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Excess Mortality in ACCORD Study Not Due to Low A1C

Last Updated: April 28, 2010.

 

Analysis finds that in intensive treatment arm, risk was actually greater with higher A1C

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A post hoc analysis of mortality data from the Action to Control Cardiovascular Risk in Diabetes study has determined that rapid glucose lowering and maintenance of lower A1C levels through intensive control -- as opposed to a standard strategy -- was not the cause of increased death rates in that arm of the study, according to research published in the May issue of Diabetes Care.

WEDNESDAY, April 28 (HealthDay News) -- A post hoc analysis of mortality data from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study has determined that rapid glucose lowering and maintenance of lower A1C levels through intensive control -- as opposed to a standard strategy -- was not the cause of increased death rates in that arm of the study, according to research published in the May issue of Diabetes Care.

Matthew C. Riddle, M.D., of the Oregon Health and Science University in Portland, and colleagues performed a multivariate analysis of data obtained over a median 3.4 years of follow-up of 10,251 patients with diabetes in the ACCORD study, which was stopped early because of excess mortality in the intensive treatment arm of the study. The participants had been randomized to the intensive treatment strategy (targeting A1C less than 6 percent) or the standard strategy (targeting A1C 7 to 7.9 percent).

The researchers found that higher average on-treatment A1C predicted mortality more strongly than first-year decrease in A1C or A1C for the last follow-up interval. The risk of death increased approximately linearly as A1C increased from 6 to 9 percent. Only when the average A1C was greater than 7 percent did there appear to be a higher risk of death in the intensive arm compared to the standard arm of the study.

"These findings confirm the earlier report warning of increased risk of death associated with the intensive treatment strategy in ACCORD, but they suggest that low A1C is unlikely to be a primary mediator of this risk. They do not support the hypothesis that overly rapid reduction of A1C from high levels increases risk of death. In fact, the opposite relationship was observed," the authors write.

Various companies provided medications, equipment or supplies for the study; several authors disclosed financial relationships with these and other pharmaceutical or medical device companies.

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