T., DiMagno, E. P., Matsumoto, Cancer S., Chowdhury, R., Mizushima, T., Ochi, K., Harada, H., Miki, H., Ozkan, Hnsan, Saisho, Hiromitsu, Yarnaguchi, Taketo, Ishihara, Takeshi, Kikuchi, Yasuharu, Tsuyuguchi, Toshio, Ohto, Masao, Pasqual, C., Sperti, C., Liesai, G., Guido, M., Pedrazzoli, S., Sperti, C., Pasquali, C., Khajeturian, E., Guolo, P., Pedrazzoli, S., Tadokoro, H., Watanabe, S., Moriyoshi, Y., Yoshida, K., Shiratori, K., Takeuchi, T., Uchida, E., Onda, M., Tajiri, T., Egami, K., Yamashita, K., Aida, K., Yamanaka, Y., Kobayashi, T., Aimoto, T., Yokoyama, T., Inoue, M., Naito, Z., Asano, G., Valentich, M. A., Monis, B., Barotto, N. N., and Herrera, P.

Published
1994
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25. Homocysteine, folate, methylation, and monoamine metabolism in depression.

Author

Bottiglieri T, Laundy M, Crellin R, Toone BK, Carney MWP, Reynolds EH, Bottiglieri, T, Laundy, M, Crellin, R, Toone, B K, Carney, M W, and Reynolds, E H

Abstract

Objectives: Previous studies suggest that folate deficiency may occur in up to one third of patients with severe depression, and that treatment with the vitamin may enhance recovery of the mental state. There are, however, difficulties in interpreting serum and red cell folate assays in some patients, and it has been suggested that total plasma homocysteine is a more sensitive measure of functional folate (and vitamin B12) deficiency. Other studies suggest a link between folate deficiency and impaired metabolism of serotonin, dopamine, and noradrenaline (norepinephrine), which have been implicated in mood disorders. A study of homocysteine, folate, and monoamine metabolism has, therefore, been undertaken in patients with severe depression.Methods: In 46 inpatients with severe DSM III depression, blood counts, serum and red cell folate, serum vitamin B12, total plasma homocysteine, and, in 28 patients, CSF folate, S-adenosylmethionine, and the monoamine neurotransmitter metabolites 5HIAA, HVA, and MHPG were examined. Two control groups comprised 18 healthy volunteers and 20 patients with neurological disorders, the second group undergoing CSF examination for diagnostic purposes.Results: Twenty four depressed patients (52%) had raised total plasma homocysteine. Depressed patients with raised total plasma homocysteine had significant lowering of serum, red cell, and CSF folate, CSF S-adenosylmethionine and all three CSF monoamine metabolites. Total plasma homocysteine was significantly negatively correlated with red cell folate in depressed patients, but not controls.Conclusions: Utilising total plasma homocysteine as a sensitive measure of functional folate deficiency, a biological subgroup of depression with folate deficiency, impaired methylation, and monoamine neurotransmitter metabolism has been identified. Detection of this subgroup, which will not be achieved by routine blood counts, is important in view of the potential benefit of vitamin replacement. [ABSTRACT FROM AUTHOR]

Published
2000

27. High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial.

Author

Aisen PS, Schneider LS, Sano M, Diaz-Arrastia R, van Dyck CH, Weiner MF, Bottiglieri T, Jin S, Stokes KT, Thomas RG, Thal LJ, Alzheimer Disease Cooperative Study, Aisen, Paul S, Schneider, Lon S, Sano, Mary, Diaz-Arrastia, Ramon, van Dyck, Christopher H, Weiner, Myron F, Bottiglieri, Teodoro, and Jin, Shelia

