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The model for rofecoxib revealed a positive relationship with counts of MIs (rate ratio 1.14; 95 percent confidence interval, 1.09 to 1.19; P<0.001), explaining 28.7 percent of the deviance.
The model for celecoxib also revealed a significant positive relationship with counts of MIs (rate ratio 1.09; 95 percent confidence interval, 1.01 to 1.18; P = 0.022), explaining 5.2 percent of the deviance.
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Among n = 1,129 MPI scans that received an appropriate grading, 148 all-cause deaths, 109 MIs, 58 cardiac deaths, 152 caths, 113 revascularization procedures occurred over a mean follow-up period of 5.4 ± 1.2 years (0.9% cardiac death rate per year, 1.8% MI rate per year).
DE was associated with an 18.5% in-hospital mortality vs. 3.0% without DE (P < 0.01) and a 25.9% MI rate vs. 5.0% without DE (P < 0.01).
Most of these errors (75%) appeared in only nine parents-offspring pairs for which the MI rate ranged from 4% to 17%, suggesting laboratory errors (either traceability errors during the controlled pollination, plant material sampling and handling, wet lab experiment, or DNA contamination) rather than genotyping errors.
The MI rate for one marker is low.
The absolute MI rate in this meta-analysis was small, with 8/399 patients reporting an MI.
The MI rate is consistent with other RA reports [ 11], including a Danish study showing similar MI rates in patients with RA, diabetes or both [ 40].
In RENAAL, which included only type 2 diabetic patients with overt nephropathy [ 9], losartan alone reduced HF and marginally reduced MI rate.
Although rates of MI were initially reported as significantly increased by dabigatran [ 40], this trend has not persisted in later analyses, in which the MI rate was similar to that with warfarin [ 48].
Direct sequencing may underestimate the MI rate; however, our conservative over selection of potential MIs (all sequence traces with any sign of mixed types were subcloned) should compensate for this.
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