Homocysteine Hypothesis for Atherothrombotic Cardiovascular Disease
Not Validated
Sanjay Kaul, MD*, ,*,
Andrew A. Zadeh, MD*, and
Prediman K. Shah, MD*,
* Division of Cardiology, Cedars-Sinai Medical Center
David Geffen School of Medicine, University of California, Los Angeles, California Drs. Kaul and Zadeh contributed equally to this work.
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Figure 1 Outline of methionine/homocysteine metabolism, causes of hyperhomocysteinemia, and therapeutic options for lowering homocysteine. Vitamin coenzymes and substrates: THF, tetrahydrofolate; B2, riboflavin; B6, vitamin B6 as its biologically active form, i.e., pyridoxal 5'-phosphate; and B12, methyl cobalamin. Intermediate metabolite: DMG, dimethylglycine. Adapted, with permission, from Malinow et al. (48).
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Figure 2 Bayesian analysis of the HOPE-2 trial. Triplots showing posterior (thick line) distributions derived from integrating evidence or likelihood (thin line) from the HOPE-2 trial and informative priors (dashed line) based on information derived from the NORVIT study (only data from comparison of combination therapy group vs. placebo are utilized to match the HOPE-2 trial treatment groups; see Table 3 for details) according to Bayes' theorem (44). Posterior probabilities are estimated using priors for the primary composite end point of death from cardiovascular cause, myocardial infarction (MI), and stroke (log odds ratio µ = 0.206, standard deviation  = 0.115), death from any cause (µ = 0.183, = 0.153), myocardial infarction (µ = 0.219, = 0.122), and stroke (µ = –0.246, = 0.293). Probability of any effect size is calculated by computing area under the curve. The probabilities of benefit (Pb, log odds ratio <0) or harm (Ph, log odds ratio >0) are shown on the right of each plot. Superiority or inferiority is inferred at a posterior probability of benefit or harm >0.950.
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