Abstract

Context: Blood levels of homocysteine may be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophysiology by vascular and direct neurotoxic mechanisms. Even in the absence of vitamin deficiency, homocysteine levels can be reduced by administration of high-dose supplements of folic acid and vitamins B(6) and B(12). Prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline.Objective: To determine the efficacy and safety of B vitamin supplementation in the treatment of AD.Design, Setting, and Patients: A multicenter, randomized, double-blind controlled clinical trial of high-dose folate, vitamin B(6), and vitamin B(12) supplementation in 409 (of 601 screened) individuals with mild to moderate AD (Mini-Mental State Examination scores between 14 and 26, inclusive) and normal folic acid, vitamin B(12), and homocysteine levels. The study was conducted between February 20, 2003, and December 15, 2006, at clinical research sites of the Alzheimer Disease Cooperative Study located throughout the United States.Intervention: Participants were randomly assigned to 2 groups of unequal size to increase enrollment (60% treated with high-dose supplements [5 mg/d of folate, 25 mg/d of vitamin B(6), 1 mg/d of vitamin B(12)] and 40% treated with identical placebo); duration of treatment was 18 months.Main Outcome Measure: Change in the cognitive subscale of the Alzheimer Disease Assessment Scale (ADAS-cog).Results: A total of 340 participants (202 in active treatment group and 138 in placebo group) completed the trial while taking study medication. Although the vitamin supplement regimen was effective in reducing homocysteine levels (mean [SD], -2.42 [3.35] in active treatment group vs -0.86 [2.59] in placebo group; P < .001), it had no beneficial effect on the primary cognitive measure, rate of change in ADAS-cog score during 18 months (0.372 points per month for placebo group vs 0.401 points per month for active treatment group, P = .52; 95% confidence interval of rate difference, -0.06 to 0.12; based on the intention-to-treat generalized estimating equations model), or on any secondary measures. A higher quantity of adverse events involving depression was observed in the group treated with vitamin supplements.Conclusion: This regimen of high-dose B vitamin supplements does not slow cognitive decline in individuals with mild to moderate AD.Trial Registration: clinicaltrials.gov Identifier: NCT00056225. [ABSTRACT FROM AUTHOR]

Published
2008
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39. The switch mechanism and the bipolar/unipolar dichotomy.

Author

Carney, M. W. P., Chary, T. K. N., Bottiglieri, T., Reynolds, E. H., Carney, M W, and Chary, T K

Subjects
METHIONINE, CLINICAL trials, PLACEBOS, BIPOLAR disorder, HYPOMANIA, CEREBROSPINAL fluid, ADENOSYLMETHIONINE, COMPARATIVE studies, EMOTIONS, INTRAVENOUS injections, RESEARCH methodology, MEDICAL cooperation, ORAL drug administration, RESEARCH, EVALUATION research, RANDOMIZED controlled trials, THERAPEUTICS, PSYCHOLOGY
Abstract

During open trials of intravenous and oral S-adenosyl methionine (SAM) and a placebo-controlled trial of intravenous SAM in 29 patients, 25 patients had SAM and four had placebo (27 courses of SAM, two of the patients receiving two trials a piece). Nine of 11 bipolar patients (all SAM-treated) switched into elevated mood state (hypomania, mania and euphoria) and two did not respond. Six endogenous unipolar patients improved and five did not. No non-endogenous patient or placebo patient responded for more than 14 days. No unipolar patient switched into elated mood. In eleven (38%) trials and nine (33%) patients there was a switch from depression to elation. Biochemical data from the cerebrospinal fluid of eight patients suggested that the role of the dopaminergic system should be further explored. [ABSTRACT FROM AUTHOR]

Published
1989
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45. Cerebrospinal fluid S-adenosylmethionine in depression and dementia: effects of treatment with parenteral and oral S-adenosylmethionine.

Author

Bottiglieri, T, Godfrey, P, Flynn, T, Carney, M W, Toone, B K, and Reynolds, E H

Abstract

Cerebrospinal fluid (CSF) S-adenosylmethionine (SAM) levels were significantly lower in severely depressed patients than in a neurological control group. The administration of SAM either intravenously or orally is associated with a significant rise of CSF SAM, indicating that it crosses the blood-brain barrier in humans. These observations provide a rational basis for the antidepressant effect of SAM, which has been confirmed in several countries. CSF SAM levels were low in a group of patients with Alzheimer's dementia suggesting a possible disturbance of methylation in such patients and the need for trials of SAM treatment. [ABSTRACT FROM AUTHOR]

Published
1990

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