Fenofibrate May Reduce CVD in Statin-Treated T2DM Patients

HealthDay News — Fenofibrate therapy may reduce cardiovascular disease (CVD) in statin-treated patients with diabetes and dyslipidemia, according to a study published online in JAMA Cardiology.

Marshal B Elam, MD, PhD, from the Memphis Veterans Affairs Medical Center and University of Tennessee Health Sciences Center, and colleagues examined whether fenofibrate reduces CVD risk in statin-treated patients with type 2 diabetes. A total of 4644 Action to Control Cardiovascular Risk in Diabetes (ACCORD) Lipid Study participants were followed for an additional 5 years, for a total of 9.7 years.

The researchers found that following completion of ACCORD, only 4.3% of study participants continued fenofibrate treatment. Among participants originally randomized to fenofibrate or placebo, high-density lipoprotein and triglyceride values rapidly equalized. During 9.7 years of follow-up, the hazard ratio for the primary study outcome (composite of fatal and nonfatal myocardial infarction and stroke) among participants originally randomized to fenofibrate versus placebo (hazard ratio, 0.93; 95% CI, 0.83 to 1.05; P = 0.25) was comparable with that originally seen in ACCORD (hazard ratio, 0.92; 95% CI, 0.79 to 1.08; P = 0.32). For participants with dyslipidemia, fenofibrate therapy effectively reduced CVD (hazard ratio, 0.73; 95% CI, 0.56 to 0.95).

“The continued observation of heterogeneity of treatment response by baseline lipids suggests that fenofibrate therapy may reduce CVD in patients with diabetes with hypertriglyceridemia and low high-density lipoprotein cholesterol,” the authors write.

Several authors disclosed financial ties to the pharmaceutical industry; several pharmaceutical companies provided study medications, equipment, and supplies during ACCORD.

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Reference

  1. Elam MB, Ginsberg HN, Lovato LC, et al. Association of Fenofibrate Therapy With Long-term Cardiovascular Risk in Statin-Treated Patients With Type 2 Diabetes. JAMA Cardiol. 28 December 2016. doi: 10.1001/jamacardio.2016.4828.