Discrepancy in mortality found for patients with diabetes treated with clopidogrel

Issue: October 2012

Among patients with diabetes, clopidogrel treatment after MI led to lower reductions in all-cause death and CV death compared with patients without diabetes, according to recent study results.

Specifically, clopidogrel was associated with a RR reduction of 25% for all-cause mortality, 23% for CV mortality and 9% for both recurrent MI and all-cause mortality in patients without diabetes. But among patients with diabetes, there was a RR reduction of 11% for all-cause mortality and no significant reduction in CV mortality.

Researchers linked data from Danish nationwide administrative registries from 2002 to 2009 among patients who were hospitalized with MI and who had survived and not undergone CABG 30 days after discharge. The trial included 58,851 patients, 7,247 (12%) with diabetes and 35,380 (60%) who received clopidogrel.

In all, 1,790 patients (25%) with diabetes and 7,931 patients (15%) without diabetes met the composite endpoint of recurrent MI and all-cause mortality. Of these, 1,225 (17%) with and 5,377 (10%) without diabetes died. In addition, 978 patients (80%) with diabetes and 4,100 patients (76%) without diabetes died of CV events.

Deepak L. Bhatt

Patients with diabetes who were treated with clopidogrel had an unadjusted mortality rate (events per 100 person-years) of 13.4 (95% CI, 12.8-14) compared with 29.3 (95% CI, 28.3-30.4) for those not treated. After examining patients without diabetes who were treated with clopidogrel, researchers observed an unadjusted mortality rate of 6.4 (95% CI, 6.3-6.6) compared with 21.3 (95% CI, 21-21.7) for those not treated with the drug.

This study highlights the elevated risk of recurrent MI and CV mortality among patients with diabetes after MI, Deepak L. Bhatt, MD, MPH, professor of medicine at Harvard Medical School, Boston, and chief medical editor of Cardiology Today Intervention, wrote in an accompanying editorial.

“More needs to be done to reduce these risks among such patients,” he said. “At least a portion of this excess risk appears due to platelet activity and function and to the effects of antiplatelet medications in patients with diabetes. Therefore, in appropriately selected patients, intensification of the antiplatelet regimen may be one method by which their outcomes might be markedly improved.”

For more information:

Andersson C. JAMA. 2012;308:882-889.

Bhatt D. JAMA. 2012;308:921-922.

Disclosure: The study was funded by an internal research foundation grant from Department of Cardiology, Gentofte Hospital. Bhatt reported that he serves on the advisory board of Medscape Cardiology, on the boards of the Boston VA Research Institute and the Society of Chest Pain Centers, and on the executive committee of PEGASUS-TIMI 54; is chair of the American Heart Association Get With The Guidelines Science Subcommittee; has received honoraria from the American College of Cardiology, Duke Clinical Research Institute, Slack Publications, and WebMD; is a senior associate editor for the Journal of Invasive Cardiology ; has won grants from Amarin, AstraZeneca, Bristol-Myers Squibb, Eisai, Ethicon, Medtronic, sanofi-aventis, and The Medicines Company; has conducted unfunded research for FlowCo, PLx Pharma, and Takeda; and served as the international principal investigator for the CHARISMA trial, on the steering committee, and as a national coordinator for the TRILOGY trial. Køber reported that he has received honorarium as speaker for Servier. Torp-Pedersen reported that he has served on advisory boards and served on study steering committees for Cardiome, Sanofi and Merck; and has obtained research grants from Bristol-Myers Squibb, and Sanofi. Andersson reported receiving a month's salary for work on the study